A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R EFERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright Ó2003 by ICON Group International, Inc. Copyright Ó2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Leukemia: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83711-2 1. Leukemia-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on leukemia. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications.
Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes & Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON LEUKEMIA ................................................................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Leukemia ....................................................................................... 5 E-Journals: PubMed Central ....................................................................................................... 63 The National Library of Medicine: PubMed ................................................................................ 97 CHAPTER 2. NUTRITION AND LEUKEMIA ..................................................................................... 187 Overview.................................................................................................................................... 187 Finding Nutrition Studies on Leukemia .................................................................................... 187 Federal Resources on Nutrition ................................................................................................. 202 Additional Web Resources ......................................................................................................... 202 CHAPTER 3. ALTERNATIVE MEDICINE AND LEUKEMIA ............................................................... 205 Overview.................................................................................................................................... 205 National Center for Complementary and Alternative Medicine................................................ 205 Additional Web Resources ......................................................................................................... 235 General References ..................................................................................................................... 240 CHAPTER 4. DISSERTATIONS ON LEUKEMIA ................................................................................. 241 Overview.................................................................................................................................... 241 Dissertations on Leukemia ......................................................................................................... 241 Keeping Current ........................................................................................................................ 248 CHAPTER 5. CLINICAL TRIALS AND LEUKEMIA ........................................................................... 249 Overview.................................................................................................................................... 249 Recent Trials on Leukemia ......................................................................................................... 249 Keeping Current on Clinical Trials ........................................................................................... 271 CHAPTER 6. PATENTS ON LEUKEMIA............................................................................................ 273 Overview.................................................................................................................................... 273 Patents on Leukemia .................................................................................................................. 273 Patent Applications on Leukemia .............................................................................................. 303 Keeping Current ........................................................................................................................ 340 CHAPTER 7. BOOKS ON LEUKEMIA ............................................................................................... 343 Overview.................................................................................................................................... 343 Book Summaries: Federal Agencies............................................................................................ 343 Book Summaries: Online Booksellers......................................................................................... 345 The National Library of Medicine Book Index ........................................................................... 360 Chapters on Leukemia ................................................................................................................ 361 CHAPTER 8. MULTIMEDIA ON LEUKEMIA .................................................................................... 363 Overview.................................................................................................................................... 363 Video Recordings ....................................................................................................................... 363 Audio Recordings....................................................................................................................... 364 Bibliography: Multimedia on Leukemia..................................................................................... 364 CHAPTER 9. PERIODICALS AND NEWS ON LEUKEMIA ................................................................. 367 Overview.................................................................................................................................... 367 News Services and Press Releases.............................................................................................. 367 Newsletter Articles .................................................................................................................... 371 Academic Periodicals covering Leukemia .................................................................................. 372 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 373 Overview.................................................................................................................................... 373 U.S. Pharmacopeia..................................................................................................................... 373 Commercial Databases ............................................................................................................... 376 Researching Orphan Drugs ....................................................................................................... 377
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APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 385 Overview.................................................................................................................................... 385 NIH Guidelines.......................................................................................................................... 385 NIH Databases........................................................................................................................... 387 Other Commercial Databases..................................................................................................... 390 The Genome Project and Leukemia ............................................................................................ 390 APPENDIX B. PATIENT RESOURCES ............................................................................................... 397 Overview.................................................................................................................................... 397 Patient Guideline Sources.......................................................................................................... 397 Associations and Leukemia ........................................................................................................ 406 Finding Associations.................................................................................................................. 407 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 409 Overview.................................................................................................................................... 409 Preparation................................................................................................................................. 409 Finding a Local Medical Library................................................................................................ 409 Medical Libraries in the U.S. and Canada ................................................................................. 409 ONLINE GLOSSARIES ................................................................................................................ 415 Online Dictionary Directories ................................................................................................... 417 LEUKEMIA DICTIONARY ......................................................................................................... 419 INDEX .............................................................................................................................................. 515
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with leukemia is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about leukemia, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to leukemia, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on leukemia. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to leukemia, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on leukemia. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON LEUKEMIA Overview In this chapter, we will show you how to locate peer-reviewed references and studies on leukemia.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and leukemia, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “leukemia” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: ·
Chronic Lymphocytic Leukemia of B-Cell Origin: Oral Manifestations and Dental Treatment Planning Source: JADA. Journal of American Dental Association. 128(2): 206-210. February 1997. Summary: Chronic lympocytic leukemia, or CLL, is the most common form of leukemia in the Western Hemisphere, accounting for approximately 30 percent of all cases. With patients having an expected life span of more than seven years, CLL is a relatively indolent hematologic malignant disease that, while incurable, often has a prognosis compatible with relatively normal dental treatment planning. In this article, the authors present four case reports of CLL in a dental setting. The authors provide an update on the diagnosis, prognosis, and dental treatment of patients with CLL of B-lymphocyte origin. Surgical considerations for procedures such as tooth extraction, periodontal surgery, apical surgery, and implant surgery in patients in beginning or intermediate
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stages of CLL usually are dictated by the patient's desires, masticatory needs, and expected life span, rather than by inherent characteristics of the hematologic malignancy. 1 table. 15 references. (AA-M). ·
Gingival Hyperplasia Complicating Acute Myelomonocytic Leukemia Source: Journal of the Canadian Dental Association. 66(2): 78-79. February 2000. Contact: Canadian Dental Association. 1815 Alta Vista Drive, Ottowa, ON K1G 3Y6. (613) 523-1770. E-mail:
[email protected]. Website: www.cda-adc.ca. Summary: Many systemic illnesses show clinical signs in the oral cavity. This article presents a case report of gingival hyperplasia (overgrowth) that was the first symptom of the presence of acute myelomonocytic leukemia (AML FAB M4). The authors review the oral manifestations of acute leukemia. The authors note that gingival hyperplasia is secondary to infiltration of the gingival tissue with leukemia cells and is well described in the literature. Generally, gingival hyperplasia resolves completely or at least partly with effective leukemia chemotherapy. This case reminds dentists and physicians of the importance of recognizing mucocutaneous manifestations of systemic diseases. 2 figures. 10 references.
·
Risky Decision Making and Allocation of Resources for Leukemia and AIDS Programs Source: Health Psychology; Vol. 12, No. 2. Contact: University of Iowa, Department of Psychology, Iowa City, IA, 52242. Summary: The goal of this study was to apply established judgement and decisionmaking paradigms to identify and understand underlying reactions to persons with AIDS compared with persons with another, less responsibility-laden, blood disease, leukemia. In the first experiment, each subject responded to treatment options for either leukemia or AIDS but did not compare the two. In the second experiment, the subjects were asked to consider treatment programs that would affect both AIDS patients and leukemia patients. In the third part of the study, subjects evaluated treatment programs described by both the number of leukemia patients saved and by the number of AIDS patients saved. In all three cases the subjects were psychology students. The results indicate a preference for less risky treatment options with positively framed information and a preference for saving the lives of leukemia patients over AIDS patients.
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Acute Promyelocytic Leukemia in Crohn's Disease Source: Journal of Clinical Gastroenterology. 13(3): 325-327. June 1991. Summary: This article presents a case study of a 19-year-old man with a documented 2year history of Crohn's disease who abruptly developed leukopenia and thrombocytopenia. A diagnosis of acute promyelocytic leukemia was established by bone marrow cytology. Chromosomal analysis of bone marrow aspirate was performed. The authors note that nine cases of Crohn's disease complicated by leukemia have been reported, including the present one; once again, a relationship between Crohn's disease and leukemia is suggested. 1 figure. 10 references. (AA).
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Incidence of Oral Complications and Application of a Preventive Protocol in Children with Acute Leukemia Source: SCD. Special Care in Dentistry. 18(5): 189-193. September- October 1998.
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Contact: Available from Special Care Dentistry. 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2660. Fax (312) 440-2824. Summary: This article reports on a prospective, controlled study that was designed to assess the effectiveness of a preventive oral protocol in children receiving antineoplastic treatment for acute lymphoblastic leukemia (ALL). During a 13 month period, 96 children from one to sixteen years of age with a diagnosis of ALL were evaluated. When the study was initiated, 60 patients already undergoing chemotherapy received palliative treatment for complications (Group 1). Thirty-six children (Group II) with newly diagnosed ALL received a daily preventive protocol consisting of elimination of bacterial plaque, application of a mouthwash with a nonalcoholic solution of chlorhexidine 0.12 percent, and topical application of iodopovidone, followed by 'swish and swallow' with nystatin 500,000 units. Children in both groups were examined every 7 to 14 days by the pediatric dentistry team. The authors found a significant improvement in oral hygiene and a significant decrease in the incidence of mucositis grade 2 and oral candidiasis in the Group II children. These findings show that the systematic application of a preventive protocol significantly reduces the incidence of oral complications. The results of the study identify a need to include a pediatric dentist in a multidisciplinary team which provides oral care for cancer patients. 5 tables. 33 references. (AA). ·
Oral Hairy Leukoplakia in a Patient with Acute Lymphocytic Leukemia Source: Oral Diseases. 5(1): 76-79. January 1999. Contact: Available from Stockton Press. Marketing Department, Houndmills, Basingstoke, Hampshire RG21 6XS, United Kingdom. (800) 747-3187. Summary: This article reports the first case of oral hairy leukoplakia (OHL) in an HIV negative 56 year old patient with acute lymphocytic leukemia (ALL). A white plaque was observed while the patient was in complete remission following chemotherapy scheme. The clinical and histopathologic findings were typical for OHL and the polymerase chain reaction method was positive for Epstein Barr virus DNA. The authors concludes that underdiagnosis and underreporting of OHL in patients with a malignant hematological disease and the apparent different environmental factors to which these non-AIDS patients have been exposed, probably constitute some of the reasons for the very few OHL cases reported in these patients. The patient, after the excisional biopsy, received prophylactic antibiotics and acyclovir and had an uneventful recovery. Careful examination of patients with a malignant hematological disease or other immunodeficiency state is suggested, in order to add knowledge to the biologic mechanisms and behavior of OHL. 3 figures. 30 references.
Federally Funded Research on Leukemia The U.S. Government supports a variety of research studies relating to leukemia. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable
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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to leukemia. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore leukemia. The following is typical of the type of information found when searching the CRISP database for leukemia: ·
Project Title: A NON MAMMALIAN MODEL FOR HUMAN ALL Principal Investigator & Institution: Walker, Charles W.; Zoology; University of New Hampshire Service Building Durham, Nh 038243585 Timing: Fiscal Year 2001; Project Start 01-MAY-2001; Project End 31-MAR-2003 Summary: The investigators take advantage of naturally occurring disease in the softshelled clam Mya arenaria. This leukemia: 1) is fatal; 2) occurs at high frequency in the wild (five-to-sixty percent); 3) is transferable to normal clams and; 4) is remarkably similar to human ALL-L3 (Burkitt's leukemia) in the morphology, behavior and cytochemistry of the leukemia cells, in the structure and expression of the p53 gene and in its response to etoposide. In preparation for this study, we have developed a mass culture system for clam leukemia cells and are the first to clone and determine expression patterns for clam c-ras and p53. Clam p53 has a binding site for MDM2 and its transcriptional activation domain is seventy-three percent conserved compared to human p53 protein. This suggests that downstream genes involved in the cell cycle and in apoptosis should also be transcriptional targets for clam p53. Much remains to be learned about this emerging leukemia model. We will use clam blood to address three specific aims that should expedite our understanding of genes involved in this disease and should help to either further validate or to discount this model. The investigators will: 1) Determine the cytotoxicity for clam leukemia of compounds widely employed in human ALL chemotherapy; 2) Determine the cytotoxicity of novel compounds that target p53 or related molecules involved in the cell cycle and/or apoptosis and; 3) Perform mutational analysis of clam p53, c-ras and c-myc. For the first two of these objectives, high throughput cytotoxicity screening will initially be accomplished using microtiter plates. Compounds that show activity against clam leukemia cells will be further tested using larger scale, parallel in vitro and in vivo clam assays for cell and organism viability, p53 expression and apoptosis. Mutational analysis using mismatch detection should reveal mutations in three genes that often cooperate during transformation inhuman leukemia. Clam leukemia offers significant advantages over currently available models for the following reasons: a) It provides an in vitro and in vivo alternative to the relatively few human leukemia cells lines; b) Populations of leukemic clams are more similar to an outbreeding, human clinical population than are those generated from inbred mouse strains or by intentional exposure to know tumor viruses; c) While existing fly and worm models have versions of some human cancer genes that contain naturally occurring or inducible mutations, resulting tumors characteristically affect embryonic and not adult somatic cells (which do not divide in these organisms) and; d) Clams have highly conserved homologs for human c-ras and p53 genes. Homologs for p53 have not yet been identified in any other non-vertebrate models, including yeast. Data that we generate in this study should point out p53related molecular mechanisms that are held in common with human ALL.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: AML1 IN NORMAL AND LEUKEMIC CELLS Principal Investigator & Institution: Downing, James R.; St. Jude Children's Research Hospital Memphis, Tn 381052794 Timing: Fiscal Year 2001; Project Start 01-AUG-1996; Project End 31-MAY-2006 Summary: The AML1/CBFbeta transcription factor complex is one of the most frequent targets of genetic alterations in human acute leukemia, being targeted in up to one-third of acute myeloid and lymphoblastic leukemia by either chromosomal induced rearrangements, or point mutation. Prior work from my laboratory has demonstrated that AMNL1 normally functions as a master regulatory transcriptional switch that is essential for the formation of the definitive hematopoietic systems. In our preliminary data, we now extend this observation to show that AML1/CBFbeta establishes, in a dose-dependent manner, a transcriptional cascade that is required for the formation of definitive hematopoietic stem cells (HSCs) in the aorta-gonad mesonephros region (AGM) of the developing embryo. Moreover, subtle alterations in the level of AML1/CBFbeta induces dramatic changes in the temporal and spatial generation of HSCs, shifting them from their normal position in the AGM to the yolk sac. The initiation of leukemia by chromosomal rearrangement-induced-induced alteration in ABL1/CBFbeta appears to result at least in part, from a partial dominant negative inhibition of normal AML1/CBFbeta, leading to alterations in the self-renewal and maturation of HSCs. Importantly, however, our preliminary data clearly demonstrates that AML1-ETO alone is insufficient to induce leukemia, but rather must cooperate with secondary genetic alterations to transform HSC. Based on these observations, our working hypothesis is that a certain threshold level of AML1/CBFbeta is required for the function of HSC. Genetic changes that decrease the activity of the complex below this level directly alter HSC growth, leading to a pool of "pre-leukemic) cells that must acquire secondary mutations before they can generate a full leukemic phenotype. To directly address this hypothesis, experiments are proposed in Specific Aim 1 that will utilize a conditional AML1-ETO knock in-mouse that was recently generated in my laboratory to define the spectrum of secondary mutations able to cooperate with AML1ETO to induce leukemia. In Specific Aim 2, we will extend these studies to determine how AML1 mutations identified in familial and sporadic cases of AML predispose to leukemia through the generation of mice containing these mutations in their germline. Together these studies should provide critical insights into the molecular pathology of the core-binding factor leukemia. Moreover, the murine models developed through these efforts should prove to be valuable reagents through which to assess the potential therapeutic use of drugs targeted toward either AML1-ETO or its bound nuclear corepressors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ANTIGEN-PRESENTING FUNCTION OF CD1 MOLECULES Principal Investigator & Institution: Brutkiewicz, Randy R.; Assistant Professor; Microbiology and Immunology; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2005 Summary: (provided by applicant): A fundamental understanding of the mechanisms involved in the processing of antigens and their presentation to cells of the immune system is critical to the design of new and more effective treatments against cancer and
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other diseases. Analyses of antigen processing, presentation and host defense have focused on studying pathways in which proteins are degraded into small peptides that are subsequently presented to the immune system. Recently, a novel pathway for antigen presentation to T cells by the major histocompatibility complex class I-like molecule, CD1, has been identified. CD1 molecules have been shown to present glycolipids, such as those derived from Mycobacterium species, rather than peptides, to T cells. Murine and human CD1d molecules are recognized by a novel subpopulation of T cells called NKT cells. NKT cells produce both Th1 and Th2 cytokines and appear to be important in regulating and/or mediating immune responses to pathogens, as well as to cancer. CD1 molecules are expressed on the surface of hematopoietic cells (e.g., T cells, B cells, macrophages) and are found on a number of T and B cell lymphomas and leukemias. Our hypothesis is that alterations in the natural glycolipid ligands bound to CD1 in hematopoietic tumor cells affect their recognition by NKT cells. To test this hypothesis, the following specific aims are proposed: 1. Assess the role of the intracellular trafficking and cell surface turnover of CD1 molecules in their recognition by NKT cells, 2. Determine the endogenous ligands in representative murine CD1+ T cell lymphoma and B cell leukemia cells, and 3. Analyze the in vitro and in vivo antitumor activity of NKT and NK cells against murine CD1+ hematopoietic tumor cells. Alterations in CD1-bound glycolipid antigens may play important roles in the ability of these tumors to evade the host's antitumor immune response. The proposed studies will also have wide-ranging applications in the development of novel treatments aimed not only at CD1 hematopoietic tumor cells, but also infectious diseases and autoimmunity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ANTILEUKEMIA ACTIVITY OF PERILLYL ALCOHOL Principal Investigator & Institution: Clark, Steven S.; Human Oncology; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2001; Project Start 01-JAN-2000; Project End 31-DEC-2003 Summary: The Bcr/Abl oncogene encodes a tyrosine kinase that is expressed in leukemias that carry the Philadelphia chromosome translocation (Ph+). The kinase interacts with different cell signaling pathways to cause factor-independent growth, resistance to apoptosis and oncogenic transformation. These pleiotropic activities of Bcr/Abl affect the pathogenesis of Ph+ leukemias by inhibiting the normal rate of cell death and by enabling Ph+ cells to resist conventional chemotherapy that induces apoptosis in other leukemias. A central hypothesis of this proposal is that inhibition of signaling pathways downstream of the Bcr/Abl kinase should render leukemia cells dependent on growth factors and sensitive to apoptosis. Perillyl alcohol (POH) belongs to a new family of chemotherapy agents and has shown excellent therapeutic rations in rodent carcinoma models. The range of potential anti-tumor activities of POH overlaps with some signaling pathways that are affected by the Bcr/Abl kinase. Thus, POH is a logical compound to test for anti- leukemia activity in Bcr/Abl-induced leukemia. Preliminary experiments demonstrated that in Bcr/Abl-transformed cells, POH rapidly induced G1 arrest and apoptosis. In contrast, Bcr/Abl- transformed cells were resistant to apoptosis induced by different conventional chemotherapy agents. This anti-leukemia activity of POH closely correlated with inhibition of the Raf-ERK signaling pathway downstream of Bcl/Abl. On the other hand, POH treatment did not affect other Bcr/Abl signals that are responsible for maintaining expression of c- Myc. Normally, expression of c-Myc is cell cycle regulated, however, when c-Myc expression is enforced during G1 arrest, cells undergo apoptosis. Therefore, POH may uncouple a Bcr/Abl signaling
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pathway through Raf that is necessary for maintaining cell growth, while not affecting other Bcr/Abl signals that induce constitutive c-Myc expression. This combination may lead to apoptosis in leukemia cells. This model will be evaluated further by examining 1) the role of the Bcr/Abl oncogene in sensitizing cells to POH, 2) how POH affects signaling through Raf, and 3) whether POH induces Myc-dependent apoptosis in leukemia cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: APE CHEMO/RADIOTHERAPY
EXPRESSION/LEUKEMIA
RESPONSE
TO
Principal Investigator & Institution: Robertson, Kent A.; Associate Professor of Pediatrics; Pediatrics; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2001; Project Start 01-AUG-1998; Project End 31-MAY-2003 Summary: DNA damage in the form of apurinic/apyrimidinic (AP) sites is induced by cytotoxic agents resulting in base substitution mutations and blocks to DNA replication. The DNA base excision repair (BER) enzyme, AP endonuclease (APE), is a multifunctional protein involved in DNA base excision repair, oxidative signaling, transcription factor regulation, cell cycle control, and apoptosis. APE is essential for the repair of AP sites thus maintaining cellular and genetic integrity. Deficient expression of APE results in a heightened sensitivity to radiation and alkylating agents with resultant tissue damage. Logically it follows that APE may also play a role in the sensitivity to malignant cells to DNA damaging therapeutic agents. Many cancer therapeutic agents will induce apoptosis or programmed cell death, however little is known about the relationship of DNA repair enzymes (particularly BER) and apoptosis. Preliminary observations indicating that APE expression can be suppressed in myeloid leukemia cells by retinoic acid or DMSO while inducing apoptosis, has led to the hypothesis that: Decreased expression of APE is functionally related to apoptosis in myeloid leukemia cells. The specific aims are: Specific Aim #1 What is the relationship of APE expression to myeloid leukemia cell differentiation and apoptosis? Specific Aim 2: What is the role of APE protein phosphorylation in APE expression, function and apoptosis. Specific Aim #3: Determination of the molecular mechanisms that are responsible for downregulation of APE expression upon induction of apoptosis. We propose to initiate studies on the relationship of APE expression and phosphorylation to cell differentiation, apoptosis, and sensitivity to cytotoxic agents, with the long-term goal of developing ways to enhance the chemo/radio sensitivity of leukemia cells by manipulating expression of APE. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ARSENIC BASED THERAPY OF BCR ABL POSITIVE LEUKEMIAS Principal Investigator & Institution: Bhalla, Kapil N.; Professor of Medicine; Moffitt Cancer Center; University of South Florida 4202 E Fowler Ave Tampa, Fl 33620 Timing: Fiscal Year 2001; Project Start 15-JUN-2001; Project End 31-MAY-2004 Summary: The leukemic clone in virtually all of the patients with chronic myeloid leukemia with blast crisis (CML-BC) and approximately one-third of the adults with acute lymphoblastic leukemia (ALL) expresses the bcr-abl fusion gene encoded p210 and p185 Bcr-Abl tyrosine kinase (TK), respectively. Although the chemotherapeutic regimens or bone marrow stem cell transplantation employed against acute leukemias can also produce complete remissions in Bcr-Abl positive ALL and CML-BC, these
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remissions are not durable and the overall clinical outcome remains dismal. This creates a strong rationale to test novel strategies in this clinical setting. Arsenic Trioxide (As2O3 or AT) is clinically active against relapsed or refractory acute promyelocytic leukemia (APL), where it downregulates the levels of the fusion protein PML-RARdelta causing partial differentiation and apoptosis of APL cells. Recently, we have demonstrated that clinically achievable levels of AT can also reduce p210 or p185 Bcr-Abl fusion protein levels and induce apoptosis of CML-BC cells. Based on these findings, we propose to conduct a Phase II clinical-pharmacologic trial of AT (NCI/CTEP sponsored) as the induction therapy for relapsed and refractory; Bcr-Abl positive adult ALL and CML-BC. In vitro studies on the patient derived leukemic blasts are proposed to determine the molecular correlates of the clinical response and apoptosis induced by AT. We have also shown that STI571, a relatively specific inhibitor of Bcr-Abl TK activity, induces differentiation and apoptosis of Bcr-Abl positive leukemic cells. Therefore, we also propose to investigate the in vitro apoptotic and differentiation effects of a combination of AT and STI571 in Bcr-Abl positive leukemic blasts. The specific aims of this proposal are: AIM 1: To determine the clinical efficacy, i.e., the rate and duration of clinical and hematologic response and overall survival, secondary to treatment with daily intravenous AT in adult patients with Philadelphia chromosome (bcr-abl fusion gene) positive relapsed or refractory ALL or CML-BC. AIM 2: To determine the pharmacokinetic parameters of AT, i.e., AUC and Css and correlate these with the clinical and cytogenetic response in patients with Bcr-Abl positive ALL or CMLBC. AIM 3: To correlate the clinical response to AT with the decline in the bcr-abl mRNA levels determined by real-time RT-PCR. AIM 4: To correlate the clinical and in vivo molecular response to AT with AT-induced in vitro downregulation of Bcr-Abl and Akt protein levels, histone hyperacetylation as well as differentiation and apoptosis, utilizing the pre-treatment samples of leukemic blasts. AIM 5: To determine the in vitro differentiation and apoptotic effects of STI-571 alone and in combination with AT in the pre-treatment samples of Bcr-Abl positive leukemic blasts. These in vitro and in vivo studies are designed to evaluate AT-based novel strategies against Bcr-Abl positive human leukemias. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: BENZODIAZEPINE RECEPTOR AND DRUG RESISTANCE IN AML Principal Investigator & Institution: Banker, Deborah E.; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2003 Summary: We are investigating molecular bases of drug resistance as markers of clinical outcome in acute myeloid leukemia (AML) and testing various drug-sensitizing strategies in hopes of improving cure rates for patients with this disease. Relevant chemotherapeutics induce apoptosis and leukemic blasts become drug resistant by downregulating apoptotic responses to these drugs. As a result of anti-apoptotic activities, expression of Bcl-2 family proteins is associated with failure to achieve remission, with short disease-free survival, and with drug-resistant relapse in AML. Bcl2 proteins are constituents of mitochondrial pore complexes (PTPC) where they block apoptosis by antagonizing mitochondrial pore dissolution that otherwise occurs after lytotoxic treatments. Like Bcl-2, peripheral benzodiazepine receptors (pBzR) reside in PTPC of normal and leukemic blood cells and can protect transfected leukemia cells from apoptosis. However, the association of pBzR expression with clinical outcome has not been directly tested. If high pBzR expression predicts clinical failures in AML, pBzR would be a rational target for molecular anti-leukemia therapies. PK11195 is a high-
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affinity pBzR antagonist that can block the PTPC protection afforded by Bcl-2 proteins, and can thereby overcome drug resistance. However, whether pBzR or Bcl-2 expresson levels determine the efficacy of PK11195 is unknown. We propose laboratory analyses that will determine the variability of BzR expression in a large number of cell samples collected from AML patients in IRB-approved clinical trials from which complete clinical data is available. We will use standard statistical analyses to determine whether pBzR is an independent prognostic marker in AML. We also propose laboratory analyses of PK11195 efficacy in primary AML cell samples treated with different relevant drugs and in isogenic cell lines over-expressing different anti-apoptotic proteins. NOD/SCID mice will be used as an in vivo model to further test PK11195 efficacy in sensitizing engrafted AML cells. In vitro analyses of normal bone marrow samples and of non-leukemia cells in engrafted mice will examine possible PK11195 toxicities: Data collected in these studies will improve our understanding of the molecular bases of drug resistance in AML. Furthermore, if drug-sensitizing by PK11195 is documented and low toxicity is confirmed in these experiments, novel treatment strategies that include PK11195 will be warranted for AML. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: BIOCHEMICAL STRATEGIES TO INCREASE LEUKEMIA RESPONSE Principal Investigator & Institution: Gandhi, Varsha; Associate Professor; Clinical Investigation; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2002; Project Start 15-SEP-1992; Project End 31-JUL-2006 Summary: (provided by applicant): This proposal is an extension of CA57629 that has been focused on understanding the metabolism, mechanism of action, and interaction of nucleoside analogs. With the success rate of analogs in leukemias, several laboratories including ours have investigated the mechanisms of cell death by these agents. The steps include formation of triphosphate of the analog, incorporation into replicating DNA, inhibition of ribonucleotide reductase (with newer analogs) and finally inhibition of DNA synthesis. Continued inhibition of DNA synthesis proceeds to cell death through apoptosis. When tested in cell lines, which are actively cycling and replicating DNA, such scenario seems to be in place. However, when one tries to validate this process during therapy, the outcome is conflicting and intriguing. The biology of leukemia cells in the body is very different from cell lines in culture. Leukemia cells in peripheral blood are generally non- or slow- cycling and with a very small percent of cells in S-phase (0-5%). Nonetheless after 5-days of effective nucleoside analog therapy, there is a massive cytoreduction (1 to 3-log decrease). Our hypothesis is built around these premises to suggest that in addition to conventional S-phase mediated pathway, there may he additional pathways that result in non-S-phase cell death during therapy. To test this hypothesis, we want to pursue three specific aims that are focused toward different mode of cell death by analogs. First, we plan to define the elements of cell death caused by conventional DNA synthesis inhibition pathway during therapy. Using nelarabine and clofarabine, two of the most successful new nucleoside analogs in the clinic, we plan to investigate the role of cellular pharmacokinetics and cellular pharmacodynamics in cell death. These parameters will be compared with clinical response to these therapies. Second, we plan to identify mitochondria induced cell death of leukemia cells during therapy. Nucleoside analogs may affect mitochondria directly and/or indirectly to induce cell death in circulating leukemia cells during therapy. Direct effect such as mitochondrial respiratory function involving ATP synthase, adenosine nucleotide translocator (ANT), and early decrease in mitochondnal
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membrane potential will be accessed to elucidate the role of mitochondria induced apoptosis. Indirect effect will include release of cytochrome c, and late effect on membrane potential. Finally, we will investigate the role of receptor-mediated cell death of leukemia cells during therapy. Following our lead in cell lines that analog incorporation results in induction of fas ligand followed by fas-mediated cell death of non-Sphase population, we plan to pursue the role of fas in cell death during therapy. We feel that knowledge gained through these aims will assist us in designing optimal therapy of leukemia with nucleoside analogs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: BIOMARKERS OF TREATMENT RELATED LEUKEMIA Principal Investigator & Institution: Felix, Carolyn A.; Associate Professor; Children's Hospital of Philadelphia 34Th St and Civic Ctr Blvd Philadelphia, Pa 19104 Timing: Fiscal Year 2001; Project Start 01-FEB-2000; Project End 31-JAN-2005 Summary: (Adapted from the investigator's abstract) The objective of this work is to develop new avenues to identify undergoing anticancer therapy who are at increased risk of leukemia as a treatment complication and to facilitate detection of the leukemic clone earlier in the course of the disease. For children with metastatic neuroblastoma receiving N6 therapy, the incidence of leukemia is 7%. About 40% of cases are related to alkylating agent therapy and have chromosome 5 and/or 7 loss; about 40% have translocation of the MLL gene at chromosome band 11q23, which occurs in leukemias related to DNA topoisomerase II inhibitors. Because of its efficacy against neuroblastoma, N6 therapy will be incorporated into the high-risk neuroblastoma trial for the Children's Cancer Group. Etoposide, doxorubicin and cyclophosphamide used in N6 therapy are metabolized by cytochrome P-450 (CYP) 3A; all are associated with leukemia as a treatment complication. The metabolites have genotoxic properties that may be relevant to leukemogenesis. The promoter of the CYP3A4 gene is polymorphic. Prior studies showed that the CYP3A4 wild-type genotype increased and CYP3A4 variant genotypes decrease the risk of treatment-related leukemia with MLL gene translocations. Prior studies also showed that the MLL gene translocation can be present early in the course therapy at how cumulative doses of DNA topoisomerase II inhibitors. MLL presents an extreme example of a translocation involving many partner genes; Southern blot analysis and cDNA panhandle PCR are two methods that can track the translocations in preleukemic samples regardless of the partner gene. They hypothesize that CYP3A4 genotype and MLL gene translocations are relevant biomarkers for treatment-related leukemia. The plans of the cooperative group to use N6 therapy not only mandate systematic investigation of who is most at risk, but also provide a unique clinical opportunity to examine CYP3A4 genotype and MLL gene translocations as a relevant biomarkders in the context of the therapeutic trial. The purpose of aim 1 is to validate the association of CYP3A4 genotype with treatmentrelated leukemia. The purpose of aims 2 and 3 is to determine and compare the utility of MLL gene translocations, detected by Southern blot analysis and cDNA panhandle PCR, as leukemia-specific markers that predict development of disease. The purpose of aim 4 is to explore the baseline frequency of MLL gene translocations in untreated pediatric patients diagnosed with neuroblastoma and to determine how chemotherapy affects this frequency during the course of treatment. Risk factors for treatment-related leukemia are poorly understood. Predictive biomarker assays will enable rational modifications of primary cancer therapies and provide new opportunities for early intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BLOCKING NEGATIVE SIGNALS TO NK CELLS TO TREAT LEUKEMIA Principal Investigator & Institution: Bennett, Michael; Professor of Pathology; Pathology; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2004 Summary: (Adapted from the investigator's abstract) NK cells are cytolytic for tumor cells but clinical use of autologous NK cell treatment has been relatively unsuccessful. A major potential cause for this is that NK cells have receptors for 'self' class I transplantation antigens, and the majority of these receptors respond by sending negative signals that prevent NK cell lysis. This explains why NK cells preferentially lyse HLA or H2 allogeneic, or class I deficient target cells. During the first 3 years of this project, the investigators have obtained evidence that blocking negative signals for two inhibitory receptors, Ly-49I and C, with F(ab')2 5E6 MAbs enhanced survival of B6 mice infused with syngeneic C1498 myeloid leukemia cells. Use of T and B cell deficient mice indicated that NK cells were the effectors. The same treatment did not inhibit growth of syngeneic BMC in irradiated B6 mice (a safety concern) but did enhance the ability of mice to reject allogeneic BMC grafts. A new 8H7 anti-Ly-49I MAb at low doses blocks negative signals without depleting NK cells and can be used as a reagent with a longer half-life than MAb fragment. The F(ab')2 reagent is limited in function due to short halflife in serum (<18h). This renewal application has 5 specific aims: Aim 1. Generate more effective MAb reagents to block negative signals to NK cells without depleting them the investigators have mutated the Fc region of 5E6 MAb to remove a critical Ncarbohydrate attachment site that is required for the MAbs to deplete cells in vivo. Generate similar reagents against Ly-49G2, an inhibitory receptor expressed on a large fraction of murine NK cells.Aim 2. Develop rapid assays for growth assessment of leukemia cells in vivo to quicken the pace of developing new reagents, e.g., infusion of leukemic cells i.v. into irradiated hosts, and assessing proliferation 5 days later by measuring DNA synthesis, an assay for proliferating cells. Use 123I-iododeoxyuridine to label proliferating cells that can be used for imaging of growing tumors and for labeling leukemia cells that are infused so that survival can be determined by whole body counting. Aim 3. Test the reagents for the ability to 'purge' leukemia cells from syngeneic marrow cells 'spiked' with different numbers of leukemia cells.Aim 4. Expand the clinical treatment protocol to include supplemental treatment of mice with IL-2 after the infusion of syngeneic or allogeneic IL-2 activated NK cells coated with anti-5E5 and/or anti-Ly49G2 F(ab')2 MAbs. Aim 5. Extend the studies to the use of human myeloid leukemia cells, human NK cells, and immunodeficient SCID mice pretreated with asialo GM1 or SCID-NOD mice, which accept grafts of human leukemia cells. Non-depleting MAbs or fragments to human negative signaling receptors for class I antigens expressed on the leukemia cells will be tested for anti-leukemia effects. Success with these studies will hopefully determine if this approach has potential for clinical application. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BRAIN NEOPLASMS, LEUKEMIA & PETROCHEMAL EXPOSURES Principal Investigator & Institution: Christiani, David C.; Professor; Environmental Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2001; Project Start 15-AUG-2000; Project End 31-JUL-2005
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Summary: (Adapted from the Applicant's Abstract): Brain tumors and leukemia are the most common children and adolescent malignancies in the U.S. Adequate information on the role of inherited genetic susceptibility and environmental exposures in the development of neoplasms in children and adolescents is lacking. In Taiwan, four large petrochemical industries are located in Kaohsiung metropolitan area. These facilities are proximal to residential areas because of the high population density in the region. Data have shown that the concentrations of ambient polycyclic aromatic hydrocarbons (PAH) and volatile organic compounds (VOC) around the petrochemical industries are at least 10 and 2 times, respectively, higher than those in U.S. industrialized communities. Our preliminary case-control study in Kaohsiung metropolitan showed that young residents (< 30 yr) living within 3 kilometers (km) of the vicinity of petrochemical industries have a 6.0 fold increase in brain neoplasms and a 2.9 fold increase in leukemia. The purpose of this proposal is to examine the association of exposure to air contaminants (PAH & VOC) emitted from the petrochemical industries, specific genetic polymorphisms (P4501A1 (MspI & exon 7) and GSTMI & Tl) from study subjects and their parents, and the risks of brain tumors and leukemia among children and youths in metropolitan Kaohsiung. Our hypothesis is that there is an increase risk of brain tumors and leukemia in patients with higher cumulative exposure to these hazards, and that heritable polymorphisms in several genes modify this association. In addition to an independent association of environmental and genetic factors with brain neoplasm and leukemia, we hypothesize that there is greater risk associated with the presence of combined environmental exposure and the high risk genotype. We also assess the role of the parental genetic polymorphisms in the development of cancer in their sibling. This proposed study uses an environmental molecular epidemiologic approach, utilizing prospective enrollment of a cohort of brain tumor and leukemia subjects and a population-based case-control design. This proposal is responsive to the recommendation of the National Research Council that risk assessment and public health policy pay special attention to the protection of children. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CANCER AND LEUKEMIA GROUP B Principal Investigator & Institution: Canellos, George P.; Chief; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-APR-1982; Project End 31-MAR-2009 Summary: (provided by applicant): The Dana-Farber Cancer Institute (DFCI) and DanaFarber/Partners CancerCare (DF/PCC) proposes to use its membership in the Cancer and Leukemia Group B (CALGB) to support participation in therapeutic research and other clinical trials, both in the Institute and its affiliate institutions. The goals of this project will be the initiation and participation in Phase I, II and III cooperative clinical trials involving chemotherapy, surgery and radiation therapy. A major emphasis will be made in developing new therapeutic strategies both at the DFCI and MGH, and in pilot collaborative investigations with interested members of CALGB. Dana-Farber investigators would continue to be actively involved in disease and modality committees of the CALGB. This project is designed to bring cooperative group trials to regional community hospitals affiliated through the Dana-Farber Cancer Institute throughout New England and to Puerto Rico through its affiliation with the University of Puerto Rico Oncology program. The Dana-Farber Cancer Institute has a broad program of Phase I trials of new treatments including biologics. The extensive involvement of members of the faculty of Dana-Farber/Partners Cancer Care in CALGB facilitates the transmission of Phase I observations and ideas into broader Phase II or
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even Phase III trials. To that end our investigators have assumed leadership roles in the modality/disease committees of CALGB (GI, Leukemia, Lymphoma, Breast, GU, Correlative Sciences, Melanoma, Clinical Economics for example). Our objectives on this grant is to increase accrual through our expanded network, which now includes Hartford Hospital (with 900 beds), and to increase interests of young investigators at DF/PCC in participation in CALGB at the administrative and scientific levels. The basic scientific efforts of the Dana-Farber/Harvard Cancer Center will be, where possible, brought to the correlative science program of CALGB. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CANCER AND LEUKEMIA GROUP B Principal Investigator & Institution: Hurd, David D.; Internal Medicine; Wake Forest University Health Sciences Winston-Salem, Nc 27157 Timing: Fiscal Year 2001; Project Start 01-APR-1979; Project End 31-MAR-2003 Summary: (adapted from the applicant's abstract): The Comprehensive Cancer Center of Wake Forest University continues to be a major accrue to Cancer and Leukemia Group B protocols. A modest decrease in accrual is noted for 1996 which reflects economic constraints and the influence of managed care. We have obtained an R13 CA-74441 demonstration grant to evaluate and strengthen the recruitment and retention of minorities in cancer clinical trials. Further, we are applying through CALGB for the minority initiative program to obtain data management support for East Carolina University. They have access to a large minority population in eastern North Carolina. The anticipation that first-line protocols for leukemia, lymphoma, and advanced breast cancer will soon be available should also strengthen our accrual in this grant period. Our institutional and CCOP accrual to protocol #9399 (chemotherapy prevention of prostate cancer with finasteride) is an expression of our ability to accrue large number of patients quickly to cancer control clinical trials. Dr. David Hurd, Chair of the Transplant committee and Dr. Electra Paskett, Chair of the Cancer Control committee provide strong scientific contributions to CALGB and further strengthen our accrual to clinical trials. Dr. Jim Atkins, Chairman of the Southeast Cancer Control Consortium (SCCC), is developing a strong regional program with increasing emphasis on the accrual of minorities to clinical trials. Our strong community outreach clinical trials program is focused to develop community techniques which will improve accrual to clinical trials. The development of multi-disciplinary affinity groups in breast, GI, GU, leukemia, lung, neuro-oncology, and oral head/neck cancer will also strengthen our institutional contributions to Cancer and Leukemia Group B. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CANCER AND LEUKEMIA GROUP B Principal Investigator & Institution: Edelman, Martin J.; Director; Medicine; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2002; Project Start 01-APR-1982; Project End 31-MAR-2003 Summary: The GCC continues to grow and develop a scientific and clinical relationship with CALGB. A number of the faculty at GCC participate in CALGB scientific and administrative committees. GCC faculty design, conduct and chair many group studies and enter large numbers of patients onto CALGB studies. The GCC faculty are on five core committees and chair the Leukemia Committee and the Subcommittee on Thoracic Surgery. The funding to continue these activities will allow further growth in the scientific and administrative participation of GCC and its affiliates. GCC is one of the
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largest accruing institutions for leukemia and one of the largest accruing institutions overall. The basic science laboratories studying acute leukemia, cellular, animal and clinical pharmacology and cellular and molecular biology form an important correlative science resource for the group. The grant will allow GCC to continue its highly effective scientific and administrative participation in the group and will continue to allow them to develop a scientific base in the greater Baltimore area and across the state and region. The grant will also allow for continuation of meritorious pilot protocols and will allow GCC to monitor and collect data which will produce mutual benefit to the GCC and CALGB. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CANCER AND LEUKEMIA GROUP B CCOP RESEARCH BASE Principal Investigator & Institution: Schilsky, Richard L.; Associate Dean for Clinical Research; Cancer Research Facility; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2001; Project Start 30-SEP-1983; Project End 31-MAY-2004 Summary: This application is submitted by the Cancer And Leukemia Group B (CALGB) to begin its sixteenth year as a primary multi-modality Research Base for seven Community Clinical Oncology Programs (CCOPs) and two Minority-Based CCOPs. CALGB is a Clinical Cooperative Group with 30 Main Member institutions and a membership of about 3000 health professionals at about 200 hospitals, clinics and physicians' offices. The overall objective is to provide an organized and collegial environment for community based health care professionals to interact with their academic counter-parts in the development and implementation of cancer prevention and control research studies and the latest cancer treatment clinical trials. CALGB proposes to enhance the translation of new information from a strong basic correlative sciences program in cancer treatment to an evolving strong program in cancer prevention and control research. Major themes are chemoprevention, intermediate markers and quality of life research. Strategies will be developed to assist CCOPs to increase accrual of minorities, women and other underserved people into ethical, high quality clinical trials which will result in a decrease in cancer incidence, morbidity and mortality. A special focus has emerged in cancer in the elderly and a new committee is charged with developing research studies of particular relevance to this rapidly growing segment of the population. CCOPs will be assisted in broadening their networks to include more primary health professionals and specialists to help in the diffusion of state-of-the-art cancer care at the community level. There are seven cancer site committees (Breast, Gastrointestinal, Leukemia, Lymphoma, Melanoma, Prostate and Respiratory) which work closely with thirteen modality committees (Pharmacology and Experimental Therapeutics, Correlative Sciences- Leukemia/Lymphoma, Correlative Sciences-Solid Tumors, Transplant, Pathology, Surgery, Radiation Oncology, PsychoOncology, Cancer Control, Oncology Nursing, Patient Issues, Clinical Research Associates, Cancer in the Elderly) to plan and implement cancer prevention and treatment studies using the latest technologies and information available. This project will bring these advances to the community hospital level where CCOP trained health care providers can apply them immediately. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CANCER AND LEUKEMIA GROUP B-LEUKEMIA CORRELATIVE SCIENCE Principal Investigator & Institution: Caligiuri, Michael A.; Professor and Director; Comprehensive Cancer Center; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2003; Project Start 13-MAY-2003; Project End 31-MAR-2009 Summary: The Cancer and Leukemia Group B (CALGB) Leukemia Correlative Sciences Program has worked to attain a highly successful integration of correlative laboratory studies into the design and implementation of CALGB leukemia trials. Dr. Michael A. Caligiuri assumed leadership of the CALGB Leukemia Correlative Science Committee (LCSC) in August of 1999 following 18 years of Committee leadership by Dr. Clara Bloomfield. The LCSC has been restructured and refocused entirely on leukemia, moving evermore into the molecular age of diagnostics, pathogenesis, and treatment. The goal is to use cytogenetics, immunology, and molecular biology to better understand the heterogeneity of leukemia with regard to diagnosis, prognosis, and ultimately treatment. In this competitive renewal application, we have assembled three Cores (Cytogenetics, Banking, and Administration) and six Projects, each of which is utilizing materials collected from patients treated on CALGB leukemia treatment protocols in order to address a scientific question and correlate it with disease outcome. Having set into motion a paradigm for stratification of leukemia treatment based on risk of relapse during this last funding cycle, the current CALGB Leukemia Correlative Science application will attempt to dissect out additional leukemia patients that can be predicted to do well or do poorly in response to standard or novel therapies, and to then work with the CALGB Leukemia disease committee to stratify their treatment based on risk. In this way, we hope to significantly impact on the cure rate of leukemia over the next six years of funding. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CHARACTERIZATION OF HUMAN LEUKEMIC STEM CELLS Principal Investigator & Institution: Bonnet, Dominique A.; Assistant Professor/Chief; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAY-2004 Summary: Understanding the processes that regulate the developmental program of normal stem cells and how aberrations in this program initiate leukemic proliferation remain a major challenge in biology. Progress to address these major questions in the human hematopoietic system has been hampered, until recently, by the lack of in vivo assays for normal and leukemic stem cells. The only way to conclusively assay stem cells is to follow their repopulating capacity. The recent development of methods to transplant human hematopoietic cells into immune-deficient mice provides an important approach to characterize stem cells and to develop animal models for hematopoietic diseases including leukemia. The development of an in vivo model that replicates many aspects of human AML and allows the identification of a novel leukemic stem cell (termed the SCID-Leukemia Initiating Cell, SL-IC) based on the ability of that cell to initiate AML in NOD/SCID mice provides the foundation of an assay to define the biological and molecular properties of such new leukemic stem cells. The major long-term objectives of my research program are to further characterize human leukemic stem cells. The research project proposed here will focus on three objectives: 1) determine the existence of an heterogeneity at the leukemic stem cell level (both Lin-CD34+ and Lin-CD341o/- subfractions have leukemic stem cell properties); 2)
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evaluate the biological properties of the leukemic stem cell pool (i.e., self-renewal, proliferation and differentiation capacities, response to cytokines and/or stromal cell environment); 3) to study the gene expression pattern of six regulatory molecules (AML1, PU.1, GATA- 1, Hox A5, Hox B4 and SCL/tal-1), known to be involved in the early stage of hematopoietic development and/or in the physiopathology of leukemia, before and after induction of differentiation of the leukemic stem cell fraction. The information obtained from these studies will gave us a more complete understanding of the nature of the leukemic stem cells, their biological properties, and the early molecular factors involved in the maintenance and/or differentiation of such leukemic stem cells. Furthermore, the knowledge gained about leukemic stem cells will allow us to devise new therapeutic strategies such as cell purging strategy, gene suicide therapy, antisense therapy and others, targeted specifically to the leukemic stem cell pool. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CHILDHOOD LEUKEMIA AND ENVIRONMENTAL EXPOSURES Principal Investigator & Institution: Buffler, Patricia A.; Professor of Epidemiology; None; University of California Berkeley Berkeley, Ca 94720 Timing: Fiscal Year 2001; Project Start 01-JAN-1999; Project End 31-DEC-2003 Summary: The causes of childhood leukemia remain largely unknown. The purpose of this proposal is to expand an existing case-control study of molecular of childhood leukemia in size and geographic region and refine the measurement of exposure to household chemicals and pesticides, and to assess exposure to electric and magnetic fields. The temporal relationship of exposure to environmental agents including dietary, occupational and residential chemical exposures are determined by use of self-report and interview data. Molecular biologic techniques are used to characterize the subtypes of leukemia and the presence of genetic changes. Biological specimens include bone marrow and peripheral blood of newly diagnosed cases, buccal cell specimens from cases, their mothers and control subjects, and archived newborn blood from cases and controls born in California will be used in the endeavor to identify the timing of exposures. Household pesticides are an environmental exposure of particular concern since previous studies have suggested that chemical and pesticide exposure during pregnancy and after birth may be related to the subsequent development of childhood leukemia. This research will expand a currently funded study of childhood leukemia which includes newly diagnosed cases ages 0-14 which present at four Bay Area referral hospitals during the period 1995-1998. This proposal will double the expected sample size to 400 cases by including cases ascertained at these hospitals an additional three years and expanding the study to include patients from the three major clinical centers for the central valleys of California for four years. Two matched control groups will be obtained for each case: friend controls and birth certificate controls. Friend controls will be randomly chosen from nominees provided by parents that match the case on age, sex, gender, county of residence at diagnosis, and ethnicity of mother. Birth certificate controls will be chosen from California births that match the case with respect to age, sex, gender, county of residence at birth, and ethnicity. A self-administered questionnaire and personal interview will be obtained to collect data related to a spectrum of environmental exposures and other risk factors including dietary history and residential history and history of chemical exposures of the mother prior to and during pregnancy and the child, occupational history and reproductive history of the mother, and health history of the child. A subsequent exposure component will focus on exposures to household pesticides during the past year and during pregnancy and the first two years of the child's life and measure electric and, magnetic fields directly in the
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home and indirectly by trained staff coding residential wiring configurations. Molecular characterization of leukemia cases allows for the subclassification of leukemias on a biological basis, and will facilitate the linkage of exposures with leukemia subtypes in the analysis. The proposed study, which will attempt to link specific chemical components with genetic changes found in childhood leukemia, will help to reduce the percentage of leukemias for which there is no known cause. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: COOPERATING GENETIC EVENTS IN MYELOID LEUKEMIA DEVELOPME Principal Investigator & Institution: Largaespada, David A.; Associate Professor; None; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2003 Summary: (adapted from the investigator's abstract) Cancer develops as a result of the accumulation of multiple genetic changes in somatic cells, all of which cooperate in inducing the transformed phenotype. In acute myeloid leukemia (AML) the number and nature of these "cooperating" oncogenic mutations is most often unknown. The BXH-2 mouse offers a model system ideal for the elucidation of interacting gene mutations. In this model, a Murine Leukemia Virus (MuLV) induces AML by acting as an insertional mutagen. The number of different gene whose expression is altered by proviral insertion and which contribute to leukemia development in BXH-2 mice is likely to be large. At least eight different loci have been identified which are mutated by proviral insertion in multiple BXH-2 leukemias, but none of these loci is involved in more than 15% of the leukemias. Therefore, new and more efficient methods for identifying and cloning these cancer genes have been developed. These techniques include the selection of tumor-specific, somatically-acquired proviruses near CpG islands, which greatly enriches for proviruses near genes involved in leukemogenesis, and the development of a highly efficient inverse PCR-based approach for cloning proviral insertion sites. The combination of these two technologies allows rapid progress toward the goal of understanding the complex network of genes mutated during myeloid leukemia development. These procedures have been used to identify mutations in two genes likely to impact the same cell signaling pathway: Nf1 and Cdc251. It is the goal of this proposal to define the overlap between the oncogenic effects of these mutations and discover other proteins involved in this pathway. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--CLINICAL RESEARCH SUPPORT COMPONENT Principal Investigator & Institution: Stone, Richard M.; Professor; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-MAR-2003 Summary: (provided by applicant): The ultimate objective of the research projects in this program project application is to improve the therapeutic results for patients with myeloid malignancies including acute myeloid leukemia, myelodysplastic syndrome, and chronic myeloid leukemia. To achieve this objective, tumor cells and other relevant clinical samples from patients will be collected, catalogued, and distributed to the relevant projects for analysis of the expected therapeutic targets and other molecules that might be important in prognosis or pathophysiology. Secondly, a clinical infrastructure is required to carry out the clinical trials described in Project 5 and additional clinical studies that will emanate from the developmental approaches
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outlined in Projects 1, 8, 9 & 10. Clinical Research Core resources are required to carry out these functions which extend beyond direct patient care and the clinical laboratory. Without the clinical research support provided in the Core it would be impossible to coordinate the proper collection of multiple research specimens, the adherence to novel complex therapeutic schedules and timely follow-up of patients enrolled on research studies. Also critical to this success of the project is the collaboration of individuals in the Core with the staff from the Biostatistics Core who will provide a quality control system for specimen tracking, computerized data entry, quality of control data and will assist in the design and analysis of the clinical research protocols. The purpose of the Clinical Research Support Core is to provide the following services that will be utilized by all the clinical research studies: 1. To collect research specimens and coordinate patient follow-up at Dana- Farber Partners Cancer Center and collaborating institutions. 2. To act as liaison with outside physicians, hospitals, and biotechnology companies to coordinate the collection of research specimens and follow-up data. 3. To insure that study parameters are followed, ancillary specimens are collected on time and processed properly, confirm eligibility, and patient registration. 4. To insure the accuracy of submitted data from outside sources. 5. To provide data management for the collection of individual patient information. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CORE--CYTOGENETICS FACILITY Principal Investigator & Institution: Bloomfield, Clara D.; Director; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2003; Project Start 13-MAY-2003; Project End 31-MAR-2009 Summary: (provided by applicant): The CALGB Cytogenetic Core provides the infrastructure for giving CALGB investigators high quality cytogenetic data in AML, ALL, MDS, CML and CLL. These data are used in the group for 3 general purposes: a) to answer specific questions regarding the clinical and biologic significance of specific cytogenetic findings in these diseases; b) to provide information required to select the correct treatment study or protocol arm, and to allow appropriate analysis of therapy being investigated; and c) to provide information required for molecular genetic studies described elsewhere in this grant application (e.g., projects 1, 2, 3, and 5). As a result of information discovered (via CALGB protocol 8461) regarding the clinical significance of cytogenetics in AML and ALL, cytogenetics are currently used in stratifying patients for specific arms on our current front-line AML protocol in adults under the age of 60 years (CALGB 19808), and for selecting appropriate protocols for adults with ALL which differ based on cytogenetic findings (CALGB 10001, 10002, 10102). In CML (CALGB 10107) and MDS (CALGB 10105) disappearance of the cytogenetic abnormality will be used for monitoring outcome. Additionally, the integral relationship of cytogenetics with other leukemia correlative science studies (e.g., CALGB 9760, 9862, 20201, 20202) and most of the molecular studies performed through the CALGB Leukemia Tissue Bank (CALGB 9665) mechanism (see Core B of this grant application) make cytogenetic studies an essential component of almost all currently planned leukemia research. Cytogenetic data for AML, ALL and MDS are obtained via CALGB 8461, for CML via CALGB 29801 and for CLL via CALGB 20106 and 20203. The processing of submitted karyotypes and fluorescence in situ hybridization (FISH) results, cytogenetic data management and central review for these studies are done at The Ohio State University (OSU) under the direction of Dr. Clara D. Bloomfield. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CYTOKINE GENE THERAPY OF RESIDUAL LEUKEMIA Principal Investigator & Institution: Gautam, Subhash C.; Internal Medicine; Case Western Reserve Univ-Henry Ford Hsc Research Administraion Cfp-046 Detroit, Mi 48202 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-MAY-2005 Summary: (Applicant's Abstract) Our long-term goal is to develop novel biotherapies that will specifically target and destroy residual leukemia. The proposed studies will test the general hypothesis that site-directed gene therapy with hematopoietic progenitor cells, genetically modified to secrete human tumor necrosis factor-alpha (hTNF-a), will significantly increase the destruction of leukemia cells remaining after high-dose chemotherapy/bone marrow (BM) transplantation. Our preliminary data show that administration of hTNF-a secreting progenitor cells following chemotherapy with cyclophosphamide (CY) and BM transplantation dramatically enhances survival (80 percent) of mice inoculated with a lethal dose of 32Dp210 murine myeloid leukemia cells without toxic side effects. We will test the hypothesis that combined therapy with CY, BM-transplant, and TNF-a secreting progenitor cells generates a greater antileukemic effect than is produced by any modality alone. We will accomplish this by the following specific aims: 1) determine the extent to which immunomodulatory effects of CY on T-helper (Th) cells and cytotoxic effector cells (CTLs and NK cells) contribute toward the antileukemic activity of CY/TNF-a gene therapy, 2) identify the cell population(s) within BM-transplant (e.g., T cells, mesenchymal cells or progenitor cells) that enhances the efficacy of combined therapy, and 3) determine whether the mechanism(s) of the antileukemic effect of CY/TNF-a treatment involves: a) augmentation of leukemia antigen presentation by dendritic cells, b) generation of leukemia specific (CTLs) and non-specific (NK cells/macrophages) cytotoxic effector cells, c) production of secondary cytokines with antileukemic activity, and d) the induction of programmed cell death (apoptosis) in leukemia cells. The results of these studies will demonstrate the value of combining this novel approach of site-directed TNFa gene therapy with other commonly used anticancer treatment strategies to achieve maximum destruction of residual leukemia. This would make possible the rapid implementation of this novel treatment strategy to eradicate residual leukemia in humans, without the toxic side effects of systemic TNF-a therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DEPSIPEPTIDE: A NOVEL HISTONE DEACYTLASE INHIBITOR IN L Principal Investigator & Institution: Byrd, John C.; Internal Medicine; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2002; Project Start 07-JUN-2002; Project End 31-MAR-2004 Summary: (provided by applicant): A fine balance between the enzymatic activity of histone acetyltransferase and histone deacetylase (HDAC) governs levels of posttranslation acetylation of histone lysine residues. Recognition of this regulatory mechanism for gene transcriptional activation is growing. In cell transformation, acetylation is profoundly altered, and accumulation of hypoacetylated histone species occurs. Depsipeptide is a novel HDAC inhibitor completing phase I development in solid tumors; clinical activity has been noted. Studies by our group have shown selective cytotoxicity of depsipeptide toward acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL) cells compared to normal hematopoetic cells. This cytotoxic effect occurs via an uncommonly exploited pathway of apoptosis, and the effect appears to be related to increasing histone H3 and H4 acetylation. We have
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demonstrated the ability of depsipeptide to induce gene transcription, cell differentiation, and expression of adhesion/co-stimulatory molecules in human myeloid cell lines and transformed lymphocytes. Synergy with decitabine and up-regulation of the 1D10 antigen was also noted. Based upon these data, we propose to perform the first clinical trial of depsipeptide in leukemia patients in two separate cohorts (AML and CLL). The objectives of our proposal are to 1) determine the safety of administering depsipeptide to two cohorts of leukemia patients (AML and CLL) 2) determine the dose at which a 100 percent increase in the baseline histone acetylation occurs, which will define a minimal effective pharmacologic dose (MEPD) 3) examine the biologic effect of depsipeptide on leukemia cells treated in vivo in patients with CLL and AML with respect to differentiation (AML) and co-stimulatory/adhesion molecule expression(AML and CLL). The specific relationship of these processes to lysine-specific H4 alterations, inhibition of HDAC enzyme activity, and enhanced ex vivo sensitivity to monoclonal antibodies will be assessed. By utilizing this novel study design that target MEPD, we may achieve significant biological effects, while avoiding excess doses of depsipeptide. The clinical and laboratory results of this trial will provide pharmacokinetic and pharmacodynamic information for additional correlative efforts in both single agent phase II and combination phase I studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: EFFECT OF ANTIBODIES/CHEMOTHERAPY ON CHILDHOOD LEUKEMIA Principal Investigator & Institution: Herrera, Larry; Scott and White Memorial Hospital 2401 S 31St St Temple, Tx 76508 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): Acute lymphoblastic leukemia (ALL) is the most common form of childhood malignancy. Chemotherapy can cure 80% of these children, but unfortunately many still relapse or develop resistant disease. Those that survive often suffer from adverse toxicity. This proposal investigates the mechanisms by which monoclonal antibodies (Mabs) induce apoptosis alone or in combination with chemotherapy in childhood B-lineage ALL. B-lineage lymphoblasts obtained from patients with leukemia undergo spontaneous and chemotherapy induced apoptosis. Like their normal counterparts (i.e., lymphocytes), they are "primed" to undergo apoptosis. Mabs have been shown to enhance the effect of chemotherapy in both laboratory and clinical settings. Mabs are capable of signaling various intracellular events and modulating the expression of genes involved in apoptosis. There exists only limited information on how Mabs and chemotherapy work together to enhance the cytotoxic effect upon leukemia. There is currently a lack of understanding of the mechanisms involved when Mabs are used to target B-lineage ALL as individual agents or in combination with chemotherapy. Our hypothesis is that the leukemia cell can undergo apoptosis in response to Mabs, the response can be enhanced with chemotherapy; and that key apoptotic related genes will be up-regulated or downregulated, thereby elucidating the pathway leading to cell death. Knowledge of this pathway may allow for the selection of agents capable of enhancing the degree of apoptosis. We plan to correlate the cellular response to a specific profile of mRNA expression. These studies may identify genes that are important in the initiation of apoptosis that have not previously been linked with this phenomenon. These studies will also allow us to determine if the degree of apoptosis demonstrated in vitro correlate with drug sensitivity in vivo. We will determine if apoptosis and gene profile analysis can predict the most effective agents in treating leukemia in a SCID/human ALL mouse
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model. We will then develop new treatment regimens for children with multiply relapsed leukemia based on this information. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: FLT3 GENOTYPES IN ACUTE MYELOID LEUKEMIA Principal Investigator & Institution: Whitman, Susan P.; Comprehensive Cancer Center; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2002; Project Start 20-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Acute leukemia is a malignancy of the hematopoietic elements that results at least in part from inappropriate activation of tyrosine kinases (TK). The most frequent somatic mutation associated with adult acute myeloid leukemia (AML) to date is the internal tandem duplication (ITD) of the FLT3 gene, a member of the Type III PDGF superfamily of receptor TKs. The FLT3 ITD defect results in the constitutive activation of the tyrosine kinase in the absence of ligand binding. Clinical studies thus far, however, have provided contradictory results with regards to presence of FLT3 ITD and prognostic significance of this defect in AML. These inconsistencies may be due to factors known to have confounding prognostic importance, such as varying cytogenetics, age, and treatment regimens. We examined a group of AML patients homogeneous for age, cytogenetics and treatment, and all considered at standard risk for relapse following therapy. We demonstrated three distinct genotypes among 82 patient samples examined: patients homozygous for the wild type (WT) FLT3 gene; patients heterozygous (FLT3ITD/WT), and patients hemizygous, i.e., FLT3 ITD in the absence of the WT gene, or FLT3ITD/-. Only the latter was a highly significant predictor of profoundly worse prognosis in AML patients compared to the others considered at standard risk. The overall research objective outlined in this proposal is to understand the mechanism by which the hemizygous genotype confers an especially poor prognosis, and to target this molecular defect in vitro and in vivo with a FLT3-specific inhibitor. To accomplish this goal, AIM 1 will investigate if a constitutively active mutant FLT3 in the absence of wild-type FLT3 confers a dominant positive gain-of-function role using in vitro and in vivo models. AIM 2 will assess whether proliferation and survival of FLT3 ITD-positive patient AML cells are selectively inhibited via induction of apoptosis by newly developed FLT3 inhibitor compounds. Funding of this K01 Mentored Minority Career Development Award will provide invaluable training for the applicant in the area of molecular mechanisms of disease, animal models for the study of human leukemia, and molecular targeted approaches to cancer therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FUNCTIONAL ANALYSIS OF THE HUMAN LEUKEMIA GENE E2APBX1 Principal Investigator & Institution: Kamps, Mark P.; Pathology; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2002; Project Start 10-APR-1992; Project End 31-MAR-2007 Summary: (provided by applicant): PBX, MEIS/PREP, and HOX genes encode interacting transcription factors that regulate development. Their mutation produces oncogenes that cause human leukemia and other tumors. Pbx, Meis/Prep, and Hox proteins are also implicated as subordinate oncoproteins functionally required for leukemogenesis by other human oncogenes. Thus, understanding oncogenesis by individual Pbx, Meis/Prep or Hox oncogenes will yield a broader understanding of
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human leukemia in general. This proposal focuses on understanding how Pbx proteins control development and hematopoiesis (Aims 1 and 2) and how the human E2a-Pbxl oncogene causes AML and preB ALL (Aims 3 and 4). Health-relatedness: Just as understanding oncogenesis by signal transduction oncoproteins led to the development of therapeutic inhibitors of cell proliferation, so also understanding the biochemical mechanism of oncoproteins that block hematopoietic differentiation will establish a rational to generate drugs that inhibit their function and promote differentiation. Because oncogenes that promote proliferation and inhibit differentiation cooperate to cause leukemia, drugs that inhibit proliferation and promote differentiation should cooperate to cure leukemia. Aim 1. Determine how Pbx homodimerization (in the absence of DNA) and Pbx:Meis/Prep heterodimerization regulate DNA-binding and nuclear import of Pbx proteins. Determine how Pbx proteins function as transcriptional coactivators. Aim 2. Using knockout technology, determine the role of Pbx2 in mouse development in general, and in regulating lineage commitment, differentiation progression, and gene transcription during hematopoiesis in particular. Make conditional Pbx2/Pbxl, or Pbx2/Pbx3 mice to determine the effect of double knockouts on hematopoietic differentiation. Aim 3: Use conditional E2a-ER-Pbxl to determine how E2 about-Pbxl prevents transcription of myeloid differentiation genes, focusing, mechanistically, on MRP8. Determine whether direct E2a-Pbxl targets reestablish a differentiation block in conditionally-immortalized E2a-ER-Pbxl myeloblasts and are activated in human t(l;19) pre-B ALL (L-Myc is one such target). Aim 4: Establish the cellular impact of E2a-Pbxl in models of pre-B cell leukemia induced by coexpression of Ras6l L plus E2a-Pbxl, or in transgenic mice expressing wild-type or conditional E2a-ERPbxl genes driven by the early, hematopoietic specific, Vav promoter. Identify the biochemical domains of E2a-Pbxl required to cause pre-B ALL, and begin to identify a genetic mechanism by which E2a-ER-Pbxl causes pre-B cell ALL. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GAT62 LEUKEMOGENESIS
IN
ONTOGENESIS,
HEMATOPOIESIS,
AND
Principal Investigator & Institution: Pandolfi, Pier P.; Professor; Sloan-Kettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAY-2002 Summary: Chronic myelogenous leukemia is characterized by the presence of the chimeric p210 bcr/abl protein which shows elevated protein tyrosine kinase activity relative to the normal c-abl tyrosine kinase. Hematopoietic progenitors isolated from CML patients in the chronic phase contain constitutively tyrosine phosphorylated protein, GAT62 (GAP-associated with tyrosine phosphorylated p62), that migrates at 62 KD by SDS page and associates with p120 bcr/abl GTPase-activating protein (GAP). The gene encoding for this protein has very recently been identified. The focus of this proposal is to elucidate the role of the GAT62 protein in development and hemopoiesis, and to clarify how GAT62 function relates to leukemogenesis with the following Specific Aims: 1. To define in knock out mice and null ES cell lines, the role of GAT62 in ontogenesis and hemopoiesis. We will characterize GAT62 expression in the developing embryo and in the adult mouse. Using homologous recombination technology, we will disrupt the GAT62 gene in mouse Embryonic Stem (ES) cells and mice or embryos homozygous for the GAT62 inactivating mutation will be generated and studied. We will define the developmental role of the GAT62 gene by characterizing the embryonic or adult phenotype resulting from its inactivation. We will specifically study hemopoiesis in GAT62 mutants. Different experimental approaches will be undertaken
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depending on whether mice lacking GAT62 re viable or on the stage of embryonic development at which they die. In parallel, we will produce GAT62 null ES cells and study the capacity of these cells to differentiate towards hemopoietic precursors in vitro and in vivo in chimeras and RAG-/- complementation assays. 2) To establish the role of GAT62 in leukemia promotion and progression. We will define whether the tyrosine phosphorylation and the resulting functional activation of GAT62 by the bcr/abl fusion products is a crucial event in CML and ALL (Acute Lymphoblastic Leukemia) leukemogenesis. To this end we will interbreed transgenic mice harboring the p210 bcr/abl and p190 bcr/abl fusion genes in the germ line, that develop leukemias through the activity of the chimeric proteins, with the GAT62 knockout mice in order to generate transgenes for the p210 bcr/abl and p120 bcr/abl fusion molecules in a GAT6 /- and -/genetic background. Hemopoiesis and leukemogenesis in the resulting transgene combinations will be analyzed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LEUKEMIA
GENE
REARRANGEMENT
AND
EXPRESSION
IN
T-CELL
Principal Investigator & Institution: Goorha, Rakesh M.; Member; St. Jude Children's Research Hospital Memphis, Tn 381052794 Timing: Fiscal Year 2001; Project Start 01-FEB-1988; Project End 31-DEC-2002 Summary: Our long-term goal is to understand the molecular mechanisms operative in proliferation and differentiation of lymphocytes because perturbations in these processes results in leukemias. LMO-2 (Rhom-2/RBTN-2/ttg-2) locus at chromosome 11p13 is specifically disrupted in 10% patients with childhood T cell acute lymphoblastic leukemia (ALL). The oncogenic effects of LMO-2 are T cell specific; transgenic mice over-expressing LMO-2 in all tissues do not show any type of cancer other than T cell leukemias. It is hypothesized that LMO-2 mediates leukemogenesis by binding to other transcription factors and modulates their activity. Oncogenic specificity of LMO-2 may be because it binds a transcription factor with thymocyte specific expression. Accordingly, we have identified a novel transcription factor (Elf-2) that binds LMO-2 and its pattern of expression in normal and leukemic thymocytes strongly suggests that it plays an important role in leukemogenesis. We will conduct structure-function studies of Elf-2 to define its normal function and its role in leukemogenesis. Elf-2, in association with LMO-2, may alter the expression of genes that regulate thymocyte proliferation. Thus, a complementary approach to understand the mechanism of LMO-2 action is to identify its downstream target genes whose expression is altered in leukemic cells. Recently, using Representational Difference Analysis technique, we have isolated several clones that represent potential LMO-2 target genes. Cognate mRNA for one of the cones (a23) is not expressed in normal thymocytes but it is highly expressed in expanded double negative (DN) thymocytes and every mouse T cell (but not in B lineage) leukemias. Clone a23's invariant but ectopic expression in DN thymocytes and in every T cell leukemia strongly suggests that it play an important early role in leukemogenesis. We plan to characterize full-length cDNA representing clone a23 and conduct functional studies to determine its normal function and its role in leukemogenesis. After achieving remission, approximately 30% of the patients with T cell acute lymphocytic leukemia (ALL) relapse due to the resurgence of residual leukemic cells that can not be detected during remission of morphological methods. We have used a very sensitive PCR based assay to detect the residual leukemic cells and found that it has great potential in predicting impending relapse. We are now conducting a prospective study employing adequate number of patients to assess the
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use of this technique in predicting relapse, monitoring the efficacy of anti-leukemic therapy, and long-term survival. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GENETIC ANALYSIS OF A FAMILIAL LEUKEMIA SYNDROME Principal Investigator & Institution: Gilliland, D Gary.; Associate Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-MAR-2002 Summary: Despite remarkable advances in therapy of leukemia over the past 3 decades, the majority of adult patients with leukemia die from complications of their disease or therapy. There is convincing evidence that leukemia, like other cancers in humans, is the consequence of multiple mutations. Although significant strides have been made in identification of genes implicated in pathogenesis of leukemia over the past decade, little is known about the initiating events in the pathogenesis of leukemia. The deficit in our understanding of the early events in the molecular pathogenesis of leukemia is due in part to the rarity of familial predisposition to leukemia. In contrast with cancers such as breast and colon cancer, in which an inherited cancer predisposition has allowed for linkage analysis and positional cloning of the "first hit" mutations transmitted in the germline, there are few leukemia-prone families that would allow for an analogous approach. However, we have identified an extended pedigree characterized by a predisposition to develop leukemia. Furthermore, the trait is "marked" at birth by a platelet defect that has allowed for reliable identification of affected individuals. The goal of this proposal is to identify the gene that is responsible for this inherited leukemia syndrome, which in turn may provide critical information about the early genetic events in the pathogenesis of leukemia. Using a generalized linkage approach, we have localized the gene that causes the inherited predisposition to leukemia to a small region of human chromosome 21q22.1. In addition, we have recently identified a second pedigree with the same clinical phenotype which also demonstrates linkage to chromosome 21q22.1. Thus, there is convincing evidence to implicate this locus in pathogenesis of inherited leukemias. The goal of this proposal is to identify the gene which is responsible for the familial platelet disorder with propensity to develop AML. Our approach, as detailed in the body of the proposal, will focus on mutational analysis of genes which map to this region. Based on experience with other inherited cancers, we would predict that mutations in the FPD disease gene will also be relevant in sporadic leukemias, and will provide valuable information about the early genetic events in leukemia. In turn, this information may provide insight into novel therapeutic approaches to treatment of leukemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC AND BIOCHEMICAL ANALYSES OF MLL CLEAVAGE Principal Investigator & Institution: Hsieh, James J.; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The mixed-lineage leukemia gene (MLL, ALL1, HRX) encodes a 3,969 amino acid nuclear protein homologous to Drosophila trithorax and is required to maintain proper Hox gene expression. Deregulation of Hox and perhaps other gene expression causes transformation of segmental identities and contributes to human malignancy. Chromosome translocations in human leukemia disrupt MLL (11q23), generating chimeric proteins between the N-terminus of MLL and
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multiple translocation partners. More than 20 MLL translocation partners have been identified. They vary widely from nuclear factors to cytoplasmic structural proteins and there are no common characteristics identified among them. However, mouse models demonstrated an indispensable role played by the various fusion partners in MLL leukemias. Gene expression profiles of human leukemia bearing an MLL translocation identified a pattern of upregulated genes. Among these genes were some of the wellrecognized targets of wild type MLL. This argues that the common MLL N-terminus is sufficient to confer at least some target gene specificity to MLL-fusion proteins. However, the mechanism by which MLL regulates downstream gene expression is still unclear. In preliminary studies, I demonstrate that MLL is normally cleaved at two conserved sites (D/GADD and D/GVDD) and that mutation of these sites abolishes the proteolysis. The cleavage site sequences are highly conserved from flies to mammals. MLL cleavage generates N-terminal p320 (N320) and C-terminal p180 (C180) fragments, which then interact to form a stable complex that localizes to a subnuclear compartment. Disruption of the interaction between N320 and C180 leads to a marked decrease in the level of N320 and a redistribution of C180 to a diffuse nuclear pattern. Based on these data, I propose a model in which a dynamic post-cleavage association confers stability to N320 and directs correct nuclear sublocalization of the complex, thereby controlling the availability of N320 for target gene regulation. This model predicts that MLL-fusion proteins of leukemia lose the ability to complex with C180 and instead have their stability conferred by the fusion partners, thus providing one mechanism for the altered target gene expression observed in MLL leukemic cells. Further characterization of MLL cleavage will help elucidate how MLL regulates target genes, which is crucial for both development and leukemogenesis. In this regard, I propose the following specific aims: (1) Characterize the MLL cleavage and determine its role in protein stability and nuclear sublocalization; (2) Generate knock-in mice with a noncleavable MLL; (3) Identify and characterize the protease responsible for MLL cleavage. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GENETIC MANIPULATION OF T CELLS--PRECLINICAL MODELS Principal Investigator & Institution: Dipersio, John F.; Cheif, Division of Oncology; Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2006 Summary: (Applicant's Description Verbatim): Allogeneic bone marrow transplantation is a curative therapy for hematologic malignancies, marrow failure states, and selected inherited metabolic diseases. Unfortunately, BMT is associated with significant morbidity and mortality related to graft vs. host disease (GvHD). Attempts to mitigate GvHD using T-cell depletion resulted in increased rates of graft failure, post-transplant lymphoproliferative diseases, leukemia relapse and opportunistic infections. We propose to genetically modify T-cells using novel cell surface chimeric suicide genes. We will test the expression and purification of novel fusion suicide genes in vitro and in vivo using instructive transgenic and "knock-in" murine pre-clinical models. The optimal method and potential role of genetically manipulated T-cells to mitigate GvHD while maintaining engraftment and graft vs. leukemia can only be defined by developing new reagents and novel pre-clinical murine transplant models. We propose to generate important new reagents to study T-cell transduction by suicide genes and to use a number of well-defined pre-clinical models to develop a rational approach and a clear foundation for future clinical trials. In Aim I, we will design methods to optimize transduction, selection, and expansion of transduced T-cells, using OKT3 and 11-3 and CD3/CD28 magnetic beads. In addition, we will generate novel second-generation
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suicide genes designed to optimize detection and killing in response to prodrug. We will also test the survival and function of transduced murine and human T cells using in vivo using allogeneic transplant models and several murine SCID models. Aims II and III, we will use the chimeric suicide genes developed in Aim I to generate informative transgenic and knock-in pre-clinical murine models in which these suicide genes will be expressed in all (Aim II) or in subsets (Aim III) of peripheral T-cells. Allogeneic bone marrow transplantation will be performed using the transgenic and knock-in mice developed in Aims II and III to further develop the optimal method of suicide in vivo, its effect on GvHD and engraftment, and its possible role in clinical trials. In Aim 1V, we will utilize three novel murine leukemia models in which the effects of genetically modified T-cells and their in vivo suicide on GvHD, engraftment and graft vs. leukemia can be compared to animals receiving unmanipulated T-cells and T-cell depleted BM. These studies will provide new insights into the pathophysiology of GvHD and its effective treatment. Issues regarding the use of genetically manipulated T-cells to control GvHD can best be investigated through the use of informative animal models and the comprehensive studies described in this proposal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GVL AGAINST MURINE CHRONIC PHASE AND BLAST CRISIS CML Principal Investigator & Institution: Shlomchik, Warren D.; Assistant Professor; Comprehensive Cancer Center; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2003; Project Start 05-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): The Graft-vs-Leukemia effect (GVL) mediated by T cells that accompany allogeneic stem cell grafts and delayed leukocyte infusions (DLI), has revolutionized the treatment of leukemia and lymphoma. Chronic phase CML (CPCML) is the prototypical GVL-sensitive neoplasm in which complete remissions are achieved in 80% of recipients of DLI. In spite of this success, alloimmune therapy has two principle weaknesses. First, many neoplasms including CML in blast crisis (BCCML), are GVL-resistant. The basis for this differential susceptibility is unknown. Second, GVL has proven difficult to separate from Graft-vs.-Host Disease (GVHD), the attack by donor T cells on recipient tissues. We hypothesize that manipulation of alloimmune responses can render GVL-resistant tumors more sensitive and lessen GVHD while retaining GVL. We believe this is possible because some patients with GVL-resistant disease do benefit from alIoSCT and some patients have GVL without GVHD. A first step in developing such strategies is to understand alloimmunity against GVL-sensitive neoplasms and how this response differs from GVHD and from GVL against less sensitive neoplasms. These are the objectives of this proposal. A major obstacle in achieving these goals has been the absence of murine models for GVLsensitive and resistant leukemias that share a common pathology and genetic etiology with their human counterparts and are inducible on different strains, including KO mice that will yield leukemias lacking critical molecules. Leukemia cell lines, the mainstay of murine GVL research, lack these features. We have adopted novel murine models of CPCML (mCP-CML) and BC-CML (mBC-CML) that address these problems, mCP-CML is a myeloproliferative disorder induced via retroviral transduction of murine progenitors with the bcr-abl fusion cDNA, the defining genetic abnormality in human CP-CML. mBC-CML is induced via the retroviral introduction of both bcr-abl and the NUP98/HOXA9 fusion, a translocation found in BC-CML. The use of retrovirus allows the induction of both leukemias in any mouse, most notably gene-deficient mice. Using
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gene deficient recipients, donors, and leukemias, we will examine antigen presentation, T cell polarization, and T cell effector mechanisms in GVL and GVHD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: HOXA9 GENE AS A THERAPEUTIC TARGET IN LEUKEMIA Principal Investigator & Institution: Lawrence, Hugh J.; Professor of Medicine; Northern California Institute Res & Educ San Francisco, Ca 941211545 Timing: Fiscal Year 2001; Project Start 12-APR-2001; Project End 31-MAR-2003 Summary: (provided by applicant) A growing body of evidence supports the notion that misexpression of the HOXA9 homeobox gene is a common and critical event in myeloid leukemogenesis. Enforced expression of HOXA9 in murine marrow cells is clearly leukemogenic, and the gene is aberrantly upregulated in a large majority of cases of human acute myelogenous leukemia (AML). In a recent survey of 6,800 human genes in acute leukemia, HOXA9 expression was shown to be highly specific for AML and was the single best marker for a poor outcome. The major hypothesis of this grant is that aberrant activation of HOXA9 is a frequent downstream consequence of many, if not most, oncogenic events that lead to AML, and that this activation is critical to the induction and maintenance of the malignant phenotype. An additional key hypothesis is that HOXA9 overexpression contributes to the drug resistance phenotype. The focus of this application is to explore strategies to inhibit HOXA9 expression and/or function as a novel therapeutic approach for AML. This project has 3 major aims: i) to test the in vitra biologic effects of over-expression of HOXA9 in a factor-dependent nonleukemogenic myeloid cell line engineered to express high levels of HOXA9 in a tetracycline-regulatable manner, and to use this inducible cell line model to test strategies to block HOXA9 expression. ii) to develop an in vivo model of a Tetregulatable HOXA9-driven AML in mice, which can be used to test treatment the strategies developed in Aim #1 in a whole animal, and iii) to study the ability of antiHOXA9 strategies to alter the proliferation, differentiation and chemotherapeutic sensitivity of fresh leukemic cells from patients, and of human myeloid leukemic cell lines that show high levels of endogenous HOXA9 expression. The specific strategies to be tested include the use of conventional antisense oligonucleotides, double-stranded DNA decoys, and double-stranded RNA to induce RNA interference. We anticipate that therapies targeting the expression and/or function of HOX proteins could have a major role in the clinical treatment of leukemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IMMUNOGLOBULIN GENE ARRANGEMENT/EXPRESSION IN LEUKEMIA Principal Investigator & Institution: Campana, Dario; Member; St. Jude Children's Research Hospital Memphis, Tn 381052794 Timing: Fiscal Year 2003; Project Start 01-JUL-1991; Project End 31-JAN-2006 Summary: (provided by applicant): By identifying patients at high risk of relapse, residual disease assessment promises to increase the cure rate of children with acute lymphoblastic leukemia (ALL). The quantity of residual, morphologically undetectable disease (minimal residual disease or MRD) present during therapy is an independent predictor of patient outcome. Although polymerase chain reaction assays can quantify MRD, simpler methods are needed for clinical application. In the previous funding period, simple automated fluorescence detection assays were developed for quantification of B- and T-cell antigen receptor gene rearrangements, which can be used
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as leukemia-specific markers in 90 percent of ALL cases. The studies now proposed will determine the utility of these assays for quantification of leukemic cells in clinical samples (Aim 1). Universally applicable ALL markers are also needed for the integration of MRD assays into clinical protocols. Our previous studies showed that the neural gene, R-cadherin, is ectopically expressed in ALL but not in normal hematopoietic cells. Expression of R-cadherin should serve as a marker of recurrent leukemic cells and as an indicator of treatment-refractory ALL. The proposed studies will determine whether expression of R-cadherin can identify patients at a high risk of relapse and evaluate the efficacy of therapy (Aim 2). The application of ultra-sensitive MRD assays can be used to address an emerging problem in the treatment of ALL. Current intensive therapy has caused a delay in the timing of hematologic relapse. Assessment of MRD at end of therapy should permit identification of those patients with greatest risk of post-therapy relapse (Aim 3). The development of new automated MRD assays and the identification of new markers of leukemia should improve residual disease evaluation and thereby improve risk-directed therapy selection for every child with ALL. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LEUKEMIA THERAPY WITH MIHA SPECIFIC T CELLS Principal Investigator & Institution: Chen, Wei; Pediatrics; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 06-AUG-1999; Project End 31-MAY-2003 Summary: Allogeneic bone marrow transplantation (BMT) has been successfully applied in the treatment of hematological malignancies. The eradication of leukemia following allogeneic BMT is in part due to due to a graft- versus-leukemia (GVL) effect mediated by the donor T cell. Clinically, the GVL effect is associated with a donor T cell-mediated graft-versus- host disease (GVHD), which is commonly fatal. In patients receiving BMT from HLA-matched donors, host antigens responsible for GVHD and GVL effect are functionally defined as the minor histocompatibility antigens (MiHA). The MiHA system is poorly characterized and few MiHA proteins responsible for GVL and/or GVH effects have been identified. Several studies indicated that MiHA may have selective tissue-restricted expression. The current grant will develop leukemia therapy with donor CD4+ and CD8+ T cell subsets specific for host hematopoietic tissuerestricted MiHA in murine models. The hypothesis to be tested is that targeting donor T-cell immunity against MiHA exclusively expressed on host hematopoietic cells may preserve a curative GVL effect without causing GVHD. The functional distinct MiHAspecific donor CD4+ and CD8+ T cell subsets may differentially mediate the processes in GVL effect and GVHD. The insights gained from this study may advance the understanding of the role of donor T cell subsets in mediating GVL and GVH effects and enable us to develop new therapeutic strategies for overcoming the clinical problem currently preventing the successful treatment of leukemia with donor T cells following allogeneic BMT. The specific aims are: 1. To analyze the therapeutic efficacy, toxicity and mechanisms of donor CD4+Th1 and Th2 subsets specific for host hematopoietic tissuerestricted MiHA. 2. To assess the therapeutic efficacy, toxicity and mechanisms of donor CD8+ Tc1 and Tc2 specific for host hematopoietic tissue-restricted MiHA. 3. To develop methods develops for in vitro induction of MiHA-specific T cells for leukemia therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS IN SUCCESSFUL THERAPY OF GVHD WITH MOAB Principal Investigator & Institution: Truitt, Robert L.; Professor; Pediatrics; Medical College of Wisconsin Po Box26509 Milwaukee, Wi 532264801 Timing: Fiscal Year 2001; Project Start 01-SEP-1984; Project End 31-JAN-2003 Summary: (Applicant's Abstract) Graft-vs-host disease (GVHD) is a potentially lethal complication of allogenic bone marrow transplantation (BMT). A reliable strategy to successfully treat GVHD once initiated has not yet been developed. The applicant has shown that F(ab')2 fragments of CD3 epsilon specific MoAb administered to mice after allogeneic BMT reverses the clinical effects of GVHD and leads to tolerance induction. In leukemia-bearing hosts, however, excessive or ill-timed administration of anti-CD3 F(ab')2 leads to leukemia relapse. The primary goal of this research is to identify mechanisms responsible for the successful treatment of GVHD with anti-CD3 F(ab')2 MoAb in vivo. Extensive preliminary data implicated cytokines in the pathology and regulation of GVHD. The two-part hypothesis to be tested states that (i) depletion of Tcells through activation-induced cell death (AICD or apoptosis) by anti-CD3 (Fab')2 MoAb is an essential prerequisite for treatment of established GVHD and (ii) anti CD3 F(ab')2 activates NK-1.1+ T-cells to secrete cytokines which lead to tolerance induction. Murine models have been developed to test this hypothesis. Four specific aims are proposed: (a) To assess the importance of AICD in the successful treatment of established GVHD with anti-CD3 F(ab')2 MoAb in vivo and correlate T-cell death with activation state of the T-cells in vitro and in vivo; (b) To determine whether NK-1.1+ Tcells or CD3+ double-negative T-cells contribute to suppression of GVHD after signaling through CD3 epsilon using phenotypic and functional assays in vitro; (c) To ascertain whether IL-4 or other cytokines are essential to the mechanism involved in therapy of GVHD with anti-CD3 F(ab')2 using homozygous deletion mutant mice ("knockout mice"); and (d) To examine immunological factors that contribute to post-BMT leukemia relapse after treatment with anti CD3 F(ab')2 MoAb and the ability of donor leukocyte infusions to prevent relapse. A unique aspect of the proposed studies is the parallel evaluation of the effects of MoAb therapy in vivo on graft-vs-leukemia (GVL) reactivity using acute T-cell lymphoblastic leukemia in AKR mice as a model. Mechanistic insights gained from the studies, together with the biological principles identified, will facilitate the translational application of MoAb to clinical BMT. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROTEINS
MECHANISMS
OF
TRANSFORMATION
BY
MLL
FUSION
Principal Investigator & Institution: Martin, Mary E.; Pediatrics; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 15-JUL-2002; Project End 31-MAY-2007 Summary: (provided by applicant): The goal of this five-year mentored clinical scientist development award is to secure for the applicant the intensive training and intellectual, scientific and educational environment requisite for development as a successful, independent physician-scientist. To this end, we propose an integrated program of research and study designed to elucidate the mechanisms of transformation by translocations of the mixed lineage leukemia gene (MLL, HRX, ALL-1) and to develop models of MLL-mediated leukemia. Despite intensive study and investigation, it remains unclear as to how MLL fusion proteins participate in leukemongenesis. MLL fusion proteins are the products of reciprocal translocation events where the MLL gene on chromosome 11q23 is combined with over 30 different translocation partners
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resulting in lymphoid, myeloid and therapy-related leukemia's. Presumably the transforming effects of MLL fusion proteins are mediated through transcriptional deregulation, a gain of function activity contributed by the translocation partner. However, the remarkable number of translocation partners and the lack of homology among them have made it difficult to explain how they contribute to the oncogenic function of MLL. Emerging evidence suggests that transformation may be mediated through dimerization/oligomerization of truncated MLL. This model is attractive because it supplies a unifying hypothesis for the function of diverse MLL fusion proteins as well as exon duplicated forms of MLL that occur in some myeloid leukemias, and suggests a possible target for therapeutic intervention. The proposed research will aim to determine if dimerization or higher order oligomerization constitutes the mechanism of transformation by MLL fusion proteins. Additionally, we seek to establish a model of ALL using murine fetal liver retrovirally transduced with MLL-AF4, which is associated with infant ALL and for which appropriate animal models are lacking. Finally, we will establish a NOD/SCID model of MLL-mediated leukemia using human hematopoietic cells retrovirally transduced with bona fide MLL fusion proteins to further explore the mechanisms of transformation and to facilitate the future development of mechanism-based therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MEMORIAL HOSPITAL AND CANCER AND ACUTE LEUKEMIA GROUP B Principal Investigator & Institution: Bosl, George J.; Chairman; Sloan-Kettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 30-JUL-1998; Project End 31-MAR-2003 Summary: (adapted from the applicant's abstract): This is the first application for support of Cancer and Leukemia Group B (CALGB) research activities by Memorial Sloan-Kettering Cancer Center (MSKCC) as a Main Member institution. MSKCC's mission is devoted to clinical and laboratory research related to cancer treatment and biology. Previously an affiliate of the New York Hospital, MSKCC became a Main Member in February 1996. This change from affiliate to Main Member represents our commitment to participate in a broad-based cooperative group in order to participate in national group and intergroup randomized trials and to interdigitate the national agenda into our extensive clinical trials program. Strong research interactions already exist between CALGB and MSKCC. Larry Norton, M.D., Chair, Breast Committee, and Jimmie Holland, M.D. first and only Chair, Psycho-Oncology Committee, both play dominant roles in shaping group and national clinical trials. In addition, Nancy Kemeny, M.D., is a member of the GI Committee and Medical Oncology Chair of CALGB 9481, studying intrahepatic chemotherapy in colorectal cancer patients with hepatic metastases. We plan to augment participation in these areas, and Clifford Hudis, M.D., and Andrew Seidman, M.D., are already actively presenting to the Breast Committee. Alice Kornblith, Ph.D., leads several psycho-oncology efforts, and Russell Porenoy, M.D., and Raymond Wesson, Ph.D., will join palliative care and minority issue efforts. Committee participation has expanded, with 19 MSKCC faculty appointed to 12 committees. Protocol accrual has increased, with 69 credits between 3/1/96 and 5/1/97, and 47 credits since 12/96 alone. Increased clinical trial accrual will result from newly activated CALGB therapeutic and nontherapeutic studies from additional disease and modality committees and, by introducing new drugs and biologics under development at MSKCC, into Group studies. This integration is under way. R.S.K. Chaganti, Ph.D., will participate in Leukemia/Lymphoma Correlative Sciences studies by providing the
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introduction of comparative genomic hybridization into the study of malignant lymphomas. Accrual from affiliation with McGill University will augment MSKCC activities in CALGB. MSKCC looks forward to participation in CALGB's excellent group science. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOBILIZED BLOOD STEM CELL TRANSPLANTATION WITHOUT GVHD Principal Investigator & Institution: Strober, Samuel; Professor of Medicine; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 01-JAN-1997; Project End 31-DEC-2002 Summary: (Adapted from applicant's abstract) The goal of this application is to test the hypothesis that the T cells in bone marrow are qualitatively different than those in peripheral blood of normal mice and that after treatment with G-CSF, marrow T cells are mobilized into the blood. Preliminary data have suggested that marrow T cells have a markedly reduced capacity to induce lethal graft-versus-host disease after allogeneic marrow transplantation as compared to blood T cells but retain graft-versus-leukemia activity and an ability to facilitate engraftment. In order to test this hypothesis, the applicant will compare the surface markers, migration pathways, cytokine secretion patterns and capacity to induce lethal graft-versus-host disease, mediate graft-versusleukemia effects and facilitate engraftment by using highly purified T cell subsets from the bone marrow and blood of normal mice and from mice treated with G-CSF. Purified donor T cell subsets will be obtained by flow cytometry and injected together with T cell-depleted marrow in lethally irradiated MHC matched or mismatched recipients. Graft-versus-leukemia activity will be measured with the use of the BCL1 B cell leukemia, and graft facilitation will be measured using purified stem cells. Results of this study should help the design of clinical protocols of allogeneic marrow or mobilized blood cell transplantation in attempts to reduce the risks of graft-versus-host disease and recurrent malignancy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR ANALYSIS OF TEL AND TEL/AML1 IN PREB LEUKEMIA Principal Investigator & Institution: Nucifora, Giuseppina; Associate Professor; Pathology; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2001; Project Start 01-AUG-1997; Project End 31-JUL-2003 Summary: (adapted from the investigator's abstract) Recently, the fusion gene TEL/AML1 was cloned from children with B-lineage acute lymphoblastic leukemia (ALL). This disease is the most common childhood cancer, and it affects about 4 in 100,000 children in the United States. TEL/AML1 results from a chromosomal translocation between chromosomes 12 and 21, the t(12:21)(pl13;q22). Gene fusion occurs between TEL, located at chromosome 12 band p13, and AML1, located on chromosome 21 band q22. Although the t(12;21) is rarely seen by cytogenetic analysis, the TEL/AML1 fusion is detected in about 25-30% of childhood ALL by using molecular analysis. In addition, almost always the leukemic cells with TEL/AML1 have deletion of the normal TEL allele. Thus, the t(12;21) is unusual in that it requires two different mutations affecting the same gene: the inactivation of one allele of TEL, and the fusion of the second TEL allele to AML1. AML1 is a DNA-binding transactivator involved in several other different translocations associated with myeloid leukemias. TEL is a
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member of the ETS family of transcription factors and contains a helix-loop-helix (HLH) motif at the N-terminal, necessary for protein dimerization. The working hypothesis is that TEL/AML1 is an altered transcription factor that inappropriately affects genes involved in B cell differentiation. In support of this hypothesis, results show that TEL/AML1 represses the activation by AML1. In addition, the investigators believe that, because the HLH motif is present in the normal TEL and in the TEL/AML1 fusion, the normal TEL might dimerize with TEL/AML1 and inactivate the inappropriate regulation by the chimeric gene. This would explain progressive deletion of the normal TEL allele. The long term objective of the proposal is to dissect the molecular mechanisms by which this chimeric protein affects the development of the hematopoietic cell and leads to leukemia. The major questions addressed in this proposal are: What proteins interact with TEL/AML1? Which genes does it regulate? and How does the leukemia progress? By using a combination of biochemical and molecular cloning techniques and tissue culture studies, the investigator will identify the proteins with which the chimeric genes interact and assess their role in cell transformation. Furthermore, they will use genetically altered animals which express the human fusion protein to evaluate the progress of the disease and to determine how hematopoietic genes are affected by the chimeric proteins. The experiments outlined in this proposal will allow them to begin to dissect the effects of TEL/AML1 in hematopoiesis and its contribution to leukogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOLECULAR DETECTION AND MONITORING OF LEUKEMIA Principal Investigator & Institution: Stock, Wendy; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2003; Project Start 13-MAY-2003; Project End 31-MAR-2009 Summary: (provided by applicant): The major translational goals of molecular diagnostic and minimal residual disease (MRD) studies in the CALGB Leukemia Correlative Science Committee (LCSC) are to identify new prognostic groups and to utilize this information to adapt therapy to improve treatment outcome. We propose to consolidate all molecular diagnostic and MRD monitoring studies into a comprehensive "Molecular Detection and Monitoring Core" that will provide high quality data to Leukemia Committee clinical trials and to other LCSC projects and cores. The work will be performed in three disease-specific laboratories: Dr. Stock's laboratory (University of Chicago) for ALL and CML; Dr. Slack's (Roswell Park) laboratory for APL; and Dr. Gribben's (Dana Farber) laboratory for CLL. Several goals are proposed for Project 5. First, we will continue to utilize Real-time PCR technology for the prospective molecular detection of specific disease subsets and evaluation of MRD, correlating these findings with response to novel therapies as they are tested in the next generation of CALGB leukemia trials in ALL, APL, CML, and CLL. We propose that assessment of response using quantitative MRD monitoring as a surrogate endpoint provides unique clinical insights that will be particularly relevant as we perform the first generation of molecularly targeted CALGB leukemia trials described below in detail. A second goal of Project 5 is to validate the use of quantitative MRD monitoring as an independent prognostic marker of outcome for patients with acute and chronic leukemia. Prospective MRD evaluation of large, uniformly treated patient cohorts is essential for identification and validation of a "threshold" level of MRD that may distinguish patients at high (or low) risk of relapse. We also propose, for the first time in CALGB Leukemia studies, to utilize MRD monitoring to adapt and individualize post-remission therapy. A fourth goal of this Project is closely linked to Project 3, Gene Profiling Studies in
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Leukemia. As new molecular "signatures" characterizing novel disease subsets are identified by gene profiling studies in Project 3, we will evaluate expression levels of new "molecular signature" genes in ALL, AML and CLL, using Real-time reverse transcriptase (RT)-PCR methodology. The correlation of gene expression using Realtime RT-PCR with microarray findings will be useful for validating these data and will provide important new diagnostic and prognostic information about new molecular genetic subsets that may be used to adapt therapy in future CALGB treatment trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOLECULAR MECHANISMS OF LEUKEMOGENESIS BY PMLRAR ALPHA Principal Investigator & Institution: Kogan, Scott C.; Assistant Professor; George Williams Hooper Foundation; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: Acute promyelocytic leukemia (APL) is a form of acute myeloid leukemia (AML) associated with fusion of the retinoic acid receptor alpha gene with the gene encoding the PML nuclear protein. In APL, the leukemic cells are blocked at the promyelocyte stage of differentiation but can be induced to develop into mature neutrophils by treatment with retinoic acid. The use of retinoic acid to treat APL is a successful example of molecularly-targeted cancer therapy. The broad long-term objectives of the proposed work are to identify the combinations of genetic changes that result in AML and to delineate the mechanisms by which these changes transform normal blood cells into leukemias. The ultimate goal is to utilize this knowledge to improve treatment for human patients with leukemias and other malignancies. The specific research proposed in this application utilizes murine models of leukemia to (i) identify activities of the fusion protein PMLRARalpha that contribute to leukemogenesis and (ii) identify the molecular events that cooperate with PMLRARalpha in leukemogenesis. Activities of PMLRARalpha that may contribute to leukemia are abrogation of the normal function of PML and disruption of normal transcription in myeloid cells (including transcriptional repression of retinoic acid responsive target genes as well as inhibition of other transcription factors). The contribution of activities of PMLRARalpha to leukemogenesis will be assessed by expressing altered forms of PMLRARalpha in mice mutant versions of PMLRARalpha differentially impaired for specific functions will be tested for their ability to initiate leukemia. The development of novel retroviral-based models of APL to complement work with transgenic mice should facilitate assessment of the leukemogenic potential of these altered forms of PMLRARalpha. Additional changes that cooperate with PMLRARalpha are required for leukemogenesis in transgenic mice. Although the nature of these cooperating events is not clear, activation of growth factor receptors may contribute to leukemia. This hypothesis will be assessed by transducing PMLRARalpha-expressing bone marrow cells with retroviral vectors that drive expression of activated forms of IL-3 receptor or activated FLT3. Further, various mutant forms of activated receptors will be compared in regard to their ability to cooperate with PMLRARalpha. Correlating the ability of these mutants to cause leukemia with their different effects on growth factor signaling pathways should identify downstream events that have a central role in transformation. In addition, by examining whether the expression or activity of candidate mediators is abnormal in leukemic cells, molecules that participate in the pre-leukemia to leukemia transition will be delineated. The proposed studies should identify molecular pathways
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and particular molecules that are central to the pathogenesis of AML. This work will aid the development of new molecularly-targeted treatments for these malignancies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOLECULAR PROFILING IN LEUKEMIA Principal Investigator & Institution: Staudt, Louis; Ohio State University 1800 Cannon Dr, Rm 1210 Columbus, Oh 43210 Timing: Fiscal Year 2003; Project Start 13-MAY-2003; Project End 31-MAR-2009 Summary: (provided by applicant): Acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) each appear to be heterogeneous at the molecular level (Bloomfield and Caligiuri, 2000). During the past two decades, there has been considerable progress in identifying cytogenetic and molecular markers that can predict outcome following standard treatment for a fraction of patients with AML, ALL, or CLL. However, there still remains a sizable fraction of cases for which molecular predictors of prognosis are not clinically useful, because the malignant clone either lacks such an abnormality or because the abnormality is too infrequent to correlate with clinical outcome. The CALGB is a leader in using cytogenetic and molecular markers to stratify patients based on the risk of failure with standard treatment, and the identification of such indicators has become central to assignment of the appropriate therapy. This trend is likely to become even more critical in the future as more and more targeted therapies that are only active in molecularly defined subsets of patients become available in the clinic. Thus, a very high priority for the CALGB is to develop better and more robust molecular means to predict outcome in the hematologic malignancies. We will do this in conjunction with the Leukemia Committee, as described in that proposal. We hypothesize that genetic expression profiling using microarrays of diagnostic AML, ALL, and CLL samples that lack cytogenetic or molecular markers predictive of clinical outcome can identify a genetic expression profile or "signature pattern" that can be used to predict clinical outcome following standard therapy. A corollary to this hypothesis is that such a molecular profile could then be used for risk stratification of treatment and ultimately to improve clinical outcome in patients with AML, ALL, and CLL. Also, we hypothesize that Restriction Landmark Genomic Scanning (RLGS) can be used to identify prognostically significant DNA methylation patterns in CLL, with the same implications for clinical outcome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR TAXONOMY OF PEDIATRIC AND ADULT ACUTE LEUKEMIA Principal Investigator & Institution: Willman, Cheryl L.; Professor; Pathology; University of New Mexico Albuquerque Controller's Office Albuquerque, Nm 87131 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JAN-2005 Summary: Although remarkable advances have been made in the treatment of the acute leukemias, particularly resistant forms of leukemia remain. In 1999, 28,000 children and adults in the U.S. will be diagnosed with leukemia and 21,000 will die of their disease. This variability in clinical response is due in part to the tremendous heterogeneity of the disease itself. Traditionally classified solely on the basis of morphology and cytochemistry, the acute lymphoid or lymphoblastic leukemias (ALL) and the acute myeloid leukemias (AML) are characterized by highly variable clinical and biologic behavior, immunophenotypes, and chromosomal abnormalities. Striking differences in
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outcome may be seen in cases with the same cytogenetic profile, implying that more subtle genetic abnormalities also impact disease biology and response. We hypothesize that cDNA microarray technology will yield quantitative, orderly, and systematic gene expression profiles that can be used to design more clinically relevant classification schemes and to predict therapeutic response. By conducting correlative science studies accompanying NCI-sponsored clinical trials in children and adults affected by acute leukemia for the Pediatric Oncology Group, Children's Cancer Study Group, and Southwest Oncology Group, and by maintaining the largest leukemia tissue repositories in the world, we are poised to propose the following specific aims: 1. To Further Optimize cDNA Microarray Technology for Studies in Primary Human Leukemia Samples. 2. To Characterize the Molecular Variations Among Highly Selected Acute Leukemia Cases Using at Least 30,000 Genes. Cases have been selected using two approaches: 1) therapeutic response/resistance and 2) the presence of specific cytogenetic abnormalities. Study sets in AML include: 1) patients with "primary resistant" disease; 2) patients in long-term remission; 3) paired pre-treatment and relapse samples; 4) patients responding or failing specific treatment regimens; and 4) cases selected by genotype [t(8.21), inv(16), t(15;17), t(4;11), t(9;11), and complex]. In ALL, cases are being selected prospectively using two approaches: 1) the presence of residual disease vs. complete molecular response during the treatment course using automated quantitative molecular monitoring methods; and 2) by genotype [hyperdiploid, t(12;21), t(9;22), t(1;19), and t(4;11)]. 3. To Apply Multivariate Clustering Methods to Group Acute Leukemias That are Coherent in their Expression Patterns. 4. To Use Automated Quantitative "Real-Time" PCR Technologies to Validate cDNA Microarray Analyses. 5. To Use High Performance Computing and Informatics Technologies to Link Large Genomic Data Sets with Clinical Databases. All leukemia samples have associated clinical databases containing detailed patient information, laboratory data (cytogenetics, correlative scientific studies), and therapeutic response data. Our experienced clinical trials biostatisticians will work with the UNM High Performance Computing Center (a National Supercomputing Facility) and Sandia National Laboratory (both world leaders in massively scalable parallel computing, statistics, informatics, and visualization tools) to meet this aim. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: NOVEL FUSION PROTEIN IN CMML Principal Investigator & Institution: Ross, Theodora S.; Internal Medicine; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 10-FEB-1998; Project End 31-JAN-2003 Summary: (Applicant's Description): The TEL-PDGFBR fusion protein was identified as the protein product of a t(5;12) translocation in a patient with chronic myelomonocytic leukemia (CMML). The protein fuses the amino portion of TEL with the transmembrane and cytoplasmic domains of the PDGFBR. TEL, a member of the ETS family of transcription factors, has subsequently been described as a common site of rearrangement in multiple forms of leukemia. This is not yet the case for the PDGFBR. The applicants find, however, in the Preliminary Results, that another patient with CMML has a novel t(5;7) translocation. Southern blotting analysis has identified a breakpoint in this patient at the same genomic localization in the PDGFBR as the t(5;12) translocation. Their hypothesis is, that in this patient, as for the t(5;12) TEL-PDGFR patients, PDGFBR is constitutively activated by fusion with a 7q24 partner. Although rare (as for identification of TEL), the PDGFBR fusion partner at 7q24 may identify a gene involved in a broader group of malignancies. Also, in light of the facts that other
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patients with CMML have PDGFR containing fusions and the region of 7q24 is frequently deleted in MDS, the cloning, characterization and manipulation of this fusion protein is paramount. Hence, in Specific Aim 1, they will use anchored PCR to clone the breakpoint. Their specific oligos will come from the known PDGFBR sequence. In Specific Aim 2, they will obtain a full length cDNA and determine the relevance of this by performing ribonuclease protection assays and mapping back to chromosome 7. Finally, for Specific Aim 3 they propose to characterize the fusion protein by determining its transforming, activity(s) and biological properties using mutational and biochemical analyses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ONCOGENES INVOLVED IN ACUTE MYELOID LEUKEMIA DEVELOPMENT Principal Investigator & Institution: Reuther, Gary W.; Comprehensive Cancer Center; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 03-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): The goal of this proposal is to identify and characterize novel oncogenes expressed in patients with acute myeloid leukemia (AML). The design of this proposal is to position the candidate for an independent career in basic cancer research, with a focus on leukemia, in an academic environment. Working in Dr. Channing Der's laboratory at the University of North Carolina at Chapel Hill has provided an excellent foundation for this career. With a little more guidance from Dr. Der, the candidate will utilize the outstanding resources that Dr. Der's laboratory and the University of North Carolina at Chapel Hill provide, in order to solidify the scientific basis for an independent career in research. The first two specific aims of this research proposal focus on characterizing a novel activator of Ras, RasGRP4, identified by the candidate in a screen for novel oncogenes in AML. RasGRP4 is primarily expressed in myeloid cells suggesting it has a specific role in these cells. Targeted disruption of the gene for RasGRP4 in mice will be utilized to characterize the normal function of RasGRP4. The development of the hematopoietic system of these mice will be analyzed along with signal transduction pathways that may utilize RasGRP4. These studies represent an excellent opportunity to expand the candidate's technical repertoire (e.g., animal model development and analyses of primary hematopoietic cells), by combining the resources provided by the UNC Chapel Hill animal model facility and Dr. Der's expertise on Ras signal transduction. The last aim of this proposal, which will be initiated in the independent phase of the award, is to perform additional screens for oncogenes in AML. AML formation requires two classes of mutations: one that induces cell proliferation and survival, and one that inhibits differentiation. AML1-Eto and CBFb-MYH11, two common oncogenes in AML, are not sufficient to induce leukemia. This proposal describes experiments to identify required mutations, expressed in AML patients whose leukemic cells harbor these fusion proteins, that cooperate with these oncogenes and also to identify members of both classes of AML oncogenes. This will provide an opportunity to expand and improve strategies aimed at identifying novel oncogenes in AML. In summary, this proposal provides an excellent opportunity for the candidate to complete his training to become an independent researcher. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ONCOGENESIS AND MYELOID TRANSCRIPTION IN AML Principal Investigator & Institution: Tenen, Daniel G.; Professor; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-MAR-2007 Summary: (provided by applicant): Knowledge of the mechanisms underlying the normal development of blood cells is important in understanding and developing new treatments for various blood diseases, including leukemias. The long range goals of this project are to further our understanding of the mechanisms involved in leukemia by understanding the effects of various leukemia oncogenes on the transcription factors which regulate normal myeloid development from stem cells. Previous work in our laboratory has led to the identification of the transcription factor CCAAT Enhancer Binding Protein a (C/EBPa) as being absolutely critical for differentiation of normal myeloid blasts, and identified abnormalities in C/EBPa as playing a critical role in a number of specific types of Acute Myeloid Leukemia (AML), as noted in the Progress Report. Over the next 5 years, we propose to extend the study of how oncogenes affect this critical transcription factor in cell differentiation. We therefore propose the following Specific Aims: (1) To test the hypothesis that the interaction between PML/RAR and C/EBPa is responsible for the differentiation block in Acute Promyelocytic Leukemia (APL); (2) To understand the role of C/EBPb in the pathogenesis of APL? (Years 1-5); and (3) To investigate the synergism between loss of function of C/EBPa and leukemia oncogenes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PEDIATRIC ONCOLOGY GROUP Principal Investigator & Institution: Kung, Faith H.; Associate Professor; Pediatrics; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2001; Project Start 01-JUL-1980; Project End 31-DEC-2002 Summary: This proposal represents a request to support continued participation in the pediatric Oncology Group (POG). This cooperative research is devoted to the investigation of chemotherapeutic, immunological and molecular biological approaches to the treatment of acute leukemia and other neoplastic diseases of childhood. Significant disease free survival has been achieved and contributions have been made in clinical pharmacology, tumor immunology and biology of cancer. However the real objective of these studies is the eradication of neoplastic diseases by treatment. Studies are being designed to reflect an increasing intensity of attack on the neoplastic cell. The cooperative group technique permits prompt evaluation in series of reasonable size of promising leads in chemotherapy. These leads or new approaches are often suggested by the results of the group's own work in clinical oncology. Thus, a completed protocol often suggests new avenues to be explored in new protocols. POG led in the investigation in the immunophenotyping of acute lymphoblastic leukemia, NTX polyglutamates accumulation in leukemic cells, and N-myc gene amplication in neuroblastoma, correlated the findings with patient outcome, and then incorporated them in new treatment protocols designed to improve the survival of children with cancer. The Division of pediatric Hematology/Oncology at the University of California, San Diego has 24 years experience (10 years in CALGB and 14 in POG) in cooperative clinical trials. In the past 5 years the 4 consortium member institutions had entered 332 patients on both therapeutic and non- therapeutic studies and the satellites, 211 patients. Our investigators served on 12 committees, designed/coordinated 16 group protocol studies. We also contributed to 15 group publications/presentations. Our investigators
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will continue to design and chair therapeutic protocols,and serve on committees. Dr. Yu's laboratory will continue to explore new immunotherapeutic agents for Group use, and serve as the Group Reference Laboratory. We plan to continue our active participation in all phases of POG activities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PEDIATRIC ONCOLOGY GROUP Principal Investigator & Institution: Breitfeld, Philip P.; Pediatrics; Duke University Durham, Nc 27706 Timing: Fiscal Year 2002; Project Start 01-JAN-1983; Project End 31-DEC-2002 Summary: The goal of the proposed research is to determine optimum care for children with all types of cancer. The research mechanism involves participation by pediatric investigators in a consortium of medical institutions in North Carolina and West Virginia in collaborative multidisciplinary clinical cancer research protocols generated through the Pediatric Oncology Group. The proposed research grant will allow for the continued participation of Duke University Medical Center, Charlotte Memorial Hospital, East Carolina University School of Medicine and West Virginia University School of Medicine in Pediatric Oncology Group activities. These activities involve studies of the epidemiology and tumor biology of selected neoplasms and the natural history and optimum multimodal therapy of all childhood malignancies. Cooperative studies among physicians from a group of medical centers allow for rapid accrual of a statistically significant number of children with cancer in order to define quickly both those avenues of biologic research which have immediate clinical relevance and those therapeutic approaches which provide prolonged disease-free survival. Through participation in cooperative studies, the entire medical community engaged in the care of children with cancer has a focal point to provide not only improved patient care but also improved multidisciplinary teaching and research. Our objectives for the coming years are: 1) to develop new protocols for the immunologic stratification and chemotherapeutic management of patients with malignant lymphoproliferative and myeloproliferative disorders; 2) to develop protocols for specific brain tumor therapy which take advantage of our expanding knowledge of the biology and pharmacologic sensitivity of human brain tumors in vitro and in vivo; 3) to expand our studies of the pharmacologic agents which influence intermediary metabolism, using our in vitro data as the basis for drug scheduling in clinical trials; 4) to expand our innovative groupwide epidemiology studies to include studies of neuroblastoma and T-cell malignancies which include laboratory investigation (immunologic, biochemical and cytogenetic) where relevant; 5) to expand our multidisciplinary therapeutic research efforts in other pediatric malignancies; and 6) to expand our outreach programs for patient care and education through our regional consortium. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PEDIATRIC ONCOLOGY GROUP Principal Investigator & Institution: Lauer, Stephen J.; Professor of Pediatrics; Pediatrics; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2001; Project Start 01-JAN-1978; Project End 31-DEC-2002 Summary: The Pediatric Oncology Program at Emory University is the only comprehensive children's cancer center in Georgia and one of the largest of its kind in the Southeast. It serves a racially, ethnically, and socioeconomically diverse population from metropolitan Atlanta, the State of Georgia, and other states including Alabama,
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Arkansas, the Carolinas, Florida, and Mississippi. Since the inception of the Pediatric Oncology Group (POG), Emory is consistently one of the largest single-institution contributors to POG clinical and laboratory studies. Emory is a center for Phase I and pilot POG trials and has initiated numerous protocols that have subsequently been implemented by POG. The specific aims of the Emory POG Program are: l) to continue as a major source of patients for POG-sponsored Phase I, pilot, groupwide, and intergroup studies; 2) to provide leadership by its investigators as POG Study Coordinators, Co- coordinators, and Core Committee members; 3) to develop innovative institutional clinical trials on which to base future POG investigations; and 4) to maintain strong basic and translational research programs in pediatric oncology. To address these aims, Emory investigators are Coordinators for several major POG studies, including standard-risk new ALL (#9405), high-risk new ALL (#9006), salvage chemotherapy in relapsed neuroblastoma (#9140), and chemotherapy vs. autologous bone marrow transplantation (ABMT) in AML (#8821). Emory POG members actively participate in POG Core Committees, Subcommittees, and new protocol development. Institutional pilot studies include therapy of relapsed AML with idarubicin and chlordeoxyadenosine, treatment of relapsed solid tumors with high-dose busulfan/melphalan and ABMT, transplantation of haploidentical CD34+ cells for relapsed ALL or AML, and vincristine plus dose-escalated cyclophosphamide and infusions of peripheral blood-derived progenitor cells in refractory solid tumors. Complementary laboratory research activities include molecular biology of ALL (mechanisms of IL-6- mediated autocrine growth and aberrations in tumor-suppressor genes); in vitro sensitivity of leukemia cells to antineoplastic agents mid biological response modifiers; mechanisms of resistance of AML cells to alkylating agents; molecular neuro-oncology; and xenogeneic models to evaluate normal and neoplastic human hematopoiesis. Investigators at Emory are participating in the POG laboratory study of methotrexate metabolism by ALL cells (ALinC #16) and coordinate the study of alterations in p53 tumor-suppressor gene pathways in relapsed ALL (SIMAL #l0). Taken together, these activities of the Emory POG Program will continue to contribute to our knowledge of the biology, therapy, and prevention of neoplastic diseases in infancy, childhood and adolescence. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PEDIATRIC ONCOLOGY GROUP Principal Investigator & Institution: Ravindranath, Yaddanapudi; Pediatrics; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2001; Project Start 01-JUN-1981; Project End 31-DEC-2002 Summary: This proposal is a request for funding for our continued involvement in the Pediatric Oncology Group (POG). The aims and objectives are to find better means of management for malignant diseases in children and adolescents, and thus increase disease-free survival rates. The Children's Hospital of Michigan (CHM) provides diagnostic evaluation and multimodal therapy for children throughout the State of Michigan. While there is one other Pediatric Oncology facility in the State, the Hematology/Oncology service sees almost all children and adolescents with malignant disease who live in the greater metropolitan Detroit area, and also sees large numbers of such children referred from other parts of the State (and from Canada) regardless of their ability to pay. Until 1979, the oncology service at CHM remained "independent". In September 1979, the CHM oncology team joined the pediatric division of the Southwest Oncology Group and in January 1981 joined the Pediatric Oncology Group, which appears to have even a greater potential for development of better treatment regimens
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for childhood malignant disease. At the time of referral and/or admission to CHM for possible malignancy, each child is seen and evaluated by the appropriate oncology team members. Following appropriate diagnostic evaluation, each child is presented and discussed at the Tumor Board, which meets weekly and is attended by pediatric oncologists, pathologists, radiologists, surgeons, surgical subspecialities, and radiotherapists. A plan of action is outlined for each child's management. All such children are registered with POG, and whenever judged appropriate, children are entered on POG treatment protocols. By our participation in such a cooperative children's cancer group, our investigators are able to share new information and ideas and gain access to new multimodal therapy regimens and investigational drugs which hopefully provide the best available care to these children. Our objectives in the coming years are: 1) increased participation in POG cancer biology and epidemiology studies; 2) to continue our leukemia biology studies particularly pharmacology studies in AML/T ALL, and 3) to develop new strategies for treatment of brain tumors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PEDIATRIC ONCOLOGY GROUP Principal Investigator & Institution: Castleberry, Robert P.; Professor of Pediatrics; Pediatrics; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 01-MAR-1979; Project End 31-DEC-2002 Summary: The University of Alabama at Birmingham (UAB) is a leading contributor to the ongoing clinical and basic research activities of the Pediatric Oncology Group (POG) which are focused upon improving the care and cure for children with cancer. Current results of these trials are in some cases already published and are available in the Progress Report. The leadership from UAB in POG is evident in several areas: l) through enrollment of substantial numbers of assessable patients on Phase I, II and III therapeutic trials, including multidiscipline (surgery, chemotherapy, and radiotherapy) management studies; through participation in and development of Group-wide biological studies of selected hematopoietic and solid malignancies; through evolving, coordinating and reporting data from POG therapeutic trials; and by providing discipline and disease committee, and administrative leadership within the group. UAB will continue to enroll all eligible patients on active POG therapeutic and biological studies, including phase I investigations, and maintain high evaluability. UAB investigators will continue to coordinate clinical trials for children with neuroblastoma, bone tumors, and juvenile chronic myelogenous leukemia (JCML) and to assess the therapeutic utility of IL6. Further, UAB investigators will be principal to the development of new studies in neuroblastoma, brain tumors, JCML and acute myelogenous leukemia. UAB will continue to supervise laboratories for POG in the following areas: 1) Banded chromosomal analysis in newly diagnosed patients with lymphoid leukemia; 2) A required reference laboratory for children with JCML (POG #9265) studying the pathogenesis of myeloproliferation; 3) A required serum/plasma repository (POG #9047) with clinical and demographic data referenced on a computer data base; and 4) A non- mandatory reference laboratory to evaluate the biological and clinical significance of rnicrotubular associated protein (MAP) and tubulin isotype expression in neuroblastoma. UAB investigators will continue their scientific and administrative leadership roles on the Neuroblastoma and Other Embryonal Tumors, Myeloid Disease Core, Biologic Response Modifier Core, Executive, Principal Investigator Core, Clinical Research Associate Core, and Diagnostic Imaging Core Committees. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PEDIATRIC ONCOLOGY GROUP Principal Investigator & Institution: Kavan, Petr; Montreal Children's Hospital 2300 Tupper St Montreal, Timing: Fiscal Year 2002; Project Start 01-JAN-1983; Project End 31-DEC-2002 Summary: The Pediatric Oncology Group (POG) is a multi-disciplinary, multiinstitutional research community which collaborates to increase knowledge of and improve treatment for cancer and leukemia in children and adolescents. The Montreal Children's Hospital/McGill University (MCH), a founding member, requests funding for itself and its two affiliates, the Children's Hospital of Eastern Ontario (CHEO) and the University of Sherbrooke Medical Center (USMC) to continue to participate fully in administrative and scientific activities of the POG during the next 5 years. We expect to enroll a total of 70 patients a year on therapeutic protocols for childhood leukemias, lymphomas, solid tumors and brain tumors, with continued emphasis on Phase I and II studies of new agents and coordination or co-coordination of a minimum of 13 protocols. We expect to enroll 110 patients per year on non-therapeutic studies of cancer etiology, epidemiology, biology, psychologic impact and late effects of therapy with particular emphasis on the pharmacology and molecular pharmacology of methotrexate in acute lymphoblastic leukemia (ALL). We will comply with all requirements of the POG constitution, with MR regulations governing ethical conduct of clinical research and with OPRR and IRB requirements for informed consent and protection of subjects from research risks. In addition to an anticipated doubling of patient accruals since 5 years ago, our major contributions to POG research will include: confirmation that the extent of accumulation of methotrexate polyglutamates by lymphoblasts in B-progenitor cell ALL correlates with event-free survival (EFS) and characterization of the mechanisms regulating this metabolism (Whitehead); promotion of new agent drug development through New Agents and Pharmacology Committee leadership (Whitehead and Bernstein) and protocol coordination (Bernstein, Baruchel); introduction of stereotactic and fractionated stereotactic radiation therapy in brain tumors (Freeman); coordination of treatment protocols of newly-diagnosed and relapsed B-progenitor cell ALL (Abish, Bernstein); introduction of new agents and combinations in recurrent lymphoid disease as Sub-committee Chair, Lymphoid Relapse (Bernstein); chemotherapy and surgery of brain tumors (Baruchel, Ventureyra); and study of the biology, including p53 gene mutations, and treatment of HIV-related lymphomas (Baruchel, Whitehead). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PEDIATRIC ONCOLOGY GROUP Principal Investigator & Institution: Link, Michael P.; Professor; Pediatrics; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 01-JAN-1983; Project End 31-DEC-2002 Summary: The overall goal of this research proposal is for Stanford University, the University of Arizona, and the Kaiser Permanente Medical Centers of the South San Francisco Bay Area to continue their active involvement in Pediatric Oncology Group research activities. Stanford faculty and the University of Arizona faculty have already assumed key leadership positions in POG and have or have had major roles in the scientific and administrative aspects of the Group. Further, Stanford, the University of Arizona, and Kaiser have maintained excellent performance ratings in their participation in POG studies and have received commendations for the large numbers of evaluable patients placed on therapeutic protocols. Specifically: l) We plan to
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continue to enter patients on appropriate POG studies where they exist. The number of patient entries from Stanford has increased each year as appropriate POG studies become available. We anticipate that between 65 and 80 patients will be entered on front-line therapeutic studies each year from Stanford in addition to patients who will be entered from the affiliates; in addition, 40-50 patients or more will be entered on POG non-therapeutic studies. 2) We anticipate that the activities of individual investigators from Stanford and the University of Arizona will continue and increase during the period of this research proposal. Currently, our faculty serve as study coordinators for front- line therapeutic studies in lymphoma and leukemia, and they have coordinated and analyzed data from recently closed protocols in osteosarcoma, lymphoma, leukemia, and Ewing's sarcoma. Our faculty also serve key scientific and administrative roles as Group Vice Chair, Disease and Discipline Committee Chairmen and CoChairmen, as members of Disease and Discipline Core Committees, and as members of the Executive Committee. Thus, our faculty are in position to influence the future direction of the scientific activities of POG. 3) We anticipate that involvement of Stanford faculty in the laboratory scientific activities of POG will continue. The laboratories of Drs. Link and Cleary have served as immunology reference laboratories and molecular biologic reference laboratories for leukemia studies of POG. 4) We anticipate that non-POG related laboratory and clinical research conducted at Stanford University and its affiliates will become increasingly relevant to POG activities. Some of these activities have already been incorporated into POG laboratory and therapeutic studies and others are targeted for incorporation into future POG studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PEDIATRIC ONCOLOGY GROUP ACTIVITIES Principal Investigator & Institution: Buchanan, George R.; Pediatrics; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2001; Project Start 01-JAN-1983; Project End 31-DEC-2002 Summary: This grant application seeks continued support for the Pediatric Oncology Group (POG) activities of The University of Texas Southwestern Medical Center (UT Southwestern) Consortium, which consists of UT Southwestern (Dallas), Cook-Ft. Worth Children's Medical Center (Ft. Worth), and Scott & White Clinic (Temple). Since joining POG in 1981, this partnership of children's cancer treatment and research centers in North Texas has grown to become POG's largest contributing member with regard to patients enrolled on therapeutic studies (over 100 annually). During the current grant cycle, consortium investigators have held administrative and scientific leadership positions on major Group committees, including Executive Committee, Principal Investigator's Committee, New ALL Committee, T-cell Committee, and Lymphoid Relapse Committee. UT Southwestern Consortium investigators have also served or are serving as study coordinators on multiple POG treatment protocols studying ALL (newly diagnosed patients with B-lineage and T-cell disease as well as following relapse), non-Hodgkin's lymphoma, bone marrow transplantation and new agents being explored in Phase I-II trials. UT Southwestern Consortium investigators have also had prominent roles in the arenas of data management, protocol development, molecular and pharmacologic monitoring in authorized POG reference laboratories, and supportive care. Results of pilot projects conducted at UT Southwestern have been instrumental in the construct of group-wide treatment strategies, especially involving use of methotrexate for B-lineage ALL. To support the UT Southwestern Consortium's continued commitment to POG research during the next 5 years, this new grant proposal describes personnel and facilities in the 3 consortium centers. Specifically,
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during 1996-2000 the Consortium aims to advance POG research by: (l) enrolling as many patients as possible on POG treatment, biological classification, and epidemiology protocols; (2) collecting, recording, and submitting research data in an accurate and timely fashion; (3) providing administrative and scientific expertise to the Group through continued active participation on major committees, including service as disease committee chairs and protocol coordinators; and (4) continuing to conduct innovative in-house pilot studies for subsequent use by the Group. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PEDIATRIC ONCOLOGY GROUP PARTICIPATION Principal Investigator & Institution: Pui, Ching-Hon; Acting Chairman; St. Jude Children's Research Hospital Memphis, Tn 381052794 Timing: Fiscal Year 2001; Project Start 01-JAN-1982; Project End 31-DEC-2002 Summary: We propose continued participation in the Pediatric Oncology Group (POG). Our goals are as follows: (1) to improve cure rates for children with cancer through participation in Phase I, II, and III clinical trials designed to test new agents or concepts; and (2) to participate in laboratory-based research aimed at clarifying the basis of drug resistance and pathogenetic mechanisms of childhood cancers. We are committed to Group participation because we believe: (1) that collaborative efforts are both desirable and necessary for study of childhood cancers, since all are relatively rare; and (2) that well-designed randomized clinical trials provide the most definitive test of efficacy and general applicability of new therapies and that pooled intellectual resources are advantageous as well. Our contribution to the Group can be categorized as follows: (1) contribution of selected patients (those with rare tumors or less common stages of other cancers, n approximately 80-100/year) to Group studies; (2) administrative and scientific leadership (e.g., disease or discipline committee chairs, and protocol coordinators); (3) provision of multiple reference laboratories (flow cytometry analyses of leukemia and solid tumors, cell bank, AML cytogenetics, pharmacokinetics/pharmacodynamics, molecular genetics of leukemia and solid tumor); (4) regular presentation of results of in-house research to the group. Since our center has an unusually large number of patients and staff (both clinical and basic), the latter contribution assumes unusual importance. We have an extensive in-house developmental therapeutics program which is independent of, but complementary to, the Group's clinical research programs. We also have extensive programs in basic research. The aim of these programs, to determine the pathogenesis of pediatric neoplasia, is expected to positively influence the Group's central goal -- curing children with cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PEDIATRIC ONCOLOGY GROUP STUDIES Principal Investigator & Institution: Chauvenet, Allen R.; Pediatrics; Wake Forest University Health Sciences Winston-Salem, Nc 27157 Timing: Fiscal Year 2001; Project Start 01-APR-1991; Project End 31-DEC-2002 Summary: The overall objective of the proposed research effort is to continue work towards determining the optimum care for children with all types of cancer. The research mechanism involves participation by pediatric investigators at the Bowman Gray School of Medicine in the development and execution of collaborative multidisciplinary clinical protocols of the pediatric Oncology Group. The proposed research grant will support the continued participation of the Bowman Gray School of
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Medicine as a full member of the pediatric Oncology Group. Our accomplishments in the past grant period are described in detail in the proposal. Our institutional goals for the five year period of this grant include: (1) continuing our high level of patient accrual and excellent clinical contributions to the POG including our outstanding patient evaluability and protocol compliance which has merited a letter of commendation from the operations office at every 6-month analysis in the past (2) maintaining our institutional involvement in POG leukemia studies and our representation on the new ALL core committee (3) continuation and further development of our multi-disciplinary institutional commitment to POG Hodgkin's disease activities (4) a major role on the POG cytogenetics committee including optimal use of our new reference laboratory status (5) increased institutional development of late effects studies in collaboration with the POG late effects efforts (6) expansion of our efforts in neuro-oncology including increased enrollment on brain tumor studies and investigator roles on the POG brain tumor committee (7) use of in situ studies of tumor cell ploidy in collaboration with POG and other investigators (8) continued contributions to the administrative aspects of the POG. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CANCER CTR
PEDIATRIC
ONCOLOGY
GROUP--MIDWEST
CHILDREN'S
Principal Investigator & Institution: Camitta, Bruce M.; Pediatrics; Medical College of Wisconsin Po Box26509 Milwaukee, Wi 532264801 Timing: Fiscal Year 2001; Project Start 01-JAN-1983; Project End 31-DEC-2002 Summary: The primary objective of the Midwest Children's Cancer Center is to reduce the incidence of and mortality from childhood cancers. This is approached by: 1) providing the best possible patient care (diagnostic and therapeutic; 2) education of medical and nonmedical groups as to the types of, treatments for, and availability of care for different childhood cancers; and 3) clinical and laboratory research. Investigators at the Cancer Center include specialists in pediatric oncology, surgery, orthopedic surgery, neurosurgery, radiology, radiation therapy, pathology, neurology, psychology and nursing. All new patients are discussed at a multidisciplinary Tumor Board. The children are then treated on Pediatric Oncology Group (POG) or institutional protocols. Results are analyzed and reported regularly. The purpose for the Midwest Children's Cancer Center's participation in POG are: l) to enhance the probability of achieving the above objectives by collaboration with other institutions in the design and execution of clinical protocols; and 2) to evaluate, through laboratory investigations, aspects of tumor biology which result in successful and unsuccessful therapy. Pediatric tumors are relatively rare. The POG is composed of more than 50 member institutions. By pooling resources, biologic and therapeutic studies on these uncommon tumors are facilitated. Similar collaboration permits more rapid development of new drugs. In addition, participation in a common milieu promotes dissemination of information between institutions and investigators. If all children with cancer receive the best possible care, morbidity and mortality will be minimized. The Midwest Children's Cancer Center has been a major contributor to POG by: 1) patient accrual; 2) coordination of POG protocols; 3) institutional pilot studies that were advanced to POG studies; and 4) participation in POG disease and administrative committees. In the next grant period we will continue each of these activities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PEDIATRIC ONCOLOGY GROUP--THE CAROLINAS CONSORTIUM Principal Investigator & Institution: Barredo, Julio C.; Professor; Pediatrics; Medical University of South Carolina 171 Ashley Ave Charleston, Sc 29425 Timing: Fiscal Year 2001; Project Start 15-JUN-1996; Project End 31-DEC-2002 Summary: (Adapted from the applicant's description): The institutions included in this proposal have been part of the Pediatric Oncology Group (POG) and received good performance scores during the past five years. There are two primary goals of this proposed research; the first is to accrue patients to the Group clinical trials in order to determine the optimal care of children with all types of cancers. The second is to contribute scientific expertise to the Group in areas of both patient care and tumor biology. This proposed research will allow participation in POG activities through a consortium effort of East Carolina University (ECU) School of Medicine, Carolinas Medical Center, Medical University of South Carolina (MUSC), Greenville Hospital, Presbyterian Hospital, and Memorial Mission Hospital (The Carolinas' Consortium). In addition to these clinical activities, their scientific efforts in next five years will include: (1) development of new protocols for the treatment of children with cancer focusing mainly on pediatric lymphomas; (2) expansion of studies of minimal marrow residual disease (using RT-PCR analysis) and assessment of new purging techniques in neuroblastoma; (3) participation in the laboratory evaluation of folylpolyglutamate synthetase (FPGS) in lymphoblasts of newly diagnosed patients; and (4) evaluation of the role hematopoietic growth factors in the treatment of pediatric malignancies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROJECT ALLIFE - EXERCISE AND LEUKEMIA SURVIVORS Principal Investigator & Institution: Oeffinger, Kevin Charles.; Family Practice and Cmty Med; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-AUG-2007 Summary: (provided by applicant): Adult survivors of childhood leukemia are a growing population that have an excess in all-cause and cardiovascular (CVD)-related mortality and are at risk for multiple health problems, including CVD, osteoporosis, and obesity. Physical activity is protective and reduces risk for CVD, hypertension, Type 2 diabetes mellitus, and osteoporosis. The Lifestyle Physical Activity intervention has been efficacious in the general population in increasing sustainable levels of moderateintensity physical activity and cardiorespiratory fitness and improving cardiovascular risk profiles and mental health. A targeted intervention tailored to the needs of leukemia survivors and intended to increase sustainable levels of moderate-intensity physical activity is not only warranted, but critical. It is imperative that methods to reduce morbidity and mortality of this young population while enhancing quality of life and productivity be addressed. The proposed study, Project ALLIFE (Acute Leukemia Lifestyle Intervention For Everyday), is a 12- month effectiveness trial with 120 young adult survivors of childhood leukemia randomized to either the Lifestyle Physical Activity intervention (ALLIFE-I) or a standard control group who will receive a periodic generic health newsletter (ALLIFE-SC). Major data collections will be at baseline, 6- and 12-months, with the two primary outcomes being levels of physical activity, as measured by 7-day physical activity recall, and cardiorespiratory fitness, as measured by the Aerobic Adaptation Test. Secondary outcomes will include other well-established measures of physical activity, cardiovascular risk profiles, gait and balance assessment, and psychological measurements. The primary research hypothesis to be tested is that the Lifestyle intervention will significantly increase physical activity and
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cardiorespiratory fitness in adult survivors of childhood leukemia in comparison with standard care. Three additional questions to be addressed are: determining if such an intervention leads to improvement in cardiovascular risk profile; determining if gait and balance disturbances are related to physical inactivity in leukemia survivors and if these disturbances improve with the intervention; and identifying factors that are predictive of improvement or lack of improvement in outcomes. This study will represent the first clinical trial aimed at increasing physical activity in leukemia survivors and will advance our understanding of this vulnerable population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PROMYELOCYTIC LEUKEMIA PROTEINS ROLE IN APOPTOSIS Principal Investigator & Institution: Borden, Katherine L.; Associate Professr; Physiology and Biophysics; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-JAN-2004 Summary: (adapted verbatim from the investigator's abstract) The promyelocytic leukemia protein PML has been ascribed roles in growth control, transformation suppression and cell death but its mechanism of action is unknown. These functions are closely tied to the subcellular localization of the protein. In normal cells, the majority of PML forms nuclear bodies which are disrupted when the cell undergoes stress. A chromosomal translocation disrupts PML in acute promyelocytic leukemia (APL) patients resulting in loss of PML nuclear bodies. Disruption of PML's growth control and apoptotic action is thought to contribute to leukemogenesis. Most viruses have evolved mechanisms to bypass host cell defenses such as apoptosis in order to survive. Several viruses target PML bodies during infection. The investigator has studied the effect of a single stranded RNA virus on PML to better understand its physiological function. This virus, lymphocytic choriomeningitis virus (LCMV), is able to establish chronic infection in tissue culture: thus, LCMV must disrupt host cell mediates apoptosis. This establishes a system for the study of PML and its role in apoptosis. A single viral protein, Z, can translocate PML nuclear bodies to the cytoplasm. This translocation may cause the decreased propensity of infected cells to undergo cell death when serum deprived. The investigator has identified a previously unknown component of PML nuclear bodies, the ribosomal protein PO. This protein has a nuclear role in DNA repair, endonuclease activities and a cytoplasmic role in translation. PO is upregulated in colon polyps and tumors suggesting that its association with PML in the nucleus may be related to PML's apoptotic action. The investigator are involved in studying several novel aspects of PML function, in particular interactions with Z, PO and a novel proline rich homeodomain protein PRH and the function of PML in translation. The investigator hypothesizes that PML executes its pro-apoptotic actions through association with other cellular partners and that LCMV proteins block this activity. Because of the association with PML with ribosomal proteins like PO, they predict that PML is involved in translational control and that this action is linked to its pro-apoptotic function. They propose to: (1) determine other cellular partners of PML and assess whether these new partners affect PML's apoptotic action; (2) investigate the PML/Z interaction using high resolution NMR methods to elucidate that basis of this proline interaction motif; (3) determine whether PML is involved in translational control perhaps through interaction with PO and whether this action could be linked to PML's apoptotic action. Elucidating the molecular mechanism of action of PML has important implications for understanding the progression of APL and certain viral infections. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROTEINASE 3 SPECIFIC IMMUNOTHERAPY OF LEUKEMIA Principal Investigator & Institution: Molldrem, Jeffrey J.; Chief, Section of Transplant Immunology; Blood & Marrow Transplantation; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-JAN-2003 Summary: A significant graft versus leukemia (GVL) immune response, mediated by donor lymphocytes after allogeneic bone marrow transplantation (BMT), contributes to the cure of 40-50 percent of adult patients with myeloid leukemias. However, allogeneic BMT is only available for 25 percent of all patients due to patient age and donor availability. Therefore, the overall objective of this proposal is to develop strategies for the generation of antigen-specific antileukemia immune responses for the treatment of myeloid leukemias that can be applied to more patients. Proteinase 3 (Pr3) is a 26kd myeloid-restricted azurophil granule protein that is normally maximally expressed only in developing promyelocytes and is an antigen for the antineutrophil cytoplasmic antibody (ANCA) in patients with Wegener's granulomatosis. Pr3 is overexpressed by 3 to 6 fold in 75 percent of chronic myeloid leukemia (CML) and 50 percent of acute myeloid leukemia (AML) cells. An HLA-A2-restricted 9 amino acid peptide derived from Pr3, PR1, has been shown to be a target epitope of cytotoxic lymphocytes (CTL) that preferentially lyse myeloid leukemia over normal bone marrow progenitors in vitro. The amount of CTL lysis correlates with Pr3 overexpression in the target cells. Detection of immunity to PR1 in normal donors and some patients with myeloid leukemia strongly implies that patient's own leukemia cells can act as a source of immunizing protein and begs the issue of whether existent immune responses to PR1 play any role in slowing leukemia progression and whether boosting of immune responses can offer any therapeutic benefit. The current NEW INVESTIGATOR proposal will assess the clinical importance of immune responses to PR1 peptide, evaluate a PR1 peptide-based tumor vaccine in patients with myeloid leukemia, and since Pr1 is the first tissue-restricted epitope identified, will investigate other unique HLA-A2-associated Pr3 peptides as leukemic-specific epitopes for CTL. To investigate the clinical significance of immune responses to PR1, CTL precursor (CTLP) frequency against PR1 will be determined in patients with CML, AML and their normal marrow donors before and after BMT using limiting dilution analysis and by using a fluorescence-tagged PR1-tetramer to directly label PR1-specific CTL. Pr3 expression in leukemia and the surface phenotype of leukemia and PR1-specific CTL will be examined and correlated to CTLP frequency and clinical outcomes. To investigate whether an immune response to PR1 can be boosted, a phase I/II study (NCI study number T98-0017, Molldrem P.I.) of PR1 peptide-based vaccine with incomplete Freund's adjuvant (IFA) will be conducted in patients with CML, AML, and myelodysplastic syndrome. The University of Texas M. D. Anderson Cancer Center has approved the investigation, and NCI will supply GMP quality PR1 peptide and IFA. Immune responses to the vaccine will be determined by LDA of CTLP and by analyzing the number of PR1-specific CTL with the fluorescent PR1-tetramer and will be correlated to clinical response and percent of leukemia blasts in bone marrow. Lastly, other synthetic HLA-A2-associated peptides from Pr3 will be investigated for their potential to elicit peptide-specific CTL from donor PBMC in vitro and then tested for ability to lyse myeloid leukemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RETINOID INDUCED APOPTOSIS IN LEUKEMIA CELLS Principal Investigator & Institution: Piedrafita, F Javier.; Sidney Kimmel Cancer Center San Diego, Ca 92121 Timing: Fiscal Year 2001; Project Start 01-APR-1998; Project End 31-JAN-2003 Summary: Retinoids have proven to be effective cancer preventive and chemotherapeutic agents. Retinoids can be used to alleviate acute promyelocytic leukemia in humans, leading to an apparent cure when combined with chemotherapy. However, effective retinoids for the treatment of other hematopoietic malignancies are not available yet. Retinoid signals are mediated by the retinoid receptors, RARs and RXRs, which belong to the steroid/thyroid hormone/retinoic acid superfamily of transcription factors. Recent evidences have shown that retinoids can induce apoptosis in certain cancer cell lines. Apoptosis is a naturally occurring form of cell death important for defense, development, homeostasis, and ageing, and alterations in the apoptosis pathways or functions contribute to the pathogenesis of certain human diseases, including cancer. Importantly, a novel class of selective retinoids has been recently discovered which are highly effective against a human non-small cell lung cancer in an animal model. These retinoids can induce apoptosis in certain cell lines, including several leukemia cell lines, and show promise as novel direct therapeutic agents for the treatment of cancer. They aim to investigate the mechanisms of action of these novel apoptosis inducing retinoids in leukemia cells. They will analyze the potential role of two transcription factors, Sp1 and NfkB, in retinoid-induce apoptosis. They have found that treatment of leukemia cell lines with those apoptotic retinoids causes loss of the DNA binding activity of both transcription factors: Sp1 is a target for caspases, while NfkB is translocated into the cytosol. They provide evidence that activation of caspases in necessary for retinoid-induced apoptosis. This is partially affected by inhibitors of protein synthesis. However, inhibition of RNA transcription has no effect on retinoid-induced apoptosis, suggesting a new mechanism of action for those novel retinoids which is independent of transcription. Thus, understanding the role of Sp1 cleavage and the mechanism of NfkB inhibition during retinoid-induced apoptosis will significantly enhance their knowledge of this novel retinoid action, and is likely to refine the future design and improve the development of new retinoids which would result in more effective treatments of leukemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RETROVIRAL IMMUNOTOXINS FOR LEUKEMIA Principal Investigator & Institution: Vallera, Daniel A.; Professor; Therapeutic Radiology; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2003 Summary: (Applicant's Abstract) Immunotoxins (IT) are experimental pharmacologic agents that are made by linking antibodies or cytokines that specifically bind to cancer cells to potent catalytic toxins of which a single molecule can kill a cell. The major purpose is to deliver therapy selectively to cancer cells instead of nontarget organs as does conventional chemotherapy. Although these agents selectively bind and kill cancer cells, clinically they have been limited by their 1) failure to penetrate and localize in adequate concentrations in cancer target tissue 2) localization in nontarget organs limiting the tolerated dose and collapsing the therapeutic window. In this application, the applicant will explore a solution to this problem. Cells of the immune system such as T cells are the most prominent cell types that penetrate, attack, and destroy cancer cells
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and are naturally suited for the expression and production of cytokines in response to antigenic challenge. Therefore, he proposes using T cells to deliver retroviral IT (retIT) consisting of IL-4 spliced to genetically modified diphtheria toxin at the site of the leukemia cells. He has established a model of retIT therapy that he will use as a foundation for future attempts to modify and improve retIT. He will test the usefulness of retIT for therapy of myeloid leukemia, the most common adult form of leukemia. In this model, the applicant has produced an antigen specific CTL cell line called T15 by hyperimmunization with irradiated murine myeloid leukemia C1498. When T15 is transduced with retrovirus encoding IL-4 spliced to truncated DT, T15 cells have been shown to express and secrete IL-4 retIT which specifically kills IL-4R+ C1498 cells, but not IL-4R- cells in vitro. More importantly, mice given C1498 tumors show significantly enhanced anti-C1498 effects when treated with transduced T15 cells as compared to controls. In this application in the first aim, the applicant intends to use this model first to answer important questions regarding the role of IL-4 IT and T15 CTL in the first retroviral model. Is secretion of IL-4 IT necessary and how much must be secreted to get an anti-cancer effect? Does the amount of secreted retIT correlate with the magnitude of the anti-cancer effect? What is the role of the CTL vehicle in the retIT response? Can we enhance secretion and CTL delivery of retIT? In the second aim, he will determine if retIT administration has advantages over conventional IT administration particularly regarding their toxic effects on non-target organ systems and effects on the immune response. With the anti-C1498 effects that he has already established as a baseline, in the last aim he will ask whether or not important genetic modifications can improve retIT. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ROLE TRANSFORMATION
OF
THE
PNH
PHENOTYPE
IN
LEUKEMIC
Principal Investigator & Institution: Bessler, Monica; Barnes-Jewish Hospital Ms 90-94212 St. Louis, Mo 63110 Timing: Fiscal Year 2001; Project Start 20-JAN-2001; Project End 31-DEC-2005 Summary: (adapted from the applicant's abstract): Paroxysmal nocturnal hemoglobinuria (PNH) is a blood disorder, which is caused by the clonal expansion of a hematopoietic progenitor cell that carries a somatic mutation in the X-linked PIGA gene. It presented classically with hemoglobinuria due to intravascular hemolysis, thrombotic complications, and pancytopenia. The PIGA gene encodes a protein subunit of a glycosyltransferase essential in the synthesis of glycosyl phosphatidylinositol (GPI) anchor molecules. Patients with PNH therefore have a proportion of blood cells deficient in all GPI-linked surface molecules. PNH is frequently found in patients with aplastic anemia (AA) and in patients with myelodysplasia (MDS). Although not a neoplastic disease on its own, patients with PNH have an increased risk of developing acute myeloid leukemia (AML). Promoted by the clinical association of PNH with AA, MDS, and AML, we raised the hypothesis that a PIGA gene mutation alone does not cause clonal expansion or leukemic transformation. But due to their inability to like certain proteins to the cell surface through a GPI-anchor PNH cells escape immuno surveillance and cell death that causes bone marrow aplasia in AA and controls neoplastic cell growth in early leukemogenesis. In the proposed research we will use a mouse model that closely mimics the human disease and investigate the association of PNH with MDS and AML. We will obtain mice with blood cells lacking GPI-linked proteins by disrupting the murine Piga gene in early hematopoietic progenitor cells in the bone marrow using the Cre-loxP system. By this approach we will generate two types of mice, one with all blood cells deficient in GPI-linked proteins whereas the other
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will have both PIGA (+) and PIGA(-) circulating blood cells. We will then compare PIGA(+) and PIGA(-) hematopoiesis in these mice in vitro and in vivo under a variety of circumstances, including the administration of stimuli that trigger cell death along with agents known to cause leukemia transformation. Competition between cells expressing wild type Piga and those expressing the recombined Piga allele will enable us to uncover even subtle differences in cell death and proliferation in any stages of hematopoietic differentiation. These experiments will demonstrate whether PIGA(-) blood cells are more resistant to specific stimuli that activate apoptotic cell death and whether mice with PIGA(-) blood cells develop leukemia earlier and more frequent compared to mice with phenotypically normal blood cells. In this way we hope to identify the factors that differentially influence growth and death of PNH and normal hematopoietic progenitor cells and to elucidate mechanisms that may lead to leukemia transformation in patients with PNH. The availability of a mouse model for PNH will provide us with a powerful tool to test new therapeutic agents for the treatment of PNH, PNH/MDS, PNH,AML and possibly other clonal blood disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: SEQUENCE CHROMOSOMES
BASED
FISH
ANALYSIS
OF
PHILADELPHIA
Principal Investigator & Institution: Knoll, Joan H.; Children's Mercy Hosp (Kansas City, Mo) 2401 Gillham Rd Kansas City, Mo 64108 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2004 Summary: (provided by applicant) One of the most prevalent abnormalities in leukemia patients, the Philadelphia chromosome, a translocation of the ABL1 oncogene on chromosome 9 to the BCR gene on chromosome 22, occurs in adult chronic myelogenous leukemia and childhood acute chronic leukemia. In addition to the translocation, the commercial ES-probe used in clinical cytogenetics laboratories sometimes detects deletions of DNA sequences upstream of the ABL1 gene on the derivative 9 chromosome (in 1/10 to 1/3 of patients). These deletions appear to be prognostic for early blast crisis. We hypothesize that these deletions result in hemizygosity of additional genes adjacent to ABLI. These deletion breakpoints can be refined with high- resolution fluorescence in situ studies (scFISH), which uses short single copy (sc) DNA probes designed from the draft genome sequence. Chromosomal preparations of patient specimens diagnosed with Philadelphia chromosomes in clinical cytogenetic laboratories will be analyzed with these probes. ScFISH, which has been developed in our laboratories, provides an unprecedented level of resolution for delineating sequences associated with inherited chromosomal rearrangements by FISH (Rogan, Cazcarro, Knoll, 2001; Knoll, Cazcarro, Rogan, 2000). We have developed and validated single copy DNA probes (quickly and without cloning) for FISH analysis of more than 20 distinct chromosomal regions. We aim (1) to develop scFISH probes for ABL1 oncogene, BCR and their adjacent regions from the draft genome sequence and verify their locations by FISH; (2) to compare results with scFISH probes to those obtained using the commercially available ES-probes for t(9;22) on the same patient specimens; and (3a) to categorize cytogenetically positive t(9;22) into molecular subgroups based on the sizes of deletion centromeric to ABL1 and the breakpoints within the BCR gene, (3b) to determine if there are preferential sites of breakage on chromosome 9 adjacent to ABL1, and to localize these sites. In contrast with scFISH probes, commercial reagents detecting this translocation routinely used in clinical laboratories comprise large multigenic segments. We anticipate that both the commercial and scFISH probes will detect the chromosomal translocation in some
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patients, however, only the scFISH probes are expected to delineate deletions in sequences immediately adjacent to ABL 1, and to distinguish the major and minor sites of breakage in the BCR gene that correspond to chronic myelogenous leukemia and acute lymphocytic leukemia, respectively. The proposed study will delineate the chromosomal regions that undergo breakage in these types of leukemia and will establish whether there are common deletion breakage intervals on the translocated chromosome 9. Our long range goal is to classify patients based on the sites of translocation and deletion size, and then to determine if the disease complications can be attributed to the loss of specific genes adjacent to ABL1. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: SIGNALS DOWNSTREAM OF NOTCH REGULATING LYMPHOID CELL FATE AND FUNCTION Principal Investigator & Institution: Pear, Warren S.; Associate Professor; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 13-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): The human homologue of Notchl was originally identified at the chromosomal breakpoint in a recurrent chromosomal translocation in T-cell leukemia. We have previously shown that constitutive expression of activated Notchl causes T-cell leukemia in mice and that its role in leukemia may be related to its normal function in lymphoid development. As part of our long-term plan to understand the role of Notch in leukemia, we have initiated studies to understand Notch function in hematopoiesis. Notch proteins are a conserved family that regulates cell fate choice in many lineages, including stem cells. Recently, we have provided evidence that Notch plays a key role in regulating lymphoid cell fate decisions from hematopoietic stem cells. To further understand this process, we have undertaken studies to understand Notch function in B cell development. Our preliminary results suggest that Notch signaling promotes apoptosis of B cells and that inhibition of Notch signaling leads to B cell development at the expense of T cell development, both in vivo and in organ cultures. The proposed studies focus on the role of Notch signaling in B cell development and survival. In Specific Aim 1, we will focus on Deltex, a poorly understood modulator of Notch signaling. We have found that Deltex antagonizes Notch signaling in lymphoid progenitors and promotes B cell development from hematopoietic stem cells. The studies in this aim will use a combination of in vivo, organ culture, and in vitro methods to understand the function of this protein in lymphoid development. In Specific Aim 2, we will characterize Notch signaling in B lymphoid subsets and determine the mechanism by which Notch signaling specifically promotes B cell death. These studies will lead to an improved understanding of lymphoid development and function, and in doing so, will provide therapeutic insights into treating leukemia and other diseases of the immune and hematopoietic systems. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: STAT ACTIVATION IN LEUKEMIAS Principal Investigator & Institution: Zuckerman, Kenneth S.; Professor; Internal Medicine; University of South Florida 4202 E Fowler Ave Tampa, Fl 33620 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2006 Summary: (Applicant's Abstract) The first purpose of this project is to understand the molecular mechanisms responsible for the constitutive activation of the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signal transduction
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pathways in some cases of acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), and chronic myelogenous leukemia (CML). The second purpose of this project is to determine the importance of constitutive JAK2/STAT5 activation in development and maintenance of the leukemic phenotype, both in vitro and in vivo. The primary hypotheses being tested are that specific activating mutations that lead to constitutive activation of JAK/STAT signal transduction pathways are responsible for the development and/or maintenance of leukemic cell survival and proliferation, and that, in leukemic cells expressing constitutively activated STAT5, inhibition of STAT5 activation or function. Three specific aims are proposed to test these hypotheses. Specific Aim 1 is to determine the mechanism(s) of constitutive activation in the HEL/Dami and Meg-01 human leukemic cell lines. Specific Aim 2 is to determine whether constitutive JAK/STAT signaling pathway activation plays an important role in maintenance of the leukemic phenotype of primary human AML cells. Specific Aim 3 is to determine the ability of double-stranded "decoy" oligonucleotides containing the STAT5 binding domain to inhibit the unregulated survival and proliferation of leukemic cells in vivo. The models to be tested include: (1) human HEL/Dami and Meg-01 cell lines implanted in sublethally irradiated NOD/SCID mice; (2) tet-off bcr/abl transgenic mice, which develop leukemia when mice are deprived of tetracycline in their drinking water (obtained from Dan Tenen); and (3) mice transplanted with bone marrow cells transfected with TEL/JAK2 or TEL/ABL retroviruses, which result in development of leukemias that have constitutively activated STAT5. These studies should lead to new understanding approaches for treatment of leukemias in which STAT activation plays a role in maintenance of the leukemic phenotype. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: STUDIES OF BCR/ABL LEUKEMOGENESIS IN MICE Principal Investigator & Institution: Van Etten, Richard A.; Director, Hematologic Malignancies; Cbr Institute for Biomedical Research 800 Huntington Ave Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2006 Summary: (Adapted from the investigator's abstract) The human Philadelphia (Ph) chromosome-positive leukemias, including chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia, are among the most common hematological malignancies, and current therapy for these diseases is inadequate. Expression of the product of the t(9;22) Ph chromosome, the BCR!ABL fusion gene, in the hematopoietic system of mice by generation of transgenic mice or through retroviral transduction and transplantation of bone marrow has demonstrated that BCR/ABL is a leukemia specific oncogene and the direct cause of CML. The long term objective of this application is a more complete molecular and genetic understanding of the pathophysiology of human Ph-positive leukemias, particularly the myeloproliferative disease CML. These goals will be accomplished by the use of a retroviral bone marrow infection/transplantation mouse model system that accurately and quantitatively models both human CML and Ph-positive B-lymphoid leukemia, and will have two Specific Aims. In the first Aim, the signaling pathways important for leukemogenesis by BCR/ABL will be identified by testing BCR/ABL mutants, by further analysis of the requirement for direct binding of the Grb2 adapter protein by the Bcr/Abl fusion protein, and through the use of mice with germline mutations in signaling molecules. In the second Aim, the bone marrow target cells that initiate the CML-like disease and B-lymphoid leukemia induced by BCR/ABL will be characterized and isolated by physical and immunological methods. These investigations will add important new information to our understanding of these
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leukemias, that would be difficult if not impossible to obtain from studies in vitro, in cultured cells, or in primary human CML cells. This knowledge will be valuable for improving the diagnosis and treatment of the Ph-positive leukemias. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: SUBNUCLEAR TARGETING OF TRANSCRIPTION FACTORS Principal Investigator & Institution: Stein, Gary S.; Professor and Chairman; Univ of Massachusetts Med Sch Worcester Office of Research Funding Worcester, Ma 01655 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2006 Summary: Nuclear architecture is dramatically modified during hematopoietic differentiation, as well as during the onset and progression of leukemias. Project 2 addresses the hypothesis that fidelity of subnuclear targeting of the key hematopoietic regulatory factor AML-1 is abrogated by leukemia-related chromosomal translocations that delete specific intranuclear trafficking signals. We postulate that the misrouting of the gene regulatory factor is a dominant defect that causes deregulation of AMLmediated control of cell growth and differentiation. These investigators have shown that AML1 contains a 31 amino acid nuclear matrix targeting signal (NMTS) that facilitates trans-activation by mediating association with components of nuclear architecture which support transcription. Additionally, the applicant has demonstrated that the 8;21 chromosomal translocation in AML leukemia modifies intranuclear targeting of the AML-1 transcription factor. Thus, the specific aims are to: (i) characterize the subnuclear targeting signal in AML-1-1 by establishing the structural basis for and functional consequences of interactions with the nuclear matrix; (ii) determine the saturability and dynamics of intranuclear trafficking of AML-1 in hematopoietic cells in functional nuclear domains; (iii) assess the spatio- functional distribution of AM-1 and leukemia related AML-1 fusion proteins during cell growth and myeloid differentiation; (iv) examine the physiological consequences of subnuclear targeting for hematopoiesis by genetically ablating the NMTS in the murine AML-1 locus; and (v) define key protein/protein interactions which regulate intranuclear trafficking in hematopoietic cells by cloning the nuclear docking protein of AML-1. The results of the proposed studies will provide an in-depth understanding of the interrelationships between subnuclear targeting of gene regulatory factors, chromosomal translocations involving trafficking signals and modifications in gene expression characteristic of leukemias. GRANT-P01CA82834-01A2-0003 The long term objective of this work is to understand how centrosomes contribute to tumorigenesis. Centrosomes are poorly understood organelles required for organization of mitotic spindles and accurate segregation of chromosomes during cell division. Thus, centrosomes are critical players in the redistribution and reorganization of the genome as it is assembled into nascent nuclei following mitosis. There is no other single cellular event that has a greater impact on the quantity, composition and organization of chromatin within the nucleus. We recently made the striking observation that malignant tumors had increased levels of the centrosome protein pericentrin, abnormal centrosomes, aberrant mitotic spindles and missegregated chromosomes. Moreover, artificial elevation of pericentrin in normal cells induced nearly identical features including aneuploidy, a condition linked to tumor malignancy, metastasis and fatality. Pericentrin over-expression also appeared to abrogate the mitotic checkpoint that normally induces mitotic arrest in the presence of unattached chromosomes. Over- expressed pericentrin bound and mislocalized cytoplasmic dynein, a molecular motor known to function in spindle organization and possibly checkpoint control. Based on these observations, we propose a model in which centrosome defects contribute to tumorigenesis by causing improper segregation of the
56 Leukemia
genome and creating aneuploid cells. The discovery of centromsomes as potential contributors to malignant tumor progression provides us with a unique opportunity to elucidate a novel mechanism for tumorigenesis. The specific aims of this proposal are: 1. To determine whether proteins of the centrosome and nucleus are altered in tumors. 2. To test whether pericentrin has oncogenic potential. 3. To determine how elevated levels of pericentrin cause aneuploidy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: TARGETED MYELODYSPLASTIC S
INHIBITION
OF
ANGIOGENESIS
IN
Principal Investigator & Institution: List, Alan F.; Professor; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 31-DEC-2006 Summary: Description (provided by applicant) The MDSs represent some of the most common hematologic malignancies, with an incidence that approximates that for chronic lymphocytic leukemia. Given the aging of the United States population and the absence of a standard effective treatment for these disorders, management of patients with MUDS has become increasingly problematic. The MDSs share the distinguishing features of ineffective hematopoiesis and increased risk of leukemia transformation. Recent studies have shown that these disorders display an increase in bone marrow (EM) microvessel density, the magnitude of which directly correlates with myeloblast percentage. We have shown that vascular endothelial growth factor (VEGF) and its receptors are expressed by myelomonocytic precursors in MDS and acute myelogenous leukemia (AML), and that VEGF elaboration contributes to suppression of committed progenitor growth and excess medullary generation of TNF alpha. Using the VEGFreceptor competent KG-1 AML cells as a model, we have characterized the biologic effects of VEGF in AML cells, which include suppression of nuclear translocation of NEB, stimulation of leukemia self renewal via interaction with either of the Fit-1 or KDR VEGF receptors, and activation of the phosphoinositol-3-kinase/Akt signaling pathway. We propose that agents which modify cellular VEGF elaboration or VEGF receptor signaling will impair leukemia progenitor self renewal, lower resistance to maturation signals, impair generation of inflammatory cytokines, and promote more effective hematopoiesis in MDS. Our efforts to delineate the VEGF receptor signaling pathway in AML progenitors provides a unique opportunity to validate in vivo target inhibition as an endpoint for biologic activity of novel therapeutics. In this project, we will investigate three Specific Aims that evaluate novel therapeutics which inhibit the actions of VEGF or its receptor signaling in patients with MDS, and delineate the relationship between in vivo target inhibition, and biologic and hematologic endpoints. The Specific Aims of this proposal are: 1) To determine the biologic effects of the VEGF inhibitor, thalidomide, in patients with MDS, and the relationship between target inhibition and hematologic response. 2) To investigate the molecular and pharmacologic effects of the VEGF receptor tyrosine kinase inhibitor, SU-5416, in vitro and in animal models. 3)To determine the biological effects of SU-5416 in patients with MDS, and the relation between hematologic response and VEGF -receptor tyrosine kinase inhibition in clinical specimens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TARGETING FLT3 AS A NOVEL SPECIFIC THERAPY FOR LEUKEMIA Principal Investigator & Institution: Levis, Mark J.; Oncology; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Leukemia remains a deadly disease in both adults and children. The majority of patients still die, and new treatments are urgently needed. There is now substantial data indicating that the receptor tyrosine kinase FLT3 plays a role in a significant fraction of leukemias. FLT3, which is expressed in most cases of acute myeloid and acute lymphocytic leukemia (AML and ALL), is constitutively activated by internal tandem duplication (ITD) mutations of the juxtamembrane region, by point mutations in the kinase domain, and by co-expression of FLT3 ligand (FL). 30% or more of AML cases harbor an activating mutation of FLT3, and this subset of patients has been shown to have a worse prognosis. Preliminary data presented here provides evidence that a FLT3 tyrosine kinase inhibitor is specifically cytotoxic to AML cells harboring FLT3 activating mutations. This proposal's scientific objective is the development of a FLT3 tyrosine kinase inhibitor for use in the treatment of leukemia. The immediate goal is to characterize the responses of different types of leukemias to the inhibitors in order to predict which patients may benefit from this therapy. The specific aims will be to test human leukemia cell lines and primary leukemic blasts for cytotoxic response to FLT3 inhibitors, with and without chemotherapy, and to correlate this cytotoxic response with changes in downstream signaling proteins and gene expression. Similar correlative studies will be performed on samples from patients receiving the inhibitor as part of a clinical trial. A FLT3 inhibitor has tremendous potential as an alternative or adjunct to conventional therapy for acute leukemias. This proposal has two goals. The first is to address the urgent need for new leukemia therapies. The second is to allow the principal investigator, Dr. Mark Levis, to develop into a laboratory-based researcher whose focus is to translate basic science research into clinical applications. With the guidance of a mentor who has expertise in the pathogenesis of leukemia, along with a structured educational program and a supportive academic environment, the principal investigator will use the support provided by this award to complete the transition to independent clinician scientist. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TEL AND THE T(12--21) AND B CELL ALL Principal Investigator & Institution: Hiebert, Scott W.; Professor; Biochemistry; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 01-AUG-1997; Project End 31-MAY-2002 Summary: The t(12;21) is the most frequent genetic abnormality associated with pediatric B-cell ALL, present in 25-30% of all cases. This translocation fuses the Nterminal 333 amino acids of TEL, a putative ets family transcription factor, to the DNA binding and transactivation domains of AML-lB, a transcription factor that is the target of multiple translocations in myeloid leukemia. Our preliminary work indicates that the addition of the N-terminal 3/4 of TEL to AML-lB converts AML-lB from an activator to a repressor of transcription. This proposal tests the hypothesis that the inhibition of AML- lB transcriptional activity by the t(12;21) fusion protein is a key event in leukemogenesis. Up to 90% of patients with the t(12;21), also have mutations in their second TEL allele. The high frequency of loss of TEL function suggests that TEL is a tumor suppressor and that its deletion cooperates with t( 12;21) in leukemogenesis.
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Specific aim 1 will determine the molecular mechanism of TEL/AML- lB-mediated transcriptional regulation. These experiments will define both the mechanism of repression and the subdomains of TEL and AML-lB that bring about this repression. With this information, the factors that mediate these transcriptional effects can be identified. Specific aim 2 will test the hypothesis that TEL is a tumor suppressor by determining whether its overexpression inhibits cellular proliferation both in vitro and in vivo. In specific aim 3, transgenic mice will be engineered to inducibly express the t(12;21) fusion protein to examine whether TEL/AML-lB is a dominant interfering protein that induces leukemia, and whether its continuous expression is required to maintain the leukemic state. By crossing these mice with TEL-deficient mice, we will directly test whether the two lesions observed in the clinic cooperate in leukemogenesis. The experiments proposed will answer fundamental questions about the role of the t(12;21) in the generation and maintenance of leukemia and will provide a murine model for t 12;21 -associated leukemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: THE PLZF PROTEIN OF T(11;17)-PROMYELOCYTIC LEUKEMIA Principal Investigator & Institution: Licht, Jonathan D.; Professor and Vice Chairman; Ruttenberg Cancer Center; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2003; Project Start 01-APR-1993; Project End 31-JAN-2008 Summary: The promyelocytic leukemia zinc finger (PLZF) protein is a transcription factor, expressed in hematopoietic progenitor cells, fused to the retinoic acid receptoralpha (RAR alpha) in t(11;17)-associated acute promyelocytic leukemia (APL). Over the past 9 years, through two periods of funding, our group characterized t(11;17) APL as a distinct syndrome, unresponsive to retinoic acid. We determined that the PLZFRARalpha fusion generated in t(11;17) is a dominant negative form of PAR that actively recruits corepressors and histone deacteylase molecules to RAR target genes. The study of the PLZF fusion protein helped solidify the model of aberrant transcriptional repression as a pathogenic basis of leukemia. Though progress has been gratifying, many questions remain. The nature of the critical target genes of the retinoid receptor blocked by the fusion proteins of APL is not certain. The way in which genes are repressed is incompletely understood. Histone deacetylases are critically involved but other modes of chromatin modification, chromatin remodeling and epigenetic silencing of repressed genes are likely. The PLZF protein represses through a number of corepressors attracted though the BTB/POZ Domain. Further structure of this domain will yield further insights and potential therapeutic modalties in the disease. APL in animal models occurs after a considerable delay, indicating that other mutations are required for the disease to occur. One such cooperating mutation may be the mutation of the fit3 receptor tyrosine kinase molecule. One mode of cooperation may be the ability of the APL fusion proteins to abrogate the p53 pathway and prevent premature cellular senescence in response to activation of ras/map kinasse pathways. PML is a modulator of p53 function and PLZF may be as well. The proposed research will: 1. Determine of how PLZF controls myeloid cell growth and differentiation by elucidation of PLZF target genes which bind the PLZF protein in vitro and in vivo such as IL-6, cyclin A and other to be identified by whole genome PCR. 2. Define how an evolutionarily conserved protein motif, the POZ domain, functions in transcriptional regulation, though mutagensis of conserved residues and identification of partner proteins using the yeast two hybrid system. 3. Define protein-protein interaction networks that play a role in normal myelopoiesis and leukemogenesis (PML-PLZF, N-Cor-PLZF) 4. Extend
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knowledge of gene regulation in early hematopoiesis through characterization of the cisacting sequences controlling expression of PLZF. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: THE ROLE OF CYCLIN A1 IN ACUTE MYELOID LEUKEMIA Principal Investigator & Institution: Wolgemuth, Debra J.; Professor; Obstetrics and Gynecology; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2007 Summary: (provided by applicant): We have identified a novel mammalian A-type cyclin, cyclin AI, that our targeted mutagenesis in mice revealed to be essential for the progression of male germ cells into meiosis. Human cyclin AI is also highly expressed in myeloid leukemia cell lines and in leukemic cells from patients with acute myeloid leukemias, in the promyelocytic form (APL) in particular. We have tested the hypothesis that the aberrant high levels of cyclin AI were causal in the leukemic phenotype, i.e., acting as an oncogene. Transgenic mice in which cyclin AI was expressed under the control of the human cathepsin G promoter in myeloid precursor cells were generated. They exhibited abnormal myelopoiesis and developed acute myeloid leukemia with low penetrance and long latency. Interestingly, in the transgenic mouse model and in human NB4 cells, the localization of cyclin A1 is predominantly cytoplasmic, distinct from its nuclear localization in germ cells. We wish to understand the cellular mechanisms in myelopoiesis that are altered in the presence of elevated levels of cyclin A1 that is now mostly cytoplasmic. The distinct cytoplasmic localization of cyclin A1 will be studied, testing the hypothesis that this property contributes to the tumorigenesis. We will also address the role of cyclin A1 during normal hematopoiesis by studying hematopoietic parameters in mice that are null for the cyclin A1 gene. The hypothesis that cyclin A1 will have distinct Cdk partners, other interacting partners, and substrates in normal versus leukemic cells will be tested using immunoprecipitation and a yeast 2-hybrid screen. As high levels of cyclin A1 protein have been shown to be characteristic of APL, we will ask whether manipulating the expression of cyclin A1 will affect the development of the leukemia. We will test this idea by performing genetic studies in which we will manipulate the expression of cyclin A1 in the fusion oncogene X-RARalpha transgenic animal models of APL. The question is whether these mice will be more resistant to the development of leukemia in the absence of cyclin AI. These studies will provide important insight into the etiology of myeloid leukemia, the role of cell cycle control in the oncogenic process, and the development of new and potentially highly tissue-specific target molecules for pharmacologic intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THE TRANSFORMING PROPERTIES OF THE MEIS1 GENE FAMILY Principal Investigator & Institution: Buchberg, Arthur M.; Associate Professor; Microbiology and Immunology; Thomas Jefferson University Office of Research Administration Philadelphia, Pa 191075587 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: (Adapted from the investigator's abstract) BXH-2 mice develop a high incidence of myeloid leukemia that is causally associated with the expression of an ecotropic murine leukemia virus (MuLV). The MuLVs act as insertional mutagens to alter the expression of cellular protooncogenes or tumor suppressor genes that contribute to leukemia. Dr. Buchberg has identified a new common site of integration, Meis1 (Myeloid ecotropic viral integration site 1), in BXH-2 myeloid tumors. Sequence
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analysis of Meis 1 reveals it to be a novel homeobox gene: the homeodomain of Meis1 is related to the PBX homeodomain family. PBX1 was identified as a Hox cofactor, cooperatively interacting with a subset of Hox genes in specifying its DNA target. Recent evidence has demonstrated that Meis1 can interact with a number of other homeodomain containing proteins, including a subset of Hox proteins, as well as Pbx1. This interaction, in some instances, results in the increased stabilization of protein-DNA complexes and is required for the nuclear localization of PBX proteins. The specific aims of this proposal are designed to understand how Meis1 cooperates with its partners to contribute to transformation. Specifically, Dr. Buchberg will dissect the interaction between Meis1 and other homeodomain containing proteins by both in vitro and in vivo assays. These aims will ultimately identify the domains required for transformation in a bioassay and correlate physical interactions with biological interactions. Moreover, using the yeast-two hybrid assay and protein pull-down assays, additional proteins will be identified that interact with the various spliced forms of Meis1, to begin the functional dissection of the alternative forms of Meis1. The goals of this proposal are to understand the molecular basis of cellular transformation mediated by Meis1. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: TOPOISOMERASE I INHIBITORS IN LEUKEMIA AND SOLID TUMORS Principal Investigator & Institution: Kaufmann, Scott H.; Professor; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2001; Project Start 01-APR-1997; Project End 31-MAR-2005 Summary: (Applicant's Abstract) Two topoisomerase I (topo I) poisons, topotecan (TPT) and irinotecan (CPT-l1), are currently licensed for use in the U.S. Clinical responses to these agents are highly variable. Although preclinical studies have identified numerous factors that can affect the action of topo I poisons in vitro, few of these parameters have been examined in tumor samples or correlated with clinical response. Studies supported by this grant have investigated 1) mechanisms of resistance to topo I poisons in clinical leukemia specimens and 2) effects of combining topo I poisons with other agents. In pursuing the first goal, we have demonstrated during the current funding period that topo I content in acute myelogenous leukemia specimens varies widely but correlates with other markers of proliferation (e.g., PCNA); that the TPT concentration required to stabilize topo I-DNA complexes in acute leukemia specimens ex vivo varies over a 30fold range irrespective of topo I content; and that this variation in TPT concentration required to stabilize topo I-DNA cleavage complexes can been recapitulated in a tissue culture model. Additional tissue culture studies have demonstrated enhanced sensitivity to TPT or SN-38 (the active metabolite of CPT-11) when activity of the DNA damage checkpoint kinase ATR is inhibited. While addressing the second goal, we have demonstrated that cytotoxic effects are more than additive when SN-38 is combined with the quinazoline-based kinase inhibitor CI1033 or with gemcitabine. Further studies have demonstrated that the SN-38/CI1033 synergy reflects enhanced drug accumulation as a result of CI1033-mediated inhibition of the ABC cassette transporter BCRP. To build on these results, we now propose to 1) evaluate the relationship between response of three well-defined cohorts of solid tumor patients receiving single-agent CPT-11 or TPT and various tumor cell parameters that have been implicated in drug resistance in preclinical models (including topo I content, p53 status, proliferative index, levels of anti-apoptotic Bcl-2 family members, and expression of replication checkpoint proteins); 2) use the recently developed tissue culture model to determine the mechanistic basis for the observation that different TPT concentrations are required to stabilize topo I-DNA
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complexes in different leukemia specimens; and 3) examine the mechanistic basis for the unanticipated synergy of the gemcitabine + SN-38 combination and determine the effect of combining SN-38 with other agents currently undergoing early clinical testing. Collectively, these studies should provide insight into factors that affect response to topo I poisons in the clinical setting and aid in the rational integration of topo I poisons into multidrug regimens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: TREATMENT OF BCR/ABL CAUSED LEUKEMIAS WITH FTIS Principal Investigator & Institution: Heisterkamp, Nora C.; Associate Professor; Children's Hospital Los Angeles 4650 Sunset Blvd Los Angeles, Ca 90027 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2006 Summary: The Bcr/Abl oncoprotein causes the development of Ph-chromosomepositive leukemias. Bcr/Abl P210 and P190 share a domain of Abi which encodes a deregulated tyrosine kinase. This activity perturbs a number of downstream signal transduction pathways including that of the small GTPase Ras. Inhibitors of the enzyme farnesyltransferase (FTIs) have been tested as possible therapeutic agents against Rasassociated solid tumors in man. We have generated a transgenic mouse model which clinically mimics Ph-positive acute lymphoblastic leukemia and tested the potential therapeutic properties of an FTI in this model. Our data show that FTIs are surprisingly potent in preventing the emergence of overt leukemia in our mice. We therefore hypothesize that Ffls are effective in the treatment of Bcr/AbI caused leukemias by interfering with specific small CTPases necessary for disease progression. We will explore this by determining which cellular characteristics known to be altered by Bcr/AbI expression including apoptosis, cytokine independence, mitogenesis and adhesion are affected by the FTIs in BaF3 lymphoid cells with regulatable Bcr/Abl expression. It will also be investigated which small GTPases including Ras are activated by Bcr/Abl in cell line and animal models, and which are targeted by treatment with the FTIs. In addition, we will evaluate whether the FTls are effective against terminal-stage disease in the Bcr/AbI P190 transgenic mouse model, whether they can cure P190caused leukemia/lymphoma in a bone marrow transplant model and whether Bcr/Ablexpressing cells develop resistance to FTIs. By utilizing a compound which apparently acts on downstream targets of Bcr/Abl in vivo, these experiments will provide unique insights into the mechanisms by which Bcr/AbI causes leukemia. These studies will also help pinpoint which pathway(s) are critical in transducing the oncogenic signals of Bcr/Abl, which could provide additional targets for therapeutic intervention. Finally, data will emerge which will be invaluable in the assessment nf Using FTIs in the treatment nf Ph-positive leukemia in man Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TREATMENT OF CHILDHOOD CANCER Principal Investigator & Institution: Brecher, Martin L.; Roswell Park Cancer Institute Corp Buffalo, Ny 14263 Timing: Fiscal Year 2001; Project Start 01-JUL-1980; Project End 31-DEC-2002 Summary: Cooperative trials in pediatric cancer patients have played a major role in the remarkable improvement in cure of childhood cancers. Because most childhood cancers are rare, it is only through this mechanism that adequate numbers of patients can be accrued in reasonable lengths of time for randomized controlled studies. The Department of Pediatrics at Roswell Park Cancer Institute (RPCI) has actively
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participated in cooperative group trials via the Pediatric Oncology Group (POG) to answer treatment questions which would be impossible to answer were we to conduct only single institution studies. Some pediatric solid tumors are so rare that national intergroup studies are required. We also participate in these intergroup studies. RPCI investigators are coordinators for a number of POG protocols including front-line studies for the treatment of advanced Hodgkin's disease, advanced small non- cleaved cell lymphoma, non-rhabdomyosarcoma soft tissue sarcomas, acute lymphoblastic leukemia in relapse, the National Wilms Tumor Study, brain tumors in infants, and the Intergroup Ewing's Sarcoma Study. Roswell Park investigators have also developed POG phase II studies of continuous infusion 5-fluouracil and the combination of cisplatin, ifosfamide and etoposide. Roswell Park investigators chair the Wilms Tumor Committee, the Neuroscience Subcommittee of the Brain Tumor Committee, and cochair the Pathology Discipline Core Committee, as well as being active on a number of other POG Core Committees. They have made major contributions over the last few years in the areas of solid tumor oncology, neuro- oncology and the treatment of lymphoid malignancies. We are strongly committed to the interdisciplinary approach to pediatric cancer and have established collaboration with the necessary clinical specialties including Radiation Medicine, Pediatric Surgery, Pediatric Neurology, Neurosurgery, and Orthopedic Surgery, as well as with researchers in immunology, pharmacology and molecular biology. As more children are cured of their cancers, the identification and prevention, when feasible, of complications of therapy have become imperative. We have been a major contributor to the identification and understanding of the long-term medical and psychosocial effects of the treatment of leukemia, Hodgkin's disease, and a number of solid tumors, both through the cooperative group mechanism and through institutional studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: TUMOR SUPPRESSORS HEMATOPOIESIS AND LEUKEMIA Principal Investigator & Institution: Amatruda, James F.; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001; Project Start 13-AUG-1999; Project End 31-JUL-2004 Summary: Hematopoiesis and leukemogenesis are developmental phenomena, in which complex interactions of multiple genes give rise to orderly differentiation or to maturation arrest and uncontrolled proliferation. While many of the terminal events in these pathways have been elucidated by cellular, biochemical and transgenic mouse studies, the genes responsible for the most fundamental developmental decisions in hematopoiesis and leukemogenesis have been less well-defined. Tumor suppressor genes (TSGs), first identified in hereditary human cancers, are likely to be among this group of fundamental genes. TSGs are key elements of cellular pathways that regulate growth and differentiation. Specific TSGs have been shown to be mutated or deleted in primary human leukemias and leukemic cell lines. Mouse knock-out models and patients deficient in several of these genes demonstrate defective hematopoiesis or develop leukemias. To better understand the function of tumor suppressor genes in normal hematopoiesis and leukemogenesis we have chosen as a model the zebrafish (Danio rerio), a vertebrate system that combines physiology and development with powerful genetics. We plan to create zebrafish strains deficient in known TSGs and to characterize hematopoietic defects and the development of leukemia in these strains. A suppressor or enhancer screen for mutations that correct the defects or cure the leukemia will lead to the isolation of additional genes in these pathways. The experiments described in this proposal are likely to identify novel proteins that play key
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roles in the control of hematopoiesis and the genesis of leukemia. These proteins will be potential therapeutic targets for the treatment of aplastic anemia, myelodysplasia and leukemia in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: WUMC-CANCER AND LEUKEMIA GROUP B Principal Investigator & Institution: Bartlett, Nancy L.; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 08-MAY-1998; Project End 31-MAR-2009 Summary: (adapted from the applicant's abstract): Washington University has been a CALGB main member institution since 1986. Over the last five years, the cancer research program at the Washington University Medical Center (WUMC) has experienced tremendous growth. Barnes-Jewish Hospital, the largest hospital in St. Louis, diagnoses more than 5,400 patients a year with cancer and remains the major referral center for southeast Missouri and southern Illinois. The Siteman Cancer Center (SCC) at WUMC received NCI-designated Cancer Center status in August 2001. The infrastructure developed by the SCC to compete successfully for the NCI Cancer Center Support Grant has significantly enhanced our ability to carry out all aspects of clinical cancer research, including cooperative group trials. Our recent efforts to expand institutional research studies will significantly enhance our ability to contribute concepts to CALGB during the next grant cycle, specifically in the areas of Hematologic malignancies, thoracic oncology, and pharmacogenomics. Between 1998 and 2002, 16 Washington University physicians and research assistants served on 36 different CALGB scientific and administrative committees. WUMC investigators chaired 12 CALGB studies, including Phase II studies in non-Hodgkin's lymphoma, Hodgkin's lymphoma, prostate cancer, mesothelioma, and several pharmacokinetic and pharmacogenomic correlative science studies. Six additional studies are in the final stages of development. Accrual to CALGB trials has continued to increase during this grant period, with an average of 183 patients per year registered to therapeutic and non-therapeutic trials from 1998 to 2001. Accrual to therapeutic trials increased from 61 patients in 1998 to 105 in 2001. Based on registrations to date, projected accrual to CALGB trials for 2002 is estimated to be 312, with 136 to therapeutic studies. Plans for the next grant cycle include 1) continued involvement by all current WUMC investigators, 2) increased participation by our Phase I investigators to facilitate development of Phase II studies within CALGB, 3) involvement of at least five additional WUMC investigators in CALGB activities including faculty interested in GU oncology, quality of life, stem cell transplant and leukemia, leukemia correlative sciences, and radiation oncology, and 5) continued efforts to increase accruals, particularly minority accruals, to CALGB trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National
3
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
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Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “leukemia” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for leukemia in the PubMed Central database: ·
[gamma][delta] + T-Lymphocyte Cytotoxicity against Envelope-Expressing Target Cells Is Unique to the Alymphocytic State of Bovine Leukemia Virus Infection in the Natural Host. by Lundberg P, Splitter GA.; 2000 Sep 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=116339
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11q23 Translocations Split the "AT-Hook" Cruciform DNA-Binding Region and the Transcriptional Repression Domain from the Activation Domain of the MixedLineage Leukemia (MLL) Gene. by Zeleznik-Le NJ, Harden AM, Rowley JD.; 1994 Oct 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45071
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A bcr-3 isoform of RAR[alpha]-PML potentiates the development of PMLRAR[alpha]-driven acute promyelocytic leukemia. by Pollock JL, Westervelt P, Kurichety AK, Pelicci PG, Grisolano JL, Ley TJ.; 1999 Dec 21; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24780
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A Lymphokine, Provisionally Designated Interleukin T and Produced by a Human Adult T-Cell Leukemia Line, Stimulates T-Cell Proliferation and the Induction of Lymphokine-Activated Killer Cells. by Burton JD, Bamford RN, Peters C, Grant AJ, Kurys G, Goldman CK, Brennan J, Roessler E, Waldmann TA.; 1994 May 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43904
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A Lysine-to-Arginine Change Found in Natural Alleles of the Human T-Cell Lymphotropic/Leukemia Virus Type 1 p12I Protein Greatly Influences Its Stability. by Trovato R, Mulloy JC, Johnson JM, Takemoto S, de Oliveira MP, Franchini G.; 1999 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112727
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A Moloney Murine Leukemia Virus-Based Retrovirus with 4070A Long Terminal Repeat Sequences Induces a High Incidence of Myeloid as Well as Lymphoid Neoplasms. by Wolff L, Koller R, Hu X, Anver MR.; 2003 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=152129
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A multistep process of leukemogenesis in Moloney murine leukemia virus-infected mice that is modulated by retroviral pseudotyping and interference. by Lavignon M, Evans L.; 1996 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190262
4
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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·
A Novel Ubiquitin-Specific Protease, UBP43, Cloned from Leukemia Fusion Protein AML1-ETO-Expressing Mice, Functions in Hematopoietic Cell Differentiation. by Liu LQ, Ilaria R Jr, Kingsley PD, Iwama A, van Etten RA, Palis J, Zhang DE.; 1999 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=84097
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A PMLRAR[alpha] transgene initiates murine acute promyelocytic leukemia. by Brown D, Kogan S, Lagasse E, Weissman I, Alcalay M, Pelicci PG, Atwater S, Bishop JM.; 1997 Mar 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20126
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A Point Mutation in the N-Terminal Coiled-Coil Domain Releases c-Fes Tyrosine Kinase Activity and Survival Signaling in Myeloid Leukemia Cells. by Cheng HY, Schiavone AP, Smithgall TE.; 2001 Sep 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=87334
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A Yeast Artificial Chromosome-Based Map of the Region of Chromosome 20 Containing the Diabetes-Susceptibility Gene, MODY1, and a Myeloid Leukemia Related Gene. by Stoffel M, Beau MM, Espinosa R, Bohlander SF, Paslier DL, Cohen D, Xiang K, Cox NJ, Fajans SS, Bell GI.; 1996 Apr 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39463
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Aberrant B cell receptor signaling from B29 ( Ig[beta], CD79b) gene mutations of chronic lymphocytic leukemia B cells. by Gordon MS, Kato RM, Lansigan F, Thompson AA, Wall R, Rawlings DJ.; 2000 May 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=25858
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Aberrant Recruitment of the Nuclear Receptor Corepressor-Histone Deacetylase Complex by the Acute Myeloid Leukemia Fusion Partner ETO. by Gelmetti V, Zhang J, Fanelli M, Minucci S, Pelicci PG, Lazar MA.; 1998 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109300
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Abnormal integrin-mediated regulation of chronic myelogenous leukemia CD34 + cell proliferation: BCR /ABL up-regulates the cyclin-dependent kinase inhibitor, p27Kip, which is relocated to the cell cytoplasm and incapable of regulating cdk2 activity. by Jiang Y, Zhao RC, Verfaillie CM.; 2000 Sep 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27060
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Acquired, nonrandom chromosomal abnormalities associated with the development of acute promyelocytic leukemia in transgenic mice. by Zimonjic DB, Pollock JL, Westervelt P, Popescu NC, Ley TJ.; 2000 Nov 21; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27220
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Acrophialophora fusispora Brain Abscess in a Child with Acute Lymphoblastic Leukemia: Review of Cases and Taxonomy. by Al-Mohsen IZ, Sutton DA, Sigler L, Almodovar E, Mahgoub N, Frayha H, Al-Hajjar S, Rinaldi MG, Walsh TJ.; 2000 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=87638
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Activation of c-myb is an Early Bone-Marrow Event in a Murine Model for Acute Promonocytic Leukemia. by Nason-Burchenal K, Wolff L.; 1993 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45926
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Activation of EVI1 Gene Expression in Human Acute Myelogenous Leukemias by Translocations Spanning 300-400 Kilobases on Chromosome Band 3q26. by Morishita K, Parganas E, Willman CL, Whittaker MH, Drabkin H, Oval J, Taetle R, Valentine MB, Ihle JN.; 1992 May 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48987
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Acute leukemia with promyelocytic features in PML /RAR[alpha] transgenic mice. by He LZ, Tribioli C, Rivi R, Peruzzi D, Pelicci PG, Soares V, Cattoretti G, Pandolfi PP.; 1997 May 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24673
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Acute Leukemias of Different Lineages Have Similar MLL Gene Fusions Encoding Related Chimeric Proteins Resulting from Chromosomal Translocation. by Corral J, Forster A, Thompson S, Lampert F, Kaneko Y, Slater R, Kroes WG, van der Schoot CE, Ludwig W, Karpas A, Pocock C, Cotter F, Rabbitts TH.; 1993 Sep 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47392
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Acute Mixed-Lineage Leukemia t(4;11)(q21;q23) Generates an MLL-AF4 Fusion Product. by Domer PH, Fakharzadeh SS, Chen C, Jockel J, Johansen L, Silverman GA, Kersey JH, Korsmeyer SJ.; 1993 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47247
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Acute myeloid leukemias with reciprocal rearrangements can be distinguished by specific gene expression profiles. by Schoch C, Kohlmann A, Schnittger S, Brors B, Dugas M, Mergenthaler S, Kern W, Hiddemann W, Eils R, Haferlach T.; 2002 Jul 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126615
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Adaptive immunity cooperates with liposomal all-trans-retinoic acid (ATRA) to facilitate long-term molecular remissions in mice with acute promyelocytic leukemia. by Westervelt P, Pollock JL, Oldfather KM, Walter MJ, Ma MK, Williams A, DiPersio JF, Ley TJ.; 2002 Jul 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123164
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AF5q31, a newly identified AF4-related gene, is fused to MLL in infant acute lymphoblastic leukemia with ins(5;11)(q31;q13q23). by Taki T, Kano H, Taniwaki M, Sako M, Yanagisawa M, Hayashi Y.; 1999 Dec 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24471
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Altered myelopoiesis and the development of acute myeloid leukemia in transgenic mice overexpressing cyclin A1. by Liao C, Wang XY, Wei HQ, Li SQ, Merghoub T, Pandolfi PP, Wolgemuth DJ.; 2001 Jun 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34442
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Amino-Terminal Protein-Protein Interaction Motif (POZ-Domain) is Responsible for Activities of the Promyelocytic Leukemia Zinc Finger-Retinoic Acid Receptor-[alpha] Fusion Protein. by Dong S, Zhu J, Reid A, Strutt P, Guidez F, Zhong H, Wang Z, Licht J, Waxman S, Chomienne C, Chen Z, Zelent A, Chen S.; 1996 Apr 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39661
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AML1 /ETO-expressing nonleukemic stem cells in acute myelogenous leukemia with 8;21 chromosomal translocation. by Miyamoto T, Weissman IL, Akashi K.; 2000 Jun 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16578
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AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations. by Yuan Y, Zhou L, Miyamoto T, Iwasaki H, Harakawa N, Hetherington CJ, Burel SA, Lagasse E, Weissman IL, Akashi K, Zhang DE.; 2001 Aug 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=56972
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An Antisense Oligodeoxynucleotide Targeted Against the Type II[beta] Regulatory Subunit mRNA of Protein Kinase Inhibits cAMP-Induced Differentiation in HL-60 Leukemia Cells Without Affecting Phorbol Ester Effects. by Tortora G, Clair T, ChoChung YS.; 1990 Jan 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53334
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An Enhancer Variant of Moloney Murine Leukemia Virus Defective in Leukemogenesis Does not Generate Detectable Mink Cell Focus-Inducing Virus in vivo. by Brightman BK, Rein A, Trepp DJ, Fan H.; 1991 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51211
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An ets-Related Gene, ERG, is Rearranged in Human Myeloid Leukemia with t(16;21) Chromosomal Translocation. by Shimizu K, Ichikawa H, Tojo A, Kaneko Y, Maseki N, Hayashi Y, Ohira M, Asano S, Ohki M.; 1993 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47758
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An XPG DNA repair defect causing mutagen hypersensitivity in mouse leukemia L1210 cells. by Vilpo JA, Vilpo LM, Szymkowski DE, O'Donovan A, Wood RD.; 1995 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231955
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Analysis of p53 Inactivation in a Human T-Cell Leukemia Virus Type 1 Tax Transgenic Mouse Model. by Portis T, Grossman WJ, Harding JC, Hess JL, Ratner L.; 2001 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=114802
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Analysis of the Disease Potential of a Recombinant Retrovirus Containing Friend Murine Leukemia Virus Sequences and a Unique Long Terminal Repeat from Feline Leukemia Virus. by Nishigaki K, Hanson C, Thompson D, Yugawa T, Hisasue M, Tsujimoto H, Ruscetti S.; 2002 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=135779
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Antileukemia effect of c-myc N3[prime prime or minute][right arrow]P5[prime prime or minute] phosphoramidate antisense oligonucleotides in vivo. by Skorski T, Perrotti D, Nieborowska-Skorska M, Gryaznov S, Calabretta B.; 1997 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20551
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Antiviral Activity of Shiga Toxin 1: Suppression of Bovine Leukemia Virus-Related Spontaneous Lymphocyte Proliferation. by Ferens WA, Hovde CJ.; 2000 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=98349
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Apoptosis and Interleukin 7 Gene Expression in Chronic B-Lymphocytic Leukemia Cells. by Long BW, Witte PL, Abraham GN, Gregory SA, Plate JM.; 1995 Feb 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=42530
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Appearance of Mink Cell Focus-Inducing Recombinants during In Vivo Infection by Moloney Murine Leukemia Virus (M-MuLV) or the Mo +PyF101 M-MuLV Enhancer Variant: Implications for Sites of Generation and Roles in Leukemogenesis. by Lander JK, Chesebro B, Fan H.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112626
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Approach to a Retrovirus Vaccine: Immunization of Mice Against Friend Virus Disease with a Replication-Defective Friend Murine Leukemia Virus. by Ruan K, Lilly F.; 1992 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=50727
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Arsenic Trioxide Is a Potent Inhibitor of the Interaction of SMRT Corepressor with Its Transcription Factor Partners, Including the PML-Retinoic Acid Receptor [alpha] Oncoprotein Found in Human Acute Promyelocytic Leukemia. by Hong SH, Yang Z, Privalsky ML.; 2001 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=99892
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Arsenic-induced PML targeting onto nuclear bodies: Implications for the treatment of acute promyelocytic leukemia. by Zhu J, Koken MH, Quignon F, Chelbi-Alix MK, Degos L, Wang ZY, Chen Z, de The H.; 1997 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20553
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Association of CYP 3A4 genotype with treatment-related leukemia. by Felix CA, Walker AH, Lange BJ, Williams TM, Winick NJ, Cheung NK, Lovett BD, Nowell PC, Blair IA, Rebbeck TR.; 1998 Oct 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23750
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Autocrine production and action of IL-3 and granulocyte colony-stimulating factor in chronic myeloid leukemia. by Jiang X, Lopez A, Holyoake T, Eaves A, Eaves C.; 1999 Oct 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23105
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BAALC, the human member of a novel mammalian neuroectoderm gene lineage, is implicated in hematopoiesis and acute leukemia. by Tanner SM, Austin JL, Leone G, Rush LJ, Plass C, Heinonen K, Mrozek K, Sill H, Knuutila S, Kolitz JE, Archer KJ, Caligiuri MA, Bloomfield CD, de la Chapelle A.; 2001 Nov 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=61139
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Backtracking leukemia to birth: Identification of clonotypic gene fusion sequences in neonatal blood spots. by Gale KB, Ford AM, Repp R, Borkhardt A, Keller C, Eden OB, Greaves MF.; 1997 Dec 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28413
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Bacteremia Due to a Novel Microbacterium Species in a Patient with Leukemia and Description of Microbacterium paraoxydans sp. nov. by Laffineur K, Avesani V, Cornu G, Charlier J, Janssens M, Wauters G, Delmee M.; 2003 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154712
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Biological Characteristics of the Leukemia-Associated Transcriptional Factor AML1 Disclosed by Hematopoietic Rescue of AML1-Deficient Embryonic Stem Cells by Using a Knock-in Strategy. by Okuda T, Takeda K, Fujita Y, Nishimura M, Yagyu S, Yoshida M, Akira S, Downing JR, Abe T.; 2000 Jan 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85087
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Blast Crisis in a Murine Model of Chronic Myelogenous Leukemia. by Daley GQ, Etten RA, Baltimore D.; 1991 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53129
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Both wild-type and strongly attenuated bovine leukemia viruses protect peripheral blood mononuclear cells from apoptosis. by Dequiedt F, Hanon E, Kerkhofs P, Pastoret PP, Portetelle D, Burny A, Kettmann R, Willems L.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191094
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Bovine Leukemia Virus Structural Gene Vectors Are Immunogenic and Lack Pathogenicity in a Rabbit Model. by Kucerova L, Altanerova V, Altaner C, BorisLawrie K.; 1999 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112833
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Bovine Leukemia Virus SU Protein Interacts with Zinc, and Mutations within Two Interacting Regions Differently Affect Viral Fusion and Infectivity In Vivo. by Gatot JS, Callebaut I, Van Lint C, Demonte D, Kerkhofs P, Portetelle D, Burny A, Willems L, Kettmann R.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=155115
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Bovine Leukemia Virus-Induced Lymphocytosis and Increased Cell Survival Mainly Involve the CD11b + B-Lymphocyte Subset in Sheep. by Chevallier N, Berthelemy M, Le Rhun D, Laine V, Levy D, Schwartz-Cornil I.; 1998 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109673
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Calcium signaling induces acquisition of dendritic cell characteristics in chronic myelogenous leukemia myeloid progenitor cells. by Engels FH, Koski GK, Bedrosian I, Xu S, Luger S, Nowell PC, Cohen PA, Czerniecki BJ.; 1999 Aug 31; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17888
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Calorie restriction reduces the incidence of myeloid leukemia induced by a single whole-body radiation in C3H /He mice. by Yoshida K, Inoue T, Nojima K, Hirabayashi Y, Sado T.; 1997 Mar 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20137
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Calorie Restriction Suppresses Subgenomic Mink Cytopathic Focus-Forming Murine Leukemia Virus Transcription and Frequency of Genomic Expression While Impairing Lymphoma Formation. by Shield BA, Engelman RW, Fukaura Y, Good RA, Day NK.; 1991 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53089
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Case of Catheter Sepsis with Ralstonia gilardii in a Child with Acute Lymphoblastic Leukemia. by Wauters G, Claeys G, Verschraegen G, De Baere T, Vandecruys E, Van Simaey L, De Ganck C, Vaneechoutte M.; 2001 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=88595
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CD4-T-Cell Antigen Receptor Complexes on Human Leukemia T Cells. by Chuck RS, Cantor CR, Tse DB.; 1990 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54253
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CD5 Is Dissociated from the B-Cell Receptor in B Cells from Bovine Leukemia VirusInfected, Persistently Lymphocytotic Cattle: Consequences to B-Cell ReceptorMediated Apoptosis. by Cantor GH, Pritchard SM, Dequiedt F, Willems L, Kettmann R, Davis WC.; 2001 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=114078
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CD8 + minor histocompatibility antigen-specific cytotoxic T lymphocyte clones eliminate human acute myeloid leukemia stem cells. by Bonnet D, Warren EH, Greenberg PD, Dick JE, Riddell SR.; 1999 Jul 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17569
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Cell death induction by the acute promyelocytic leukemia-specific PML /RAR[alpha] fusion protein. by Ferrucci PF, Grignani F, Pearson M, Fagioli M, Nicoletti I, Pelicci PG.; 1997 Sep 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23524
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Cellular pathways involved in the ex vivo expression of bovine leukemia virus. by Kerkhofs P, Adam E, Droogmans L, Portetelle D, Mammerickx M, Burny A, Kettmann R, Willems L.; 1996 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190055
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Characteristics of Erythroleukemia Cells Selected for Vincristine Resistance That Have Accelerated Inducer-Mediated Differentiation. by Richon VM, Weich N, Leng L, Kiyokawa H, Ngo L, Rifkind RA, Marks PA.; 1991 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51085
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Characterization of a High-Molecular-Weight Notch Complex in the Nucleus of Notchic-Transformed RKE Cells and in a Human T-Cell Leukemia Cell Line. by Jeffries S, Robbins DJ, Capobianco AJ.; 2002 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=133837
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Characterization of a Polytropic Murine Leukemia Virus Proviral Sequence Associated with the Virus Resistance Gene Rmcf of DBA/2 Mice. by Jung YT, Lyu MS, Buckler-White A, Kozak CA.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=155147
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Chronic Lymphocytic Leukemia Cells with Allelic Deletions at 13q14 Commonly have One Intact RB1 Gene: Evidence for a Role of an Adjacent Locus. by Liu Y, Szekely L, Grander D, Soderhall S, Juliusson G, Gahrton G, Linder S, Einhorn S.; 1993 Sep 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47425
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Chronic myelogenous leukemia shapes host immunity by selective deletion of highavidity leukemia-specific T cells. by Molldrem JJ, Lee PP, Kant S, Wieder E, Jiang W, Lu S, Wang C, Davis MM.; 2003 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151894
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Chronic Myeloproliferative Disease Induced by Site-Specific Integration of Abelson Murine Leukemia Virus-Infected Hemopoietic Stem Cells. by Han X, Wong PM, Chung S.; 1991 Nov 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52881
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Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop. by Roumiantsev S, Shah NP, Gorre ME, Nicoll J, Brasher BB, Sawyers CL, Van Etten RA.; 2002 Aug 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=125018
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Cloning of a gene (RIG-G) associated with retinoic acid-induced differentiation of acute promyelocytic leukemia cells and representing a new member of a family of interferon-stimulated genes. by Yu M, Tong JH, Mao M, Kan LX, Liu MM, Sun YW, Fu G, Jing YK, Yu L, Lepaslier D, Lanotte M, Wang ZY, Chen Z, Waxman S, Wang YX, Tan JZ, Chen SJ.; 1997 Jul 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23834
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Cloning of ELL, a Gene that Fuses to MLL in a t(11;19)(q23;p13.1) in Acute Myeloid Leukemia. by Thirman MJ, Levitan DA, Kobayashi H, Simon MC, Rowley JD.; 1994 Dec 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45386
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Clustering of Syk is sufficient to induce tyrosine phosphorylation and release of allergic mediators from rat basophilic leukemia cells. by Rivera VM, Brugge JS.; 1995 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230382
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CML66, a broadly immunogenic tumor antigen, elicits a humoral immune response associated with remission of chronic myelogenous leukemia. by Yang XF, Wu CJ, McLaughlin S, Chillemi A, Wang KS, Canning C, Alyea EP, Kantoff P, Soiffer RJ, Dranoff G, Ritz J.; 2001 Jun 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34696
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Combined expression of pT[alpha] and Notch3 in T cell leukemia identifies the requirement of preTCR for leukemogenesis. by Bellavia D, Campese AF, Checquolo S, Balestri A, Biondi A, Cazzaniga G, Lendahl U, Fehling HJ, Hayday AC, Frati L, von Boehmer H, Gulino A, Screpanti I.; 2002 Mar 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122602
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Complete Bovine Leukemia Virus (BLV) Provirus Is Conserved in BLV-Infected Cattle throughout the Course of B-Cell Lymphosarcoma Development. by Tajima S, Ikawa Y, Aida Y.; 1998 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=110004
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Conditional Expression of the Ubiquitous Transcription Factor MafK Induces Erythroleukemia Cell Differentiation. by Igarashi K, Itoh K, Hayashi N, Nishizawa M, Yamamoto M.; 1995 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41356
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Constitutive retinoid receptors expressed from adenovirus vectors that specifically activate chromosomal target genes required for differentiation of promyelocytic leukemia and teratocarcinoma cells. by Lipkin SM, Grider TL, Heyman RA, Glass CK, Gage FH.; 1996 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190771
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Core Binding Factor [beta]--Smooth Muscle Myosin Heavy Chain Chimeric Protein Involved in Acute Myeloid Leukemia Forms Unusual Nuclear Rod-Like Structures in Transformed NIH 3T3 Cells. by Wijmenga C, Gregory PE, Hajra A, Schrock E, Ried T, Eils R, Liu PP, Collins FS.; 1996 Feb 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39993
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Cutaneous Infection Caused by Cylindrocarpon lichenicola in a Patient with Acute Myelogenous Leukemia. by Iwen PC, Tarantolo SR, Sutton DA, Rinaldi MG, Hinrichs SH.; 2000 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=87389
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Defining Roles for HOX and MEIS1 Genes in Induction of Acute Myeloid Leukemia. by Thorsteinsdottir U, Kroon E, Jerome L, Blasi F, Sauvageau G.; 2001 Jan 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=88796
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DEK, an autoantigen involved in a chromosomal translocation in acute myelogenous leukemia, binds to the HIV-2 enhancer. by Fu GK, Grosveld G, Markovitz DM.; 1997 Mar 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19999
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Deregulated expression of TCL1 causes T cell leukemia in mice. by Virgilio L, Lazzeri C, Bichi R, Nibu KI, Narducci MG, Russo G, Rothstein JL, Croce CM.; 1998 Mar 31; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19932
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Detection of leukemia-associated MLL-GAS7 translocation early during chemotherapy with DNA topoisomerase II inhibitors. by Megonigal MD, Cheung NK, Rappaport EF, Nowell PC, Wilson RB, Jones DH, Addya K, Leonard DG, Kushner BH, Williams TM, Lange BJ, Felix CA.; 2000 Mar 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16012
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Development of Leukemia in Mice Transgenic for the tax Gene of Human T-Cell Leukemia Virus Type I. by Grossman WJ, Kimata JT, Wong F, Zutter M, Ley TJ, Ratner L.; 1995 Feb 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=42636
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Dietary bioflavonoids induce cleavage in the MLL gene and may contribute to infant leukemia. by Strick R, Strissel PL, Borgers S, Smith SL, Rowley JD.; 2000 Apr 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18311
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Dietary flavonoids and the MLL gene: A pathway to infant leukemia? by Ross JA.; 2000 Apr 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34309
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Discordance between Bovine Leukemia Virus Tax Immortalization In Vitro and Oncogenicity In Vivo. by Twizere JC, Kerkhofs P, Burny A, Portetelle D, Kettmann R, Willems L.; 2000 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=102026
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Disruption of Hematopoiesis and Thymopoiesis in the Early Premalignant Stages of Infection with SL3-3 Murine Leukemia Virus. by Rulli K, Lenz J, Levy LS.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=135944
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Dissecting the Immune Response to Moloney Murine Sarcoma/Leukemia VirusInduced Tumors by Means of a DNA Vaccination Approach. by Milan G, Zambon A, Cavinato M, Zanovello P, Rosato A, Collavo D.; 1999 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=104473
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Disseminated Infection Caused by Scedosporium prolificans in a Patient with Acute Multilineal Leukemia. by de Batlle J, Motje M, Balanza R, Guardia R, Ortiz R.; 2000 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=86531
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Distinct leukemia phenotypes in transgenic mice and different corepressor interactions generated by promyelocytic leukemia variant fusion genes PLZF -RAR[alpha] and NPM --RAR[alpha]. by Cheng GX, Zhu XH, Men XQ, Wang L, Huang QH, Jin XL, Xiong SM, Zhu J, Guo WM, Chen JQ, Xu SF, So E, Chan LC, Waxman S, Zelent A, Chen GQ, Dong S, Liu JX, Chen SJ.; 1999 May 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26879
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DNA Methylation Profiles in the Human Genes for Tumor Necrosis Factor [alpha] and [beta] in Subpopulations of Leukocytes and in Leukemias. by Kochanek S, Radbruch A, Tesch H, Renz D, Doerfler W.; 1991 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51957
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Domains with Transcriptional Regulatory Activity within the ALL1 and AF4 Proteins Involved in Acute Leukemia. by Prasad R, Yano T, Sorio C, Nakamura T, Rallapalli R, Gu Y, Leshrkowitz D, Croce CM, Canaani E.; 1995 Dec 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40316
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Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias. by Tanaka T, Mitani K, Kurokawa M, Ogawa S, Tanaka K, Nishida J, Yazaki Y, Shibata Y, Hirai H.; 1995 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230467
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Dual Transforming Activities of the FUS (TLS)-ERG Leukemia Fusion Protein Conferred by Two N-Terminal Domains of FUS (TLS). by Ichikawa H, Shimizu K, Katsu R, Ohki M.; 1999 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=84797
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EEN encodes for a member of a new family of proteins containing an Src homology 3 domain and is the third gene located on chromosome 19p13 that fuses to MLL in human leukemia. by So CW, Caldas C, Liu MM, Chen SJ, Huang QH, Gu LJ, Sham MH, Wiedemann LM, Chan LC.; 1997 Mar 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20128
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Effect of intravenous infusions of 12-O-tetradecanoylphorbol-13-acetate (TPA) in patients with myelocytic leukemia: Preliminary studies on therapeutic efficacy and toxicity. by Han ZT, Zhu XX, Yang RY, Sun JZ, Tian GF, Liu XJ, Cao GS, Newmark HL, Conney AH, Chang RL.; 1998 Apr 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20265
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Efficient Transplantation of BCR-ABL-Induced Chronic Myelogenous LeukemiaLike Syndrome in Mice. by Gishizky ML, Johnson-White J, Witte ON.; 1993 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46380
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ELL and EAF1 are Cajal Body Components That Are Disrupted in MLL-ELL Leukemia. by Polak PE, Simone F, Kaberlein JJ, Luo RT, Thirman MJ.; 2003 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153119
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Endocarditis and Aortal Embolization Caused by Aspergillus terreus in a Patient with Acute Lymphoblastic Leukemia in Remission: Diagnosis by Peripheral-Blood Culture. by Schett G, Casati B, Willinger B, Weinlander G, Binder T, Grabenwoger F, Sperr W, Geissler K, Jager U.; 1998 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=105327
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Essential Roles for Ankyrin Repeat and Transactivation Domains in Induction of TCell Leukemia by Notch1. by Aster JC, Xu L, Karnell FG, Patriub V, Pui JC, Pear WS.; 2000 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=86303
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ETO, a Target of t(8;21) in Acute Leukemia, Interacts with the N-CoR and mSin3 Corepressors. by Lutterbach B, Westendorf JJ, Linggi B, Patten A, Moniwa M, Davie JR, Huynh KD, Bardwell VJ, Lavinsky RM, Rosenfeld MG, Glass C, Seto E, Hiebert SW.; 1998 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109299
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ETO, a Target of t(8;21) in Acute Leukemia, Makes Distinct Contacts with Multiple Histone Deacetylases and Binds mSin3A through Its Oligomerization Domain. by Amann JM, Nip J, Strom DK, Lutterbach B, Harada H, Lenny N, Downing JR, Meyers S, Hiebert SW.; 2001 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=99794
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ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex. by Wang J, Hoshino T, Redner RL, Kajigaya S, Liu JM.; 1998 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27986
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Expression of a gene encoding a tRNA synthetase-like protein is enhanced in tumorigenic human myeloid leukemia cells and is cell cycle stage- and differentiation-dependent. by Sen S, Zhou H, Ripmaster T, Hittelman WN, Schimmel P, White RA.; 1997 Jun 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21020
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Expression of Alternatively Spliced Human T-Lymphotropic Virus Type I pX mRNA in Infected Cell Lines and in Primary Uncultured Cells from Patients with Adult TCell Leukemia/Lymphoma and Healthy Carriers. by Berneman ZN, Gartenhaus RB, Reitz MS Jr, Blattner WA, Manns A, Hanchard B, Ikehara O, Gallo RC, Klotman ME.; 1992 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48792
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Expression of dominant-negative and mutant isoforms of the antileukemic transcription factor Ikaros in infant acute lymphoblastic leukemia. by Sun L, Heerema N, Crotty L, Wu X, Navara C, Vassilev A, Sensel M, Reaman GH, Uckun FM.; 1999 Jan 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15196
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Expression of Interferon Consensus Sequence Binding Protein (ICSBP) Is Downregulated in Bcr-Abl-Induced Murine Chronic Myelogenous Leukemia-Like Disease, and Forced Coexpression of ICSBP Inhibits Bcr-Abl-Induced Myeloproliferative Disorder. by Hao SX, Ren R.; 2000 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85233
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Expression profiling reveals fundamental biological differences in acute myeloid leukemia with isolated trisomy 8 and normal cytogenetics. by Virtaneva K, Wright FA, Tanner SM, Yuan B, Lemon WJ, Caligiuri MA, Bloomfield CD, de la Chapelle A, Krahe R.; 2001 Jan 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=14719
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Fatal Penicillium citrinum pneumonia with pericarditis in a patient with acute leukemia. by Mok T, Koehler AP, Yu MY, Ellis DH, Johnson PJ, Wickham NW.; 1997 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230029
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Fetal origins of the TEL-AML1 fusion gene in identical twins with leukemia. by Ford AM, Bennett CA, Price CM, Bruin MC, Van Wering ER, Greaves M.; 1998 Apr 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22533
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Friend Leukemia Virus Infection Enhances DNA Damage-Induced Apoptosis of Hematopoietic Cells, Causing Lethal Anemia in C3H Hosts. by Kitagawa M, Yamaguchi S, Hasegawa M, Tanaka K, Sado T, Hirokawa K, Aizawa S.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=136359
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Functional Analysis of the Leukemia Protein ELL: Evidence for a Role in the Regulation of Cell Growth and Survival. by Johnstone RW, Gerber M, Landewe T, Tollefson A, Wold WS, Shilatifard A.; 2001 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=86713
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Functional and Physical Interactions between AML1 Proteins and an ETS Protein, MEF: Implications for the Pathogenesis of t(8;21)-Positive Leukemias. by Mao S, Frank RC, Zhang J, Miyazaki Y, Nimer SD.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=84165
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Fusion of the NUP98 gene with the LEDGF/p52 gene defines a recurrent acute myeloid leukemia translocation. by Hussey DJ, Moore S, Nicola M, Dobrovic A.; 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=60524
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Fusion of the TEL Gene on 12p13 to the AML1 Gene on 21q22 in Acute Lymphoblastic Leukemia. by Golub TR, Barker GF, Bohlander SK, Hiebert SW, Ward DC, Bray-Ward P, Morgan E, Raimondi SC, Rowley JD, Gilliland DG.; 1995 May 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41818
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Gene Targeting of X Chromosome-Linked Chronic Granulomatous Disease Locus in a Human Myeloid Leukemia Cell Line and Rescue by Expression of Recombinant gp91phox. by Zhen L, King AA, Xiao Y, Chanock SJ, Orkin SH, Dinauer MC.; 1993 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47666
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Generation of a novel Fli-1 protein by gene targeting leads to a defect in thymus development and a delay in Friend virus-induced erythroleukemia. by Melet F, Motro B, Rossi DJ, Zhang L, Bernstein A.; 1996 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231261
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Generation of Novel Syncytium-Inducing and Host Range Variants of Ecotropic Moloney Murine Leukemia Virus in Mus spicilegus. by Jung YT, Kozak CA.; 2003 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=153962
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Genes on Chromosomes 4, 9, and 19 Involved in 11q23 Abnormalities in Acute Leukemia Share Sequence Homology and/or Common Motifs. by Nakamura T, Alder H, Gu Y, Prasad R, Canaani O, Kamada N, Gale RP, Lange B, Crist WM, Nowell PC, Croce CM, Canaani E.; 1993 May 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46566
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Genetic Control of a Mouse Serum Lipoprotein Factor That Inactivates Murine Leukemia Viruses: Evaluation of Apolipoprotein F as a Candidate. by Wu T, Lee CG, Buckler-White A, Kozak CA.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=153798
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Genetic Regulation of Long-Term Nonprogression in E-55 + Murine Leukemia Virus Infection in Mice. by Panoutsakopoulou V, Hunter K, Sieck TG, Blankenhorn EP, Blank KJ.; 1999 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112957
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Genomic DNA breakpoints in AML1 /RUNX1 and ETO cluster with topoisomerase II DNA cleavage and DNase I hypersensitive sites in t(8;21) leukemia. by Zhang Y, Strissel P, Strick R, Chen J, Nucifora G, Le Beau MM, Larson RA, Rowley JD.; 2002 Mar 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122474
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Gris1, a New Common Integration Site in Graffi Murine Leukemia Virus-Induced Leukemias: Overexpression of a Truncated Cyclin D2 due to Alternative Splicing. by Denicourt C, Kozak CA, Rassart E.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=140601
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Growth Inhibition and Induction of Differentiation of t(8;21) Acute Myeloid Leukemia Cells by the DNA-Binding Domain of PEBP2 and the AML1/MTG8(ETO) Specific Antisense Oligonucleotide. by Sakakura C, Yamaguchi-Iwai Y, Satake M, Bae S, Takahashi A, Ogawa E, Hagiwara A, Takahashi T, Murakami A, Makino K, Nakagawa T, Kamada N, Ito Y.; 1994 Nov 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45304
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Growth Suppression of Pre-T Acute Lymphoblastic Leukemia Cells by Inhibition of Notch Signaling. by Weng AP, Nam Y, Wolfe MS, Pear WS, Griffin JD, Blacklow SC, Aster JC.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=151540
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Homeobox Gene Expression Plus Autocrine Growth Factor Production Elicits Myeloid Leukemia. by Perkins A, Kongsuwan K, Visvader J, Adams JM, Cory S.; 1990 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54963
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Host Sequences Flanking the Human T-Cell Leukemia Virus Type 1 Provirus In Vivo. by Leclercq I, Mortreux F, Cavrois M, Leroy A, Gessain A, Wain-Hobson S, Wattel E.; 2000 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=111712
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Human AML1 /MDS1 /EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: A model for human AML. by Cuenco GM, Nucifora G, Ren R.; 2000 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26509
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Human chronic lymphocytic leukemia modeled in mouse by targeted TCL1 expression. by Bichi R, Shinton SA, Martin ES, Koval A, Calin GA, Cesari R, Russo G, Hardy RR, Croce CM.; 2002 May 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124510
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Human T-cell leukemia retrovirus-Tax protein is a repressor of nuclear receptor signaling. by Doucas V, Evans RM.; 1999 Mar 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15820
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Human T-Cell Leukemia Virus Type 1 Tax and Cell Cycle Progression: Role of Cyclin D-cdk and p110Rb. by Neuveut C, Low KG, Maldarelli F, Schmitt I, Majone F, Grassmann R, Jeang KT.; 1998 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=108944
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Human T-Cell Leukemia Virus Type 1 Tax Induction of NF-[kappa]B Involves Activation of the I[kappa]B Kinase [alpha] (IKK[alpha]) and IKK[beta] Cellular Kinases. by Geleziunas R, Ferrell S, Lin X, Mu Y, Cunningham ET Jr, Grant M, Connelly MA, Hambor JE, Marcu KB, Greene WC.; 1998 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109101
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Hypermutability of Mouse Chromosome 2 During the Development of X-RayInduced Murine Myeloid Leukemia. by Rithidech K, Bond VP, Cronkite EP, Thompson MH, Bullis JE.; 1995 Feb 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=42656
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Identification and Characterization of an Activating TrkA Deletion Mutation in Acute Myeloid Leukemia. by Reuther GW, Lambert QT, Caligiuri MA, Der CJ.; 2000 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=86471
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Identification and characterization of the ARP1 gene, a target for the human acute leukemia ALL1 gene. by Arakawa H, Nakamura T, Zhadanov AB, Fidanza V, Yano T, Bullrich F, Shimizu M, Blechman J, Mazo A, Canaani E, Croce CM.; 1998 Apr 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22531
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Identification and Mapping of a Common Proviral Integration Site Fli-1 in Erythroleukemia Cells Induced by Friend Murine Leukemia Virus. by Ben-David Y, Giddens EB, Bernstein A.; 1990 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53469
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Identification of a gag-encoded cytotoxic T-lymphocyte epitope from FBL-3 leukemia shared by Friend, Moloney, and Rauscher murine leukemia virus-induced tumors. by Chen W, Qin H, Chesebro B, Cheever MA.; 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190847
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Identification of a gene at 11q23 encoding a guanine nucleotide exchange factor: Evidence for its fusion with MLL in acute myeloid leukemia. by Kourlas PJ, Strout MP, Becknell B, Veronese ML, Croce CM, Theil KS, Krahe R, Ruutu T, Knuutila S, Bloomfield CD, Caligiuri MA.; 2000 Feb 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15768
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Identification of Directly Infected Cells in the Bone Marrow of Neonatal Moloney Murine Leukemia Virus-Infected Mice by Use of a Moloney Murine Leukemia VirusBased Vector. by Okimoto MA, Fan H.; 1999 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=103987
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Identification of Genetic Determinants Responsible for the Rapid Immunosuppressive Activity and the Low Leukemogenic Potential of a Variant of
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Friend Leukemia Virus, FIS-2. by Dai HY, Troseth GI, Gunleksrud M, Bruland T, Solberg LA, Aarset H, Kristiansen LI, Dalen A.; 1998 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=124602 ·
Identification of Protein Instability Determinants in the Carboxy-Terminal Region of c-Myb Removed as a Result of Retroviral Integration in Murine Monocytic Leukemias. by Bies J, Nazarov V, Wolff L.; 1999 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=104446
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Identification of the Regions of Fv1 Necessary for Murine Leukemia Virus Restriction. by Bishop KN, Bock M, Towers G, Stoye JP.; 2001 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=114923
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Ikaros, a Lymphoid-Cell-Specific Transcription Factor, Contributes to the Leukemogenic Phenotype of a Mink Cell Focus-Inducing Murine Leukemia Virus. by DiFronzo NL, Leung CT, Mammel MK, Georgopoulos K, Taylor BJ, Pham QN.; 2002 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=135716
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Impaired expression of interleukin 2 receptor and CD45RO antigen on lymphocytes from children with acute lymphoblastic leukemia in response to cytomegalovirus and varicella-zoster virus. by Mizutani K, Ito M, Nakano T, Kamiya H, Sakurai M.; 1995 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=170164
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In vivo and in vitro Characterization of the B1 and B2 Zinc-Binding Domains from the Acute Promyelocytic Leukemia Protooncoprotein PML. by Borden KL, Lally JM, Martin SR, O'Reilly NJ, Solomon E, Freemont PS.; 1996 Feb 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39988
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Inactivation of murine leukemia virus by compounds that react with the zinc finger in the viral nucleocapsid protein. by Rein A, Ott DE, Mirro J, Arthur LO, Rice W, Henderson LE.; 1996 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190449
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Increased cell proliferation, but not reduced cell death, induces lymphocytosis in bovine leukemia virus-infected sheep. by Debacq C, Asquith B, Kerkhofs P, Portetelle D, Burny A, Kettmann R, Willems L.; 2002 Jul 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126622
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Increased interleukin-10 mRNA expression in tumor-bearing or persistently lymphocytotic animals infected with bovine leukemia virus. by Pyeon D, O'Reilly KL, Splitter GA.; 1996 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190539
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Induction of a Chronic Myelogenous Leukemia-Like Syndrome in Mice With V-abl and BCR/ABL. by Kelliher MA, McLaughlin J, Witte ON, Rosenberg N.; 1990 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54594
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Induction of Adult T-Cell Leukemia-Like Lymphoproliferative Disease and Its Inhibition by Adoptive Immunotherapy in T-Cell-Deficient Nude Rats Inoculated with Syngeneic Human T-Cell Leukemia Virus Type 1-Immortalized Cells. by Ohashi T, Hanabuchi S, Kato H, Koya Y, Takemura F, Hirokawa K, Yoshiki T, Tanaka Y, Fujii M, Kannagi M.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112664
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Infection of central nervous system cells by ecotropic murine leukemia virus in C58 and AKR mice and in in utero-infected CE/J mice predisposes mice to paralytic infection by lactate dehydrogenase-elevating virus. by Anderson GW, Palmer GA, Rowland RR, Even C, Plagemann PG.; 1995 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=188577
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Inhibition of both paracrine and autocrine VEGF / VEGFR-2 signaling pathways is essential to induce long-term remission of xenotransplanted human leukemias. by Dias S, Hattori K, Heissig B, Zhu Z, Wu Y, Witte L, Hicklin DJ, Tateno M, Bohlen P, Moore MA, Rafii S.; 2001 Sep 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=58564
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Inhibition of Moloney Murine Leukemia Virus-Induced Leukemia in Transgenic Mice Expressing Antisense RNA Complementary to the Retroviral Packaging Sequences. by Han L, Yun JS, Wagner TE.; 1991 May 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51649
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Inhibition of the Self-Renewal Capacity of Blast Progenitors from Acute Myeloblastic Leukemia Patients by Site-Selective 8-Chloroadenosine 3', 5'-Cyclic Monophosphate. by Pinto A, Aldinucci D, Gattei V, Zagonel V, Tortora G, Budillon A, Cho-Chung YS.; 1992 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=50028
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Interaction of SP100 with HP1 proteins: A link between the promyelocytic leukemiaassociated nuclear bodies and the chromatin compartment. by Seeler JS, Marchio A, Sitterlin D, Transy C, Dejean A.; 1998 Jun 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22602
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Interactions of Ofloxacin and Erythromycin with the Multidrug Resistance Protein (MRP) in MRP-Overexpressing Human Leukemia Cells. by Terashi K, Oka M, Soda H, Fukuda M, Kawabata S, Nakatomi K, Shiozawa K, Nakamura T, Tsukamoto K, Noguchi Y, Suenaga M, Tei C, Kohno S.; 2000 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=89936
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Intergenic Splicing of MDS1 and EVI1 Occurs in Normal Tissues as well as in Myeloid Leukemia and Produces a New Member of the PR Domain Family. by Fears S, Mathieu C, Zeleznik-Le N, Huang S, Rowley JD, Nucifora G.; 1996 Feb 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39995
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Interleukin (IL) 15/IL-T Production by the Adult T-Cell Leukemia Cell Line HuT-102 is Associated with a Human T-Cell Lymphotrophic Virus Type I R Region/IL-15 Fusion Message that Lacks Many Upstream AUGs that Normally Attenuate IL-15
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mRNA Translation. by Bamford RN, Battiata AP, Burton JD, Sharma H, Waldmann TA.; 1996 Apr 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39731 ·
Interleukin 2 Prevents Graft-Versus-Host Disease While Preserving the Graft-VersusLeukemia Effect of Allogeneic T Cells. by Sykes M, Romick ML, Sachs DH.; 1990 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54381
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Interleukin-12 p40 mRNA Expression in Bovine Leukemia Virus-Infected Animals: Increase in Alymphocytosis but Decrease in Persistent Lymphocytosis. by Pyeon D, Splitter GA.; 1998 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109906
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Interspecies transmission of macaque simian T-cell leukemia/lymphoma virus type 1 in baboons resulted in an outbreak of malignant lymphoma. by Voevodin A, Samilchuk E, Schatzl H, Boeri E, Franchini G.; 1996 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189987
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Introduction of a cis-Acting Mutation in the Capsid-Coding Gene of Moloney Murine Leukemia Virus Extends Its Leukemogenic Properties. by Audit M, Dejardin J, Hohl B, Sidobre C, Hope TJ, Mougel M, Sitbon M.; 1999 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=113102
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Introduction of the [beta] Isozyme of Protein Kinase C Accelerates Induced Differentiation of Murine Erythroleukemia Cells. by Melloni E, Pontremoli S, Sparatore B, Patrone M, Grossi F, Marks PA, Rifkind RA.; 1990 Jun 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54125
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Involvement of a human gene related to the Drosophila spen gene in the recurrent t(1;22) translocation of acute megakaryocytic leukemia. by Mercher T, Coniat MB, Monni R, Mauchauffe M, Khac FN, Gressin L, Mugneret F, Leblanc T, Dastugue N, Berger R, Bernard OA.; 2001 May 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33289
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Isolation and characterization of fluconazole- and amphotericin B-resistant Candida albicans from blood of two patients with leukemia. by Nolte FS, Parkinson T, Falconer DJ, Dix S, Williams J, Gilmore C, Geller R, Wingard JR.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=163686
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Isolation of a Yeast Artificial Chromosome Spanning the 8;21 Translocation Breakpoint t(8;21)(q22;q22.3) in Acute Myelogeneous Leukemia. by Gao J, Erickson P, Gardiner K, Beau MM, Diaz MO, Patterson D, Rowley JD, Drabkin HA.; 1991 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51771
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Latency of Viral Expression In Vivo Is Not Related to CpG Methylation in the U3 Region and Part of the R Region of the Long Terminal Repeat of Bovine Leukemia Virus. by Tajima S, Tsukamoto M, Aida Y.; 2003 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=150652
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Latent sensitivity to Fas-mediated apoptosis after CD40 ligation may explain activity of CD154 gene therapy in chronic lymphocytic leukemia. by Chu P, Deforce D, Pedersen IM, Kim Y, Kitada S, Reed JC, Kipps TJ.; 2002 Mar 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122613
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Leucine-Zipper Dimerization Motif Encoded by the AF17 Gene Fused to ALL-1 (MLL) in Acute Leukemia. by Prasad R, Leshkowitz D, Gu Y, Alder H, Nakamura T, Saito H, Huebner K, Berger R, Croce CM, Canaani E.; 1994 Aug 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=44554
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Leukemia Initiated by Hemopoietic Stem Cells Expressing the v-abl Oncogene. by Chung S, Wong PM, Durkin H, Wu Y, Petersen J.; 1991 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51064
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Leukemia-associated retinoic acid receptor [alpha] fusion partners, PML and PLZF, heterodimerize and colocalize to nuclear bodies. by Koken MH, Reid A, Quignon F, Chelbi-Alix MK, Davies JM, Kabarowski JH, Zhu J, Dong S, Chen SJ, Chen Z, Tan CC, Licht J, Waxman S, de The H, Zelent A.; 1997 Sep 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23349
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Localization of human T-cell leukemia virus type 1 tax to subnuclear compartments that overlap with interchromatin speckles. by Semmes OJ, Jeang KT.; 1996 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190661
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Loss of functional cell surface transforming growth factor [beta] (TGF-[beta]) type 1 receptor correlates with insensitivity to TGF-[beta] in chronic lymphocytic leukemia. by DeCoteau JF, Knaus PI, Yankelev H, Reis MD, Lowsky R, Lodish HF, Kadin ME.; 1997 May 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20874
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Low-frequency loss of heterozygosity in Moloney murine leukemia virus-induced tumors in BRAKF1/J mice. by Lander JK, Fan H.; 1997 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191546
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Lymphocyte Deficiencies Increase Susceptibility to Friend Virus-Induced Erythroleukemia in Fv-2 Genetically Resistant Mice. by Hasenkrug KJ.; 1999 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112728
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Lymphomas and High-Level Expression of Murine Leukemia Viruses in CFW Mice. by Taddesse-Heath L, Chattopadhyay SK, Dillehay DL, Lander MR, Nagashfar Z, Morse HC III, Hartley JW.; 2000 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112200
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Major Histocompatibility Complex Class I Gene Controls the Generation of Gamma Interferon-Producing CD4 + and CD8 + T Cells Important for Recovery from Friend
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Retrovirus-Induced Leukemia. by Peterson KE, Iwashiro M, Hasenkrug KJ, Chesebro B.; 2000 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=110893 ·
Mapping Chromosome Band 11q23 in Human Acute Leukemia with Biotinylated Probes: Identification of 11q23 Translocation Breakpoints with a Yeast Artificial Chromosome. by Rowley JD, Diaz MO, Espinosa R III, Patel YD, van Melle E, Ziemin S, Taillon-Miller P, Lichter P, Evans GA, Kersey JH, Ward DC, Domer PH, Beau MM.; 1990 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=55164
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Meis1, a PBX1-related homeobox gene involved in myeloid leukemia in BXH-2 mice. by Moskow JJ, Bullrich F, Huebner K, Daar IO, Buchberg AM.; 1995 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230793
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Meis1a suppresses differentiation by G-CSF and promotes proliferation by SCF: Potential mechanisms of cooperativity with Hoxa9 in myeloid leukemia. by Calvo KR, Knoepfler PS, Sykes DB, Pasillas MP, Kamps MP.; 2001 Nov 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=60834
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Methylenetetrahydrofolate reductase (MTHFR) polymorphisms and risk of molecularly defined subtypes of childhood acute leukemia. by Wiemels JL, Smith RN, Taylor GM, Eden OB, Alexander FE, Greaves MF.; 2001 Mar 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=31169
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Milk and Fat Yields Decline in Bovine Leukemia Virus-Infected Holstein Cattle with Persistent Lymphocytosis. by Da Y, Shanks RD, Stewart JA, Lewin HA.; 1993 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46967
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Mink Cell Focus-Forming Murine Leukemia Virus Infection Induces Apoptosis of Thymic Lymphocytes. by Yoshimura FK, Wang T, Yu F, Kim HR, Turner JR.; 2000 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112345
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MLL is fused to CBP, a histone acetyltransferase, in therapy-related acute myeloid leukemia with a t(11;16)(q23;p13.3). by Sobulo OM, Borrow J, Tomek R, Reshmi S, Harden A, Schlegelberger B, Housman D, Doggett NA, Rowley JD, Zeleznik-Le NJ.; 1997 Aug 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23102
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Molecular Cloning, Primary Structure, and Expression of the Human Platelet/ Erythroleukemia Cell 12-Lipoxygenase. by Funk CD, Furci L, FitzGerald GA.; 1990 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54382
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Molecular emergence of acute myeloid leukemia during treatment for acute lymphoblastic leukemia. by Blanco JG, Dervieux T, Edick MJ, Mehta PK, Rubnitz JE, Shurtleff S, Raimondi SC, Behm FG, Pui CH, Relling MV.; 2001 Aug 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=56962
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Molecular Relapse in Chronic Myelogenous Leukemia Patients After Bone Marrow Transplantation Detected by Polymerase Chain Reaction. by Sawyers CL, Timson L, Kawasaki ES, Clark SS, Witte ON, Champlin R.; 1990 Jan 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53305
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Moloney Murine Leukemia Virus-Induced Tumors Show Altered Levels of Proapoptotic and Antiapoptotic Proteins. by Bonzon C, Fan H.; 2000 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112349
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Mouse Af9 Is a Controller of Embryo Patterning, Like Mll, Whose Human Homologue Fuses with AF9 after Chromosomal Translocation in Leukemia. by Collins EC, Appert A, Ariza-McNaughton L, Pannell R, Yamada Y, Rabbitts TH.; 2002 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=139815
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Mouse Model for the Equilibration Interaction between the Host Immune System and Human T-Cell Leukemia Virus Type 1 Gene Expression. by Furuta RA, Sugiura K, Kawakita S, Inada T, Ikehara S, Matsuda T, Fujisawa JI.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=135962
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MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25). by Osaka M, Rowley JD, Zeleznik-Le NJ.; 1999 May 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26898
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mSin3A Regulates Murine Erythroleukemia Cell Differentiation through Association with the TAL1 (or SCL) Transcription Factor. by Huang S, Brandt SJ.; 2000 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=110841
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Multimeric Complexes of the PML-Retinoic Acid Receptor [alpha] Fusion Protein in Acute Promyelocytic Leukemia Cells and Interference with Retinoid and PeroxisomeProliferator Signaling Pathways. by Jansen JH, Mahfoudi A, Rambaud S, Lavau C, Wahli W, Dejean A.; 1995 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41347
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Multimerization via Its Myosin Domain Facilitates Nuclear Localization and Inhibition of Core Binding Factor (CBF) Activities by the CBF[beta]-Smooth Muscle Myosin Heavy Chain Myeloid Leukemia Oncoprotein. by Kummalue T, Lou J, Friedman AD.; 2002 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=134059
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Murine Erythroleukemia Cell Line GM979 Contains Factors that Can Activate Silent Chromosomal Human [gamma]-Globin Genes. by Zitnik G, Hines P, Stamatoyannopoulos G, Papayannopoulou T.; 1991 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51266
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Near-precise interchromosomal recombination and functional DNA topoisomerase II cleavage sites at MLL and AF-4 genomic breakpoints in treatment-related acute lymphoblastic leukemia with t(4;11) translocation. by Lovett BD, Lo Nigro L,
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Rappaport EF, Blair IA, Osheroff N, Zheng N, Megonigal MD, Williams WR, Nowell PC, Felix CA.; 2001 Aug 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=55533 ·
Novel integration sites at the distal 3' end of the c-myb locus in retrovirus-induced promonocytic leukemias. by Nazarov V, Wolff L.; 1995 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189110
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NUP98 --HOXA9 expression in hemopoietic stem cells induces chronic and acute myeloid leukemias in mice. by Kroon E, Thorsteinsdottir U, Mayotte N, Nakamura T, Sauvageau G.; 2001 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=133485
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Oligomerization of the ABL tyrosine kinase by the Ets protein TEL in human leukemia. by Golub TR, Goga A, Barker GF, Afar DE, McLaughlin J, Bohlander SK, Rowley JD, Witte ON, Gilliland DG.; 1996 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231407
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Oncogene Activation in Myeloid Leukemias by Graffi Murine Leukemia Virus Proviral Integration. by Denicourt C, Edouard E, Rassart E.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=104225
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Oncogenic homeodomain transcription factor E2A-Pbx1 activates a novel WNT gene in pre-B acute lymphoblastoid leukemia. by McWhirter JR, Neuteboom ST, Wancewicz EV, Monia BP, Downing JR, Murre C.; 1999 Sep 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18056
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Oncogenic Transformation by the Tax Gene of Human T-Cell Leukemia Virus Type I In vitro. by Tanaka A, Takahashi G, Yamaoka S, Nosaka T, Maki M, Hatanaka M.; 1990 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53412
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Opposite effects of the acute promyelocytic leukemia PML-retinoic acid receptor alpha (RAR alpha) and PLZF-RAR alpha fusion proteins on retinoic acid signalling. by Ruthardt M, Testa U, Nervi C, Ferrucci PF, Grignani F, Puccetti E, Grignani F, Peschle C, Pelicci PG.; 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=232338
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Origin and Rapid Evolution of a Novel Murine Erythroleukemia Virus of the Spleen Focus-Forming Virus Family. by Hoatlin ME, Gomez-Lucia E, Lilly F, Beckstead JH, Kabat D.; 1998 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109581
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Overexpression of HOXA10 in murine hematopoietic cells perturbs both myeloid and lymphoid differentiation and leads to acute myeloid leukemia. by Thorsteinsdottir U, Sauvageau G, Hough MR, Dragowska W, Lansdorp PM, Lawrence HJ, Largman C, Humphries RK.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231774
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p45NFE2 Is a Negative Regulator of Erythroid Proliferation Which Contributes to the Progression of Friend Virus-Induced Erythroleukemias. by Li YJ, Higgins RR, Pak BJ, Shivdasani RA, Ney PA, Archer M, Ben-David Y.; 2001 Jan 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=88781
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p53 in Chronic Myelogenous Leukemia in Acute Phase. by Feinstein E, Cimino G, Gale RP, Alimena G, Berthier R, Kishi K, Goldman J, Zaccaria A, Berrebi A, Canaani E.; 1991 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52069
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p53 Mutations in Human Lymphoid Malignancies: Association with Burkitt Lymphoma and Chronic Lymphocytic Leukemia. by Gaidano G, Ballerini P, Gong JZ, Inghirami G, Neri A, Newcomb EW, Magrath IT, Knowles DM, Dalla-Favera R.; 1991 Jun 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51883
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Panhandle PCR strategy to amplify MLL genomic breakpoints in treatment-related leukemias. by Megonigal MD, Rappaport EF, Jones DH, Kim CS, Nowell PC, Lange BJ, Felix CA.; 1997 Oct 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23546
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Parameters of disease progression in long-term experimental feline retrovirus (feline immunodeficiency virus and feline leukemia virus) infections: hematology, clinical chemistry, and lymphocyte subsets. by Hofmann-Lehmann R, Holznagel E, Ossent P, Lutz H.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=170472
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Pbx1 is Converted into a Transcriptional Activator Upon Acquiring the N-Terminal Region of E2A in Pre-B-Cell Acute Lymphoblastoid Leukemia. by Dijk MA, Voorhoeve PM, Murre C.; 1993 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46867
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PIC-1/SUMO-1-Modified PML-Retinoic Acid Receptor [alpha] Mediates Arsenic Trioxide-Induced Apoptosis in Acute Promyelocytic Leukemia. by Sternsdorf T, Puccetti E, Jensen K, Hoelzer D, Will H, Ottmann OG, Ruthardt M.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=84360
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PLZF-RAR[alpha] Fusion Proteins Generated from the Variant t(11;17)(q23;q 21) Translocation in Acute Promyelocytic Leukemia Inhibit Ligand-Dependent Transactivation of Wild-Type Retinoic Acid Receptors. by Chen Z, Guidez F, Rousselot P, Agadir A, Chen S, Wang Z, Degos L, Zelent A, Waxman S, Chomienne C.; 1994 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43117
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Polar/Apolar Compounds Induce Leukemia Cell Differentiation by Modulating CellSurface Potential. by Arcangeli A, Carla M, Bene MR, Becchetti A, Wanke E, Olivotto M.; 1993 Jun 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46822
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Polyclonal bovine sera but not virus-neutralizing monoclonal antibodies block bovine leukemia virus (BLV) gp51 binding to recombinant BLV receptor BLVRcp1. by Orlik O, Ban J, Hlavaty J, Altaner C, Kettmann R, Portetelle D, Splitter GA.; 1997 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191461
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Polymorphism in glutathione S-transferase P1 is associated with susceptibility to chemotherapy-induced leukemia. by Allan JM, Wild CP, Rollinson S, Willett EV, Moorman AV, Dovey GJ, Roddam PL, Roman E, Cartwright RA, Morgan GJ.; 2001 Sep 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=58774
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Polymorphisms in the methylenetetrahydrofolate reductase gene are associated with susceptibility to acute leukemia in adults. by Skibola CF, Smith MT, Kane E, Roman E, Rollinson S, Cartwright RA, Morgan G.; 1999 Oct 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23109
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Polymorphisms of the Cell Surface Receptor Control Mouse Susceptibilities to Xenotropic and Polytropic Leukemia Viruses. by Marin M, Tailor CS, Nouri A, Kozak SL, Kabat D.; 1999 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112970
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Pondering the Promyelocytic Leukemia Protein (PML) Puzzle: Possible Functions for PML Nuclear Bodies. by Borden KL.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=133952
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Potential role of natural killer cells in controlling tumorigenesis by human T-cell leukemia viruses. by Feuer G, Stewart SA, Baird SM, Lee F, Feuer R, Chen IS.; 1995 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=188715
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Potentiation of GATA-2 Activity through Interactions with the Promyelocytic Leukemia Protein (PML) and the t(15;17)-Generated PML-Retinoic Acid Receptor [alpha] Oncoprotein. by Tsuzuki S, Towatari M, Saito H, Enver T.; 2000 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=86102
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Powerful and prolonged protection of human retinal pigment epithelial cells, keratinocytes, and mouse leukemia cells against oxidative damage: The indirect antioxidant effects of sulforaphane. by Gao X, Dinkova-Kostova AT, Talalay P.; 2001 Dec 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=65010
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Prevention of Adult T-Cell Leukemia-Like Lymphoproliferative Disease in Rats by Adoptively Transferred T Cells from a Donor Immunized with Human T-Cell Leukemia Virus Type 1 Tax-Coding DNA Vaccine. by Ohashi T, Hanabuchi S, Kato H, Tateno H, Takemura F, Tsukahara T, Koya Y, Hasegawa A, Masuda T, Kannagi M.; 2000 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112393
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Productive Nonlytic Human Immunodeficiency Virus Type 1 Replication in a Newly Established Human Leukemia Cell Line. by Banerjee R, Bekesi JG, Tarcsafalvi A, Sperber K, Deak G, Choi HH, Paronetto F, Holland JF, Acs G.; 1992 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=50264
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Progression to persistent lymphocytosis and tumor development in bovine leukemia virus (BLV)-infected cattle correlates with impaired proliferation of CD4+ T cells in response to gag- and env-encoded BLV proteins. by Orlik O, Splitter GA.; 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190827
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Progressive de novo DNA Methylation at the bcr-abl Locus in the Course of Chronic Myelogenous Leukemia. by Zion M, Ben-Yehuda D, Avraham A, Cohen O, Wetzler M, Melloul D, Ben-Neriah Y.; 1994 Oct 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45094
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Proliferation of adult T cell leukemia /lymphoma cells is associated with the constitutive activation of JAK /STAT proteins. by Takemoto S, Mulloy JC, Cereseto A, Migone TS, Patel BK, Matsuoka M, Yamaguchi K, Takatsuki K, Kamihira S, White JD, Leonard WJ, Waldmann T, Franchini G.; 1997 Dec 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28404
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Proteins associated with the promyelocytic leukemia gene product (PML)-containing nuclear body move to the nucleolus upon inhibition of proteasome-dependent protein degradation. by Mattsson K, Pokrovskaja K, Kiss C, Klein G, Szekely L.; 2001 Jan 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=14700
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Pulmonary Infection Caused by Gymnascella hyalinospora in a Patient with Acute Myelogenous Leukemia. by Iwen PC, Sigler L, Tarantolo S, Sutton DA, Rinaldi MG, Lackner RP, McCarthy DI, Hinrichs SH.; 2000 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=88727
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Putative Tyrosine Kinases Expressed in K-562 Human Leukemia Cells. by Partanen J, Makela TP, Alitalo R, Lehvaslaiho H, Alitalo K.; 1990 Nov 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=55070
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Quantification of Bcr-Abl transcripts in chronic myelogenous leukemia (CML) using standardized, internally controlled, competitive differential PCR (CD-PCR). by Nagel S, Schmidt M, Thiede C, Huhn D, Neubauer A.; 1996 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=146207
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Rapid Tumor Formation of Human T-Cell Leukemia Virus Type 1-Infected Cell Lines in Novel NOD-SCID/[gamma]cnull Mice: Suppression by an Inhibitor against NF[kappa]B. by Dewan MZ, Terashima K, Taruishi M, Hasegawa H, Ito M, Tanaka Y, Mori N, Sata T, Koyanagi Y, Maeda M, Kubuki Y, Okayama A, Fujii M, Yamamoto N.; 2003 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=153944
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Recombinant mink cell focus-inducing virus and long terminal repeat alterations accompany the increased leukemogenicity of the Mo+PyF101 variant of Moloney
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murine leukemia virus after intraperitoneal inoculation. by Belli B, Patel A, Fan H.; 1995 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=188674 ·
Regulation of Phospholipase A2 in Human Leukemia Cell Lines: Its Implication for Intracellular Signaling. by Tsujishita Y, Asaoka Y, Nishizuka Y.; 1994 Jul 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=44183
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Replication and Pathogenicity of Primer Binding Site Mutants of SL3-3 Murine Leukemia Viruses. by Lund AH, Schmidt J, Luz A, Sorensen AB, Duch M, Pedersen FS.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112678
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Resistance to Friend Murine Leukemia Virus Infection Conferred by the Fv-4 Gene Is Recessive but Appears Dominant from the Effect of the Immune System. by Zhang F, Ya LT, Iwatani Y, Higo K, Suzuki Y, Tanaka M, Nakahara T, Ono T, Sakai H, Kuribayashi K, Ishimoto A.; 2000 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=112120
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Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RAR[alpha] and PLZF-RAR[alpha] oncoproteins. by Rego EM, He LZ, Warrell RP Jr, Wang ZG, Pandolfi PP.; 2000 Aug 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27786
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Retinoids down-regulate telomerase and telomere length in a pathway distinct from leukemia cell differentiation. by Pendino F, Flexor M, Delhommeau F, Buet D, Lanotte M, Segal-Bendirdjian E.; 2001 Jun 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=34517
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Retroviral Integration at the Epi1 Locus Cooperates with Nf1 Gene Loss in the Progression to Acute Myeloid Leukemia. by Blaydes SM, Kogan SC, Truong BT, Gilbert DJ, Jenkins NA, Copeland NG, Largaespada DA, Brannan CI.; 2001 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=114510
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Retroviral integration at the Evi-2 locus in BXH-2 myeloid leukemia cell lines disrupts Nf1 expression without changes in steady-state Ras-GTP levels. by Largaespada DA, Shaughnessy JD Jr, Jenkins NA, Copeland NG.; 1995 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189327
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Retrovirus-mediated gene transfer of MLL-ELL transforms primary myeloid progenitors and causes acute myeloid leukemias in mice. by Lavau C, Luo RT, Du C, Thirman MJ.; 2000 Sep 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27135
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Reverse Transcription Polymerase Chain Reaction for the Rearranged Retinoic Acid Receptor [alpha] Clarifies Diagnosis and Detects Minimal Residual Disease in Acute Promyelocytic Leukemia. by Miller WH Jr, Kakizuka A, Frankel SR, Warrell RP Jr, DeBlasio A, Levine K, Evans RM, Dmitrovsky E.; 1992 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48728
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Ribozyme Cleaves rex/tax mRNA and Inhibits Bovine Leukemia Virus Expression. by Cantor GH, McElwain TF, Birkebak TA, Palmer GH.; 1993 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47895
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RIG-E, a Human Homolog of the Murine Ly-6 Family, is Induced by Retinoic Acid during the Differentiation of Acute Promyelocytic Leukemia Cell. by Mao M, Yu M, Tong J, Ye J, Zhu J, Huang Q, Fu G, Yu L, Zhao S, Waxman S, Lanotte M, Wang Z, Tan J, Chan S, Chen Z.; 1996 Jun 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39161
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Role of Natural Killer Cells in Resistance against Friend Retrovirus-Induced Leukemia. by Iwanami N, Niwa A, Yasutomi Y, Tabata N, Miyazawa M.; 2001 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=114109
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Selection for Loss of p53 Function in T-Cell Lymphomagenesis Is Alleviated by Moloney Murine Leukemia Virus Infection in myc Transgenic Mice. by Baxter EW, Blyth K, Cameron ER, Neil JC.; 2001 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=114551
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Seroepidemiological Survey of Infection by Feline Leukemia Virus and Immunodeficiency Virus in Madrid and Correlation with Some Clinical Aspects. by Arjona A, Escolar E, Soto I, Barquero N, Martin D, Gomez-Lucia E.; 2000 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=87403
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SFA-1, a novel cellular gene induced by human T-cell leukemia virus type 1, is a member of the transmembrane 4 superfamily. by Hasegawa H, Utsunomiya Y, Kishimoto K, Yanagisawa K, Fujita S.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190191
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SMRT corepressor interacts with PLZF and with the PML-retinoic acid receptor [alpha] (RAR[alpha]) and PLZF-RAR[alpha] oncoproteins associated with acute promyelocytic leukemia. by Hong SH, David G, Wong CW, Dejean A, Privalsky ML.; 1997 Aug 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23013
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Spi-1/PU.1 transgenic mice develop multistep erythroleukemias. by Moreau-Gachelin F, Wendling F, Molina T, Denis N, Titeux M, Grimber G, Briand P, Vainchenker W, Tavitian A.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231234
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Stability of AML1 (core) site enhancer mutations in T lymphomas induced by attenuated SL3-3 murine leukemia virus mutants. by Amtoft HW, Sorensen AB, Bareil C, Schmidt J, Luz A, Pedersen FS.; 1997 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191741
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Structure and function of the long terminal repeats of feline leukemia viruses derived from naturally occurring acute myeloid leukemias in cats. by Nishigaki K, Okuda M, Endo Y, Watari T, Tsujimoto H, Hasegawa A.; 1997 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230298
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Studies on Leukemia Developing Spontaneously in an Inbred Family of Rats. by Gross L, Dreyfuss Y.; 1993 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46664
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Subcellular localization of the alpha and beta subunits of the acute myeloid leukemia-linked transcription factor PEBP2/CBF. by Lu J, Maruyama M, Satake M, Bae SC, Ogawa E, Kagoshima H, Shigesada K, Ito Y.; 1995 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230389
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Substitution of Leucine for Isoleucine in a Sequence Highly Conserved Among Retroviral Envelope Surface Glycoproteins Attenuates the Lytic Effect of the Friend Murine Leukemia Virus. by Sitbon M, D'Auriol L, Ellerbrok H, Andre C, Nishio J, Perryman S, Pozo F, Hayes SF, Wehrly K, Tambourin P, Galibert F, Chesebro B.; 1991 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51992
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Successful Hematopoietic Reconstitution with Transplantation of ErythrocyteDepleted Allogeneic Human Umbilical Cord Blood Cells in a Child with Leukemia. by Pahwa RN, Fleischer A, Than S, Good RA.; 1994 May 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43810
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Successful Outcome of Treatment of a Disseminated Infection Due to Fusarium dimerum in a Leukemia Patient. by Letscher-Bru V, Campos F, Waller J, Randriamahazaka R, Candolfi E, Herbrecht R.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=120274
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Suppression of H-2b-Associated Resistance to Friend Erythroleukemia Virus by a Class I Gene from the H-dd Major Histocompatibility Complex Haplotype. by Polsky D, Lilly F.; 1991 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52690
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Suppression of Philadelphia1 Leukemia Cell Growth in Mice by BCR-ABL Antisense Oligodeoxynucleotide. by Skorski T, Nieborowska-Skorska M, Nicolaides NC, Szczylik C, Iversen P, Iozzo RV, Zon G, Calabretta B.; 1994 May 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43814
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Surface expression and function of p75 /AIRM-1 or CD33 in acute myeloid leukemias: Engagement of CD33 induces apoptosis of leukemic cells. by Vitale C, Romagnani C, Puccetti A, Olive D, Costello R, Chiossone L, Pitto A, Bacigalupo A, Moretta L, Mingari MC.; 2001 May 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33287
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Susceptibility of nude mice carrying the Fv-4 gene to Friend murine leukemia virus infection. by Higo K, Kubo Y, Iwatani Y, Ono T, Maeda M, Hiai H, Masuda T, Kuribayashi K, Zhang F, Lamin TY, Adachi A, Ishimoto A.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191112
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T cells recognizing leukemic CD34 + progenitor cells mediate the antileukemic effect of donor lymphocyte infusions for relapsed chronic myeloid leukemia after allogeneic stem cell transplantation. by Smit WM, Rijnbeek M, van Bergen CA, Fibbe WE, Willemze R, Falkenburg JH.; 1998 Aug 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21477
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t(11;22)(q23;q11.2) in acute myeloid leukemia of infant twins fuses MLL with hCDCrel, a cell division cycle gene in the genomic region of deletion in DiGeorge and velocardiofacial syndromes. by Megonigal MD, Rappaport EF, Jones DH, Williams TM, Lovett BD, Kelly KM, Lerou PH, Moulton T, Budarf ML, Felix CA.; 1998 May 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27754
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t(8;21) Breakpoints on Chromosome 21 in Acute Myeloid Leukemia are Clustered within a Limited Region of a Single Gene, AML1. by Miyoshi H, Shimizu K, Kozu T, Maseki N, Kaneko Y, Ohki M.; 1991 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52942
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TAL1 and LIM-Only Proteins Synergistically Induce Retinaldehyde Dehydrogenase 2 Expression in T-Cell Acute Lymphoblastic Leukemia by Acting as Cofactors for GATA3. by Ono Y, Fukuhara N, Yoshie O.; 1998 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109277
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TAL2, A Helix-Loop-Helix Gene Activated by the (7;9)(q34;q32) Translocation in Human T-Cell Leukemia. by Xia Y, Brown L, Yang CY, Tsan JT, Siciliano MJ, Espinosa R III, Beau MM, Baer RJ.; 1991 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53146
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Tandemization of a Subregion of the Enhancer Sequences from SRS 19-6 Murine Leukemia Virus Associated with T-Lymphoid but Not Other Leukemias. by Granger SW, Bundy LM, Fan H.; 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=104241
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Telomere-Like DNA Polymorphisms Associated with Genetic Predisposition to Acute Myeloid Leukemia in Irradiated CBA Mice. by Silver A, Cox R.; 1993 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45882
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The (4;11)(q21;q23) Chromosome Translocations in Acute Leukemias Involve the VDJ Recombinase. by Gu Y, Cimino G, Alder H, Nakamura T, Prasad R, Canaani O, Moir DT, Jones C, Nowell PC, Croce CM, Canaani E.; 1992 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=50359
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The Bcr-Abl Leukemia Oncogene Activates Jun Kinase and Requires Jun for Transformation. by Raitano AB, Halpern JR, Hambuch TM, Sawyers CL.; 1995 Dec 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40479
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The Control of Hematopoiesis and Leukemia: From Basic Biology to the Clinic. by Sachs L.; 1996 May 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39349
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The Entire Nucleotide Sequence of Friend-Related and Paralysis-Inducing PVC-441 Murine Leukemia Virus (MuLV) and Its Comparison with Those of PVC-211 MuLV and Friend MuLV. by Tanaka A, Oka K, Tanaka K, Jinno A, Ruscetti SK, Kai K.; 1998 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=109840
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The ETO Protein Disrupted in t(8;21)-Associated Acute Myeloid Leukemia Is a Corepressor for the Promyelocytic Leukemia Zinc Finger Protein. by Melnick AM, Westendorf JJ, Polinger A, Carlile GW, Arai S, Ball HJ, Lutterbach B, Hiebert SW, Licht JD.; 2000 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=110824
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The extracellular signal-regulated kinase pathway phosphorylates AML1, an acute myeloid leukemia gene product, and potentially regulates its transactivation ability. by Tanaka T, Kurokawa M, Ueki K, Tanaka K, Imai Y, Mitani K, Okazaki K, Sagata N, Yazaki Y, Shibata Y, Kadowaki T, Hirai H.; 1996 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231393
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The human formin-binding protein 17 (FBP17) interacts with sorting nexin, SNX2, and is an MLL-fusion partner in acute myelogeneous leukemia. by Fuchs U, Rehkamp G, Haas OA, Slany R, Konig M, Bojesen S, Bohle RM, Damm-Welk C, Ludwig WD, Harbott J, Borkhardt A.; 2001 Jul 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=37508
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The human leukemia oncogene bcr-abl abrogates the anchorage requirement but not the growth factor requirement for proliferation. by Renshaw MW, McWhirter JR, Wang JY.; 1995 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230351
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The MN1-TEL Fusion Protein, Encoded by the Translocation (12;22)(p13;q11) in Myeloid Leukemia, Is a Transcription Factor with Transforming Activity. by Buijs A, van Rompaey L, Molijn AC, Davis JN, Vertegaal AC, Potter MD, Adams C, van Baal S, Zwarthoff EC, Roussel MF, Grosveld GC.; 2000 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=102185
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The partial tandem duplication of ALL1 (MLL) is consistently generated by Alumediated homologous recombination in acute myeloid leukemia. by Strout MP, Marcucci G, Bloomfield CD, Caligiuri MA.; 1998 Mar 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19353
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The partial tandem duplication of ALL1 in acute myeloid leukemia with normal cytogenetics or trisomy 11 is restricted to one chromosome. by Caligiuri MA, Strout MP, Oberkircher AR, Yu F, de la Chapelle A, Bloomfield CD.; 1997 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20539
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The PEBP2[beta]MYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia. by Kogan SC, Lagasse E, Atwater S, Bae SC, Weissman I, Ito Y, Bishop JM.; 1998 Sep 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21731
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The prevalence of proviral bovine leukemia virus in peripheral blood mononuclear cells at two subclinical stages of infection. by Mirsky ML, Olmstead CA, Da Y, Lewin HA.; 1996 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190056
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The Recombinant Immunotoxin Anti-Tac(Fv)-Pseudomonas Exotoxin 40 is Cytotoxic Toward Peripheral Blood Malignant Cells from Patients with Adult T-Cell Leukemia. by Krietman RJ, Chaudhary VK, Waldmann T, Willingham MC, FitzGerald DJ, Pastan I.; 1990 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54941
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The role of viruses in the etiology of cancer and leukemia in animals and in humans. by Gross L.; 1997 Apr 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33660
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The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells. by Klejman A, Schreiner SJ, Nieborowska-Skorska M, Slupianek A, Wilson M, Smithgall TE, Skorski T.; 2002 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=131059
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The T cell leukemia LIM protein Lmo2 is necessary for adult mouse hematopoiesis. by Yamada Y, Warren AJ, Dobson C, Forster A, Pannell R, Rabbitts TH.; 1998 Mar 31; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19933
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The t(1;12)(q21;p13) translocation of human acute myeloblastic leukemia results in a TEL-ARNT fusion. by Salomon-Nguyen F, Della-Valle V, Mauchauffe M, Busson-Le Coniat M, Ghysdael J, Berger R, Bernard OA.; 2000 Jun 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18730
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The t(10;14)(q24;q11) of T-Cell Acute Lymphoblastic Leukemia Justaposes the [delta] T-Cell Receptor with TCL3, a Conserved and Activated Locus at 10q24. by Zutter M, Hockett RD, Roberts CW, McGuire EA, Bloomstone J, Morton CC, Deaven LL, Crist WM, Carroll AJ, Korsmeyer SJ.; 1990 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53854
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The t(14;21)(q11.2;q22) chromosomal translocation associated with T-cell acute lymphoblastic leukemia activates the BHLHB1 gene. by Wang J, Jani-Sait SN, Escalon EA, Carroll AJ, de Jong PJ, Kirsch IR, Aplan PD.; 2000 Mar 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16268
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The t(8;21) chromosomal translocation in acute myelogenous leukemia modifies intranuclear targeting of the AML1 /CBF[alpha]2 transcription factor. by McNeil S, Zeng C, Harrington KS, Hiebert S, Lian JB, Stein JL, van Wijnen AJ, Stein GS.; 1999 Dec 21; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24742
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The TEL /platelet-derived growth factor [beta] receptor (PDGF[beta]R) fusion in chronic myelomonocytic leukemia is a transforming protein that self-associates and
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activates PDGF[beta]R kinase-dependent signaling pathways. by Carroll M, Tomasson MH, Barker GF, Golub TR, Gilliland DG.; 1996 Dec 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26224 ·
Thrombopoietin-induced differentiation of a human megakaryoblastic leukemia cell line, CMK, involves transcriptional activation of p21(WAF1/Cip1) by STAT5. by Matsumura I, Ishikawa J, Nakajima K, Oritani K, Tomiyama Y, Miyagawa J, Kato T, Miyazaki H, Matsuzawa Y, Kanakura Y.; 1997 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=232145
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Thy-1 Glycoprotein and src-Like Protein-Tyrosine Kinase p53/p56lyn are Associated in Large Detergent-Resistant Complexes in Rat Basophilic Leukemia Cells. by Draberova L, Draber P.; 1993 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46351
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Timed sequential chemotherapy with concomitant Granulocyte Colony-Stimulating Factor for high-risk acute myelogenous leukemia: a single arm clinical trial. by He XY, Elson P, Pohlman B, Lichtin A, Hussein M, Andresen S, Kalaycio M.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=113260
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Tissue Distribution and Timing of Appearance of Polytropic Envelope Recombinants during Infection with SL3-3 Murine Leukemia Virus or Its Weakly Pathogenic SL3[Delta]Myb5 Mutant. by Rulli K, Lobelle-Rich PA, Trubetskoy A, Lenz J, Levy LS.; 2001 Jan 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=113945
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TLS-ERG Leukemia Fusion Protein Inhibits RNA Splicing Mediated by SerineArginine Proteins. by Yang L, Embree LJ, Hickstein DD.; 2000 May 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85627
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Transcriptional regulation of the ferritin heavy-chain gene: the activity of the CCAAT binding factor NF-Y is modulated in heme-treated Friend leukemia cells and during monocyte-to-macrophage differentiation. by Marziali G, Perrotti E, Ilari R, Testa U, Coccia EM, Battistini A.; 1997 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231863
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Transcriptional Regulation of the Stem Cell Leukemia Gene (SCL) --- Comparative Analysis of Five Vertebrate SCL Loci. by Gottgens B, Barton LM, Chapman MA, Sinclair AM, Knudsen B, Grafham D, Gilbert JG, Rogers J, Bentley DR, Green AR.; 2002 May 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=186570
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Translocation Breakpoint of Acute Promyelocytic Leukemia Lies Within the Retinoic Acid Receptor [alpha] Locus. by Alcalay M, Zangrilli D, Pandolfi PP, Longo L, Mencarelli A, angelo Giacomucci, Rocchi M, Biondi A, Rambaldi A, Coco FL, Diverio D, Donti E, Grignani F, Pelicci PG.; 1991 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51149
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Triple synergism of human T-lymphotropic virus type 1-encoded tax, GATA-binding protein, and AP-1 is required for constitutive expression of the interleukin-5 gene in
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adult T-cell leukemia cells. by Yamagata T, Mitani K, Ueno H, Kanda Y, Yazaki Y, Hirai H.; 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=232280 ·
Tumorigenic Potential of a Recombinant Retrovirus Containing Sequences from Moloney Murine Leukemia Virus and Feline Leukemia Virus. by Starkey CR, LobelleRich PA, Granger S, Brightman BK, Fan H, Levy LS.; 1998 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=124580
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Two Distinct Notch1 Mutant Alleles Are Involved in the Induction of T-Cell Leukemia in c-myc Transgenic Mice. by Hoemann CD, Beaulieu N, Girard L, Rebai N, Jolicoeur P.; 2000 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85710
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Two Distinctly Regulated Events, Priming and Triggering, During Retinoid-Induced Maturation and Resistance of NB4 Promyelocytic Leukemia Cell Line. by Ruchaud S, Duprez E, Gendron MC, Houge G, Genieser HG, Jastorff B, Doskeland SO, Lanotte M.; 1994 Aug 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=44619
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UBE1L is a retinoid target that triggers PML /RAR[alpha] degradation and apoptosis in acute promyelocytic leukemia. by Kitareewan S, Pitha-Rowe I, Sekula D, Lowrey CH, Nemeth MJ, Golub TR, Freemantle SJ, Dmitrovsky E.; 2002 Mar 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122605
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Unintegrated bovine leukemia virus DNA: association with viral expression and disease. by Reyes RA, Cockerell GL.; 1996 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190448
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Unresponsiveness of Primitive Chronic Myeloid Leukemia Cells to Macrophage Inflammatory Protein 1[alpha], an Inhibitor of Primitive Normal Hematopoietic Cells. by Eaves CJ, Cashman JD, Wolpe SD, Eaves AC.; 1993 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48116
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Vancomycin-resistant Aureobacterium species cellulitis and bacteremia in a patient with acute myelogenous leukemia. by Nolte FS, Arnold KE, Sweat H, Winton EF, Funke G.; 1996 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=229168
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Variant-type PML-RAR[alpha] fusion transcript in acute promyelocytic leukemia: Use of a cryptic coding sequence from intron 2 of the RAR[alpha] gene and identification of a new clinical subtype resistant to retinoic acid therapy. by Gu BW, Xiong H, Zhou Y, Chen B, Wang L, Dong S, Yu ZY, Lu LF, Zhong M, Yin HF, Zhu GF, Huang W, Ren SX, Gallagher RE, Waxman S, Chen GQ, Wang ZG, Chen Z, Fu G, Chen SJ.; 2002 May 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124308
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The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with leukemia, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “leukemia” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for leukemia (hyperlinks lead to article summaries): ·
A 41-year-old woman with chronic myelogenous leukemia. Author(s): Antin JH. Source: Jama : the Journal of the American Medical Association. 2003 August 27; 290(8): 1083-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941682&dopt=Abstract
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A case of acute myelogenous leukemia: myelodysplastic syndrome with t(2;11)(p21;q23) without MLL rearrangement. Author(s): Gozzetti A, Tozzuoli D, Crupi R, Raspadori D, Fabbri A, Lauria F. Source: Cancer Genetics and Cytogenetics. 2003 July 15; 144(2): 177-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850382&dopt=Abstract
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A case of adult T cell leukemia and lymphoma in an Italian woman showing different malignant clones in tumor mass and in blood. Author(s): Menin C, Bulian P, Filippi F, Buttarello M, Casado C, Lopez-Galindez C, De Rossi A, Chieco-Bianchi L, Del Mistro A. Source: Haematologica. 2003 July; 88(7): Ecr23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857570&dopt=Abstract
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A case of leukemia of the appendix presenting as acute appendicitis. Author(s): Toubai T, Kondo Y, Ogawa T, Imai A, Kobayashi N, Ogasawara M, Kiyama Y, Higa T, Sato K, Miyokawa N, Tanaka J, Imamura M, Kasai M. Source: Acta Haematologica. 2003; 109(4): 199-201. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853694&dopt=Abstract
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PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A case of myelodysplastic syndrome developed blastic crisis of chronic myelogenous leukemia with acquisition of major BCR/ABL. Author(s): Onozawa M, Fukuhara T, Takahata M, Yamamoto Y, Miyake T, Maekawa I. Source: Annals of Hematology. 2003 September; 82(9): 593-5. Epub 2003 July 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898186&dopt=Abstract
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A diagnosis of chronic lymphocytic leukemia prompted by cutaneous lymphocytic infiltrates present in mohs micrographic surgery frozen sections. Author(s): Padgett JK, Parlette HL 3rd, English JC 3rd. Source: Dermatologic Surgery : Official Publication for American Society for Dermatologic Surgery [et Al.]. 2003 July; 29(7): 769-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828704&dopt=Abstract
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A fluorescence in situ hybridization study of TEL-AML1 fusion gene in B-cell acute lymphoblastic leukemia (1984-2001). Author(s): Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Le Calvez G, Marion V, Abgrall JF, Berthou C, De Braekeleer M. Source: Cancer Genetics and Cytogenetics. 2003 July 15; 144(2): 143-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850377&dopt=Abstract
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A preparatory regimen of total body irradiation, busulphan and melphalan for allogeneic bone marrow transplantation in childhood high-risk leukemia and lymphoma. Author(s): Yoshihara T, Naya M, Tsunamoto K, Hojo M, Hibi S, Morimoto A, Todo S, Imashuku S. Source: Anticancer Res. 2003 March-April; 23(2C): 1739-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820450&dopt=Abstract
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A xeno-transplantable plasma cell leukemia line with a split translocation of the IgH gene. Author(s): Ohbayashi K, Taniwaki M, Ninomiya M, Kiyoi H, Iida S, Ueda R, Naoe T. Source: Cancer Genetics and Cytogenetics. 2003 July 1; 144(1): 31-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810253&dopt=Abstract
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Activity of a novel G-quadruplex-interactive telomerase inhibitor, telomestatin (SOT095), against human leukemia cells: involvement of ATM-dependent DNA damage response pathways. Author(s): Tauchi T, Shin-Ya K, Sashida G, Sumi M, Nakajima A, Shimamoto T, Ohyashiki JH, Ohyashiki K. Source: Oncogene. 2003 August 14; 22(34): 5338-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917635&dopt=Abstract
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Acute leukemia and myelodysplasia in patients with a Philadelphia chromosome negative chronic myeloproliferative disorder treated with hydroxyurea alone or with hydroxyurea after busulphan. Author(s): Nielsen I, Hasselbalch HC. Source: American Journal of Hematology. 2003 September; 74(1): 26-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949887&dopt=Abstract
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Acute leukemia: a pediatric perspective. Author(s): Downing JR, Shannon KM. Source: Cancer Cell. 2002 December; 2(6): 437-45. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12498712&dopt=Abstract
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Acute lymphoblastic leukemia presenting with lactic acidosis and renal tubular dysfunction. Author(s): Hayek M, Srinivasan A. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 June; 25(6): 488-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794529&dopt=Abstract
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Acute lymphoblastic leukemia relapse in the breast diagnosed with gray-scale and color Doppler sonography. Author(s): Likaki-Karatza E, Mpadra FA, Karamouzis MV, Ravazoula P, Koukouras D, Margariti S, Dimopoulos I. Source: Journal of Clinical Ultrasound : Jcu. 2002 November-December; 30(9): 552-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12404522&dopt=Abstract
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Acute lymphocytic leukemia after fulminant varicella associated with severe neutropenia. Author(s): Moiz B. Source: Southern Medical Journal. 2003 July; 96(7): 726; Author Reply 726. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12940335&dopt=Abstract
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Acute myeloblastic leukemia in a patient with non-Hodgkin's lymphoma early after double peripheral blood stem-cell transplantation. Author(s): Hashino S, Toyoshima N, Chiba K, Suzuki S, Kurosawa M, Musashi M, Asaka M. Source: Transplantation. 2003 July 15; 76(1): 264-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865823&dopt=Abstract
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Acute Philadelphia chromosome-positive leukemia in an adolescent boy after liver transplantation. Author(s): Silliman CC, Tyson RW, Wei Q, Karrer FG, Davies SM, Blake M, McGavran L. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 July; 25(7): 565-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847326&dopt=Abstract
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Acute promyelocytic leukemia and aural recurrence: the importance of otoscopy in early diagnosis. Author(s): Magliulo G, Fusconi M, Pulice G. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1418-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835735&dopt=Abstract
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Adenovirus-mediated gene therapy with an antiangiogenic fragment of thrombospondin-1 inhibits human leukemia xenograft growth in nude mice. Author(s): Liu P, Wang Y, Li YH, Yang C, Zhou YL, Li B, Lu SH, Yang RC, Cai YL, Tobelem G, Caen J, Han ZC. Source: Leukemia Research. 2003 August; 27(8): 701-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801528&dopt=Abstract
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Advances in targeted therapy for chronic myeloid leukemia. Author(s): Yee KW, Keating A. Source: Expert Rev Anticancer Ther. 2003 June; 3(3): 295-310. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820774&dopt=Abstract
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Age- and sex-specific incidence of childhood leukemia by immunophenotype in the Nordic countries. Author(s): Hjalgrim LL, Rostgaard K, Schmiegelow K, Soderhall S, Kolmannskog S, Vettenranta K, Kristinsson J, Clausen N, Melbye M, Hjalgrim H, Gustafsson G. Source: Journal of the National Cancer Institute. 2003 October 15; 95(20): 1539-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14559876&dopt=Abstract
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Aggressive natural killer cell leukemia: clinical features and treatment outcome. Author(s): Song SY, Kim WS, Ko YH, Kim K, Lee MH, Park K. Source: Haematologica. 2002 December; 87(12): 1343-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495907&dopt=Abstract
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Allogeneic stem cell transplantation for advanced acute promyelocytic leukemia: results in patients treated in second molecular remission or with molecularly persistent disease. Author(s): Lo-Coco F, Romano A, Mengarelli A, Diverio D, Iori AP, Moleti ML, De Santis S, Cerretti R, Mandelli F, Arcese W. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 1930-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513040&dopt=Abstract
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Altered transcription of the stem cell leukemia gene in myelofibrosis with myeloid metaplasia. Author(s): Steunou V, Le Bousse-Kerdiles MC, Colin-Micouin A, Clay D, Chevillard S, Martyre MC; French INSERM Research Network on Myelofibrosis Myeloid Metaplasia. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 1998-2006. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513050&dopt=Abstract
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AML1 overexpression and/or mutations should be checked in trisomy 21 patients with megakaryocytic leukemia. Author(s): Huret JL, Leonard C. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1421. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835737&dopt=Abstract
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An activated receptor tyrosine kinase, TEL/PDGFbetaR, cooperates with AML1/ETO to induce acute myeloid leukemia in mice. Author(s): Grisolano JL, O'Neal J, Cain J, Tomasson MH. Source: Proceedings of the National Academy of Sciences of the United States of America. 2003 August 5; 100(16): 9506-11. Epub 2003 July 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12881486&dopt=Abstract
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An analysis of prognostic factors and the five-year survival rate in childhood acute lymphoblastic leukemia. Author(s): Karimi M, Yarmohammadi H, Sabri MR. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2002 December; 8(12): Cr792-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12503037&dopt=Abstract
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An unusual case of CD4+ CD7+ CD56+ acute leukemia with overlapping features of type 2 dendritic cell (DC2) and myeloid/NK cell precursor acute leukemia. Author(s): Anargyrou K, Paterakis G, Boutsis D, Politou M, Papadhimitriou SI, Siakandaris M, Vassiliadis J, Androulakis A, Meletis J, Rombos J, Tassiopoulou A, Vaiopoulos G. Source: European Journal of Haematology. 2003 October; 71(4): 294-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950240&dopt=Abstract
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Analysis of CD10+ hairy cell leukemia. Author(s): Jasionowski TM, Hartung L, Greenwood JH, Perkins SL, Bahler DW. Source: American Journal of Clinical Pathology. 2003 August; 120(2): 228-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12931553&dopt=Abstract
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Analysis of the impact of imatinib mesylate therapy on the prognosis of patients with Philadelphia chromosome-positive chronic myelogenous leukemia treated with interferon-alpha regimens for early chronic phase. Author(s): Kantarjian H, O'Brien S, Cortes J, Shan J, Giles F, Garcia-Manero G, Verstovsek S, Faderl S, Rios MB, Talpaz M. Source: Cancer. 2003 October 1; 98(7): 1430-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508830&dopt=Abstract
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Androgen receptor mutations in androgen-independent prostate cancer: Cancer and Leukemia Group B Study 9663. Author(s): Taplin ME, Rajeshkumar B, Halabi S, Werner CP, Woda BA, Picus J, Stadler W, Hayes DF, Kantoff PW, Vogelzang NJ, Small EJ; Cancer and Leukemia Group B Study 9663. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 15; 21(14): 2673-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860943&dopt=Abstract
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Antagonism by methotrexate on mercaptopurine disposition in lymphoblasts during up-front treatment of acute lymphoblastic leukemia. Author(s): Dervieux T, Hancock ML, Pui CH, Rivera GK, Sandlund JT, Ribeiro RC, Boyett J, Evans WE, Relling MV. Source: Clinical Pharmacology and Therapeutics. 2003 June; 73(6): 506-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12811360&dopt=Abstract
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Antithrombin supplementation III in childhood acute lymphoblastic leukemia treated with L-asparaginase. Author(s): Matsuzaki A, Suminoe A, Hara T. Source: Pediatric Hematology and Oncology. 2002 December; 19(8): 601-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12487838&dopt=Abstract
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Arsenic trioxide-induced mitotic arrest and apoptosis in acute promyelocytic leukemia cells. Author(s): Cai X, Yu Y, Huang Y, Zhang L, Jia PM, Zhao Q, Chen Z, Tong JH, Dai W, Chen GQ. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1333-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835721&dopt=Abstract
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Association of acute leukemia and autoimmune polyendocrine syndrome in two kindreds. Author(s): Willems E, Valdes-Socin H, Betea D, Beckers A, Beguin Y. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1912-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970797&dopt=Abstract
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Autoimmune cytopenia does not predict poor prognosis in chronic lymphocytic leukemia/small lymphocytic lymphoma. Author(s): Kyasa MJ, Parrish RS, Schichman SA, Zent CS. Source: American Journal of Hematology. 2003 September; 74(1): 1-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949883&dopt=Abstract
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B cell chronic lymphocytic leukemia: lessons learned from studies of the B cell antigen receptor. Author(s): Chiorazzi N, Ferrarini M. Source: Annual Review of Immunology. 2003; 21: 841-94. Epub 2001 December 19. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12615894&dopt=Abstract
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B lineage acute lymphoblastic leukemia transformation in a child with juvenile myelomonocytic leukemia, type 1 neurofibromatosis and monosomy of chromosome 7. Possible implications in the leukemogenesis. Author(s): Scrideli CA, Baruffi MR, Rogatto SR, Valera ET, Defavery R, Tone LG. Source: Leukemia Research. 2003 April; 27(4): 371-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531231&dopt=Abstract
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B3/A3 rearrangement in a patient with chronic myeloid leukemia. Author(s): Paz-Y-Mino C, Arevalo M, Leone PE. Source: Leukemia & Lymphoma. 2003 February; 44(2): 375-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688363&dopt=Abstract
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Bacteremia caused by Brevibacterium species in a patient with chronic lymphocytic leukemia. Author(s): Ogunc D, Gultekin M, Colak D, Timuragaoglu A, Ongut G, Mutlu G, Hathi D, Undar L. Source: Haematologia. 2002; 32(2): 151-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12412735&dopt=Abstract
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Bacteremia due to a novel Microbacterium species in a patient with leukemia and description of Microbacterium paraoxydans sp. nov. Author(s): Laffineur K, Avesani V, Cornu G, Charlier J, Janssens M, Wauters G, Delmee M. Source: Journal of Clinical Microbiology. 2003 May; 41(5): 2242-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12734292&dopt=Abstract
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BARCODE-ALL: accelerated and cost-effective genetic risk stratification in acute leukemia using spectrally addressable liquid bead microarrays. Author(s): Wallace J, Zhou Y, Usmani GN, Reardon M, Newburger P, Woda B, Pihan G. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1411-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835732&dopt=Abstract
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BARCODE-ALL: accelerated and cost-effective genetic risk stratification in acute leukemia using spectrally addressable liquid bead microarrays. Author(s): Wallace J, Zhou Y, Usmani GN, Reardon M, Newburger P, Woda B, Pihan G. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1404-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835731&dopt=Abstract
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B-Cell lymphoproliferative disorder not associated with Epstein-Barr Virus in a child with relapsed acute lymphoblastic leukemia. Author(s): Lehrnbecher T, Trusen A, Deinlein F, Hocht B, Marx A, Kuhl J. Source: Medical and Pediatric Oncology. 2003 January; 40(1): 13-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12426680&dopt=Abstract
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Bcl-2 and apoptosis in chronic lymphocytic leukemia. Author(s): Schimmer AD, Munk-Pedersen I, Minden MD, Reed JC. Source: Curr Treat Options Oncol. 2003 June; 4(3): 211-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718798&dopt=Abstract
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BCR/ABL amplification in chronic myelocytic leukemia blast crisis following imatinib mesylate administration. Author(s): Campbell LJ, Patsouris C, Rayeroux KC, Somana K, Januszewicz EH, Szer J. Source: Cancer Genetics and Cytogenetics. 2002 November; 139(1): 30-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12547154&dopt=Abstract
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BCR/ABL: from molecular mechanisms of leukemia induction to treatment of chronic myelogenous leukemia. Author(s): Salesse S, Verfaillie CM. Source: Oncogene. 2002 December 9; 21(56): 8547-59. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12476301&dopt=Abstract
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BCR/ABL-mediated increased expression of multiple known and novel genes that may contribute to the pathogenesis of chronic myelogenous leukemia. Author(s): Salesse S, Verfaillie CM. Source: Molecular Cancer Therapeutics. 2003 February; 2(2): 173-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12589034&dopt=Abstract
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Bcr: a negative regulator of the Bcr-Abl oncoprotein in leukemia. Author(s): Arlinghaus RB. Source: Oncogene. 2002 December 9; 21(56): 8560-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12476302&dopt=Abstract
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BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. Author(s): Donato NJ, Wu JY, Stapley J, Gallick G, Lin H, Arlinghaus R, Talpaz M. Source: Blood. 2003 January 15; 101(2): 690-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509383&dopt=Abstract
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Behavioural and anatomical effects of systemically administered leukemia inhibitory factor in the SOD1(G93A G1H) mouse model of familial amyotrophic lateral sclerosis. Author(s): Azari MF, Lopes EC, Stubna C, Turner BJ, Zang D, Nicola NA, Kurek JB, Cheema SS. Source: Brain Research. 2003 August 22; 982(1): 92-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915243&dopt=Abstract
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Bell's palsy as an early manifestation of acute lymphoblastic leukemia. Author(s): Ozcakar L, Akinci A, Ozgocmen S, Aksu S, Cetin E. Source: Annals of Hematology. 2003 February; 82(2): 124-6. Epub 2003 February 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12601494&dopt=Abstract
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Benefit of high-dose methylprednisolone in comparison with conventional-dose prednisolone during remission induction therapy in childhood acute lymphoblastic leukemia for long-term follow-up. Author(s): Yetgin S, Tuncer MA, Cetin M, Gumruk F, Yenicesu I, Tunc B, Oner AF, Toksoy H, Koc A, Aslan D, Ozyurek E, Olcay L, Atahan L, Tuncbilek E, Gurgey A. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 February; 17(2): 328-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592331&dopt=Abstract
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Beta2-microglobulin induces caspase-dependent apoptosis in the CCRF-HSB-2 human leukemia cell line independently of the caspase-3, -8 and -9 pathways but through increased reactive oxygen species. Author(s): Gordon J, Wu CH, Rastegar M, Safa AR. Source: International Journal of Cancer. Journal International Du Cancer. 2003 January 20; 103(3): 316-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12471614&dopt=Abstract
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Beta-carotene regulates NF-kappaB DNA-binding activity by a redox mechanism in human leukemia and colon adenocarcinoma cells. Author(s): Palozza P, Serini S, Torsello A, Di Nicuolo F, Piccioni E, Ubaldi V, Pioli C, Wolf FI, Calviello G. Source: The Journal of Nutrition. 2003 February; 133(2): 381-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12566471&dopt=Abstract
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Bilateral alveolar infiltrates in a 29-year-old man with chronic myelogenous leukemia. Author(s): Cheng SL, Kuo PH, Yang PC, Luh KT. Source: Chest. 2002 December; 122(6): 2238-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475870&dopt=Abstract
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Bilateral cavitary pulmonary consolidations in a patient undergoing allogeneic bone marrow transplantation for acute leukemia. Author(s): Hiltermann TJ, Bredius RG, Gesink-vd Veer BJ, Corrin B, Rabe KF, Brahim JJ. Source: Chest. 2003 March; 123(3): 929-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12628896&dopt=Abstract
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Bilateral exopthalmus due to retro-orbital chloromas in a boy with t(8;21)- positive acute myeloblastic acute leukemia. Author(s): Bonig H, Gobel U, Nurnberger W. Source: Pediatric Hematology and Oncology. 2002 December; 19(8): 597-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12487837&dopt=Abstract
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Bilateral optic nerve infiltration in central nervous system leukemia. Author(s): Schocket LS, Massaro-Giordano M, Volpe NJ, Galetta SL. Source: American Journal of Ophthalmology. 2003 January; 135(1): 94-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12504706&dopt=Abstract
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Bilateral orbital myeloid sarcoma as initial sign of acute myeloid leukemia: case report and review of the literature. Author(s): Shields JA, Stopyra GA, Marr BP, Shields CL, Pan W, Eagle RC Jr, Bernstein J. Source: Archives of Ophthalmology. 2003 January; 121(1): 138-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12523908&dopt=Abstract
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Biological and clinical heterogeneity of B-cell chronic lymphocytic leukemia. Author(s): D'Arena G, Di Renzo N, Brugiatelli M, Vigliotti ML, Keating MJ. Source: Leukemia & Lymphoma. 2003 February; 44(2): 223-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688337&dopt=Abstract
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Biology, clinical, and hematologic features of acute megakaryoblastic leukemia in children. Author(s): Paredes-Aguilera R, Romero-Guzman L, Lopez-Santiago N, Trejo RA. Source: American Journal of Hematology. 2003 June; 73(2): 71-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749007&dopt=Abstract
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Biphenotypic acute leukemia following intensive adjuvant chemotherapy for breast cancer: case report and review of the literature. Author(s): Briasoulis E, Tzouvara E, Tsiara S, Vartholomatos G, Tsekeris P, Bourantas K. Source: The Breast Journal. 2003 May-June; 9(3): 241-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752636&dopt=Abstract
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Biphenotypic acute leukemia with coexpression of CD79a and markers of myeloid lineage. Author(s): Frater JL, Yaseen NR, Peterson LC, Tallman MS, Goolsby CL. Source: Archives of Pathology & Laboratory Medicine. 2003 March; 127(3): 356-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12653584&dopt=Abstract
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Birth weight as a risk factor for childhood leukemia: a meta-analysis of 18 epidemiologic studies. Author(s): Hjalgrim LL, Westergaard T, Rostgaard K, Schmiegelow K, Melbye M, Hjalgrim H, Engels EA. Source: American Journal of Epidemiology. 2003 October 15; 158(8): 724-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14561661&dopt=Abstract
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Body composition in long-term survivors of childhood acute lymphoblastic leukemia (ALL). Author(s): van der Sluis IM, van den Heuvel MM, de Muinck Keizer-Schrama SM. Source: Medical and Pediatric Oncology. 2003 June; 40(6): 407. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692817&dopt=Abstract
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Breakthrough fungemia caused by azole-resistant Candida albicans in neutropenic patients with acute leukemia. Author(s): Myoken Y, Kyo T, Kohara T, Fujihara M, Sugata T, Mikami Y. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2003 June 1; 36(11): 1496-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12766847&dopt=Abstract
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Bryostatin 1 and UCN-01 potentiate 1-beta-D-arabinofuranosylcytosine-induced apoptosis in human myeloid leukemia cells through disparate mechanisms. Author(s): Wang S, Wang Z, Grant S. Source: Molecular Pharmacology. 2003 January; 63(1): 232-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488556&dopt=Abstract
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Bullous pyoderma gangrenosum complicated by disseminated intravascular coagulation with subsequent myelodysplastic syndrome (chronic myelomonocytic leukemia). Author(s): Rogalski C, Paasch U, Glander HJ, Haustein UF. Source: The Journal of Dermatology. 2003 January; 30(1): 59-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598711&dopt=Abstract
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Burkitt's leukemia with precursor B-cell immunophenotype and atypical morphology (atypical Burkitt's leukemia/lymphoma): case report and review of literature. Author(s): Komrokji R, Lancet J, Felgar R, Wang N, Bennett JM. Source: Leukemia Research. 2003 June; 27(6): 561-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12648517&dopt=Abstract
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Bystander transfer of functional human CD40 ligand from gene-modified fibroblasts to B-chronic lymphocytic leukemia cells. Author(s): Biagi E, Yvon E, Dotti G, Amrolia PJ, Takahashi S, Popat U, Marini F, Andreeff M, Brenner MK, Rousseau RF. Source: Human Gene Therapy. 2003 April 10; 14(6): 545-59. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718765&dopt=Abstract
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Can t(8;21) oligoblastic leukemia be called a myelodysplastic syndrome? Author(s): Kaneda K, Kojima K, Takeuchi M, Takimoto H, Takaba S, Shinagawa K, Kobayashi H, Miyata A, Hara M, Tanimoto M. Source: European Journal of Haematology. 2002 September; 69(3): 165-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12406010&dopt=Abstract
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Causation of chronic lymphocytic leukemia--insights from familial disease. Author(s): Houlston RS, Sellick G, Yuille M, Matutes E, Catovsky D. Source: Leukemia Research. 2003 October; 27(10): 871-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860003&dopt=Abstract
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CD8+ chronic lymphocytic leukemia: an extensive characterization of a bizarre hybrid neoplasia. Author(s): Richaud-Patin Y, Piedras J, Carrillo-Maravilla E, Lopez-Karpovitch X, Llorente L. Source: European Journal of Haematology. 2003 September; 71(3): 224-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930326&dopt=Abstract
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cDNA microarray analysis of altered gene expression in Ara-C-treated leukemia cells. Author(s): Takagaki K, Katsuma S, Horio T, Kaminishi Y, Hada Y, Tanaka T, Ohgi T, Yano J. Source: Biochemical and Biophysical Research Communications. 2003 September 19; 309(2): 351-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12951057&dopt=Abstract
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Centromeric transverse fission of chromosome 1 in a case of acute myelocytic leukemia. Author(s): Bakshi SR, Roy SK, Patel SJ, Trivedi PJ, Brahmbhatt M, Patel SM, Shah PM, Patel DD. Source: Cancer Genetics and Cytogenetics. 2003 October 15; 146(2): 173-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14553954&dopt=Abstract
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Changes in apoptosis-related pathways in acute myelocytic leukemia. Author(s): Casas S, Ollila J, Aventin A, Vihinen M, Sierra J, Knuutila S. Source: Cancer Genetics and Cytogenetics. 2003 October 15; 146(2): 89-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14553942&dopt=Abstract
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Changes of mitochondrial respiration, mitochondrial content and cell size after induction of apoptosis in leukemia cells. Author(s): Renner K, Amberger A, Konwalinka G, Kofler R, Gnaiger E. Source: Biochimica Et Biophysica Acta. 2003 September 23; 1642(1-2): 115-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12972300&dopt=Abstract
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Childhood leukemia--successes and challenges for survivors. Author(s): Simone JV. Source: The New England Journal of Medicine. 2003 August 14; 349(7): 627-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917297&dopt=Abstract
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Childhood T-cell acute lymphoblastic leukemia: the Dana-Farber Cancer Institute acute lymphoblastic leukemia consortium experience. Author(s): Goldberg JM, Silverman LB, Levy DE, Dalton VK, Gelber RD, Lehmann L, Cohen HJ, Sallan SE, Asselin BL. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 October 1; 21(19): 3616-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512392&dopt=Abstract
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Chronic lymphocytic leukemia manifesting in the paranasal sinuses. Author(s): Johnston R, Altman KW, Gartenhaus RB. Source: Otolaryngology and Head and Neck Surgery. 2002 December; 127(6): 582-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12501113&dopt=Abstract
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Chronic lymphocytic leukemia presenting as purpura fulminans. Author(s): Yamac K, Fen T, Erel A. Source: Haematologica. 2003 July; 88(7): Eim08. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857575&dopt=Abstract
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Chronic lymphocytic leukemia: advances in biology and therapeutics. Author(s): Aksentijevich I, Flinn IW. Source: Current Opinion in Oncology. 2003 January; 15(1): 16-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490757&dopt=Abstract
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Chronic myelocytic leukemia with eosinophilia, t(9;12)(q34;p13), and ETV6-ABL gene rearrangement: case report and review of the literature. Author(s): Keung YK, Beaty M, Steward W, Jackle B, Pettnati M. Source: Cancer Genetics and Cytogenetics. 2002 October 15; 138(2): 139-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12505259&dopt=Abstract
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Chronic myelogenous leukemia. Author(s): O'Dwyer ME. Source: Current Opinion in Oncology. 2003 January; 15(1): 10-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490756&dopt=Abstract
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Chronic myelogenous leukemia: a review and update of therapeutic strategies. Author(s): Garcia-Manero G, Faderl S, O'Brien S, Cortes J, Talpaz M, Kantarjian HM. Source: Cancer. 2003 August 1; 98(3): 437-57. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879460&dopt=Abstract
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Chronic myeloid leukemia in the elderly: long-term results from randomized trials with interferon alpha. Author(s): Berger U, Engelich G, Maywald O, Pfirrmann M, Hochhaus A, Reiter A, Metzgeroth G, Gnad U, Hasford J, Heinze B, Heimpel H, Hossfeld DK, Kolb HJ, Loffler H, Pralle H, Queisser W, Hehlmann R; German CML-Study Group. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1820-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970782&dopt=Abstract
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Chronic myeloid leukemia--advances in biology and new approaches to treatment. Author(s): Goldman JM, Melo JV. Source: The New England Journal of Medicine. 2003 October 9; 349(15): 1451-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14534339&dopt=Abstract
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Chronic myelomonocytic leukemia with abnormal bone marrow eosinophils. Author(s): Hyde J, Sun T. Source: Archives of Pathology & Laboratory Medicine. 2003 September; 127(9): 1214-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12946218&dopt=Abstract
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Clinical applications of molecular monitoring in leukemia. Author(s): Maslak P. Source: Curr Hematol Rep. 2003 January; 2(1): 43-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901153&dopt=Abstract
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Clinical features in T-cell vs. natural killer-cell variants of large granular lymphocyte leukemia. Author(s): Neben MA, Morice WG, Tefferi A. Source: European Journal of Haematology. 2003 October; 71(4): 263-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950235&dopt=Abstract
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Clinical relevance of CD95 (Fas/Apo-1) on T cells of patients with B-cell chronic lymphocytic leukemia. Author(s): Groneberg C, Pickartz T, Binder A, Ringel F, Srock S, Sieber T, Schoeler D, Schriever F. Source: Experimental Hematology. 2003 August; 31(8): 682-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901972&dopt=Abstract
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Clonal analysis of granulocyte-monocyte colony-forming unit cells with the human androgen receptor gene in chronic myeloid leukemia. Author(s): Akel S, Mavroyanni D, Yataganas X, Terpos E, Meletis J, Anargyrou K, Stavrogianni N, Pangalis GA, Loukopoulos D, Viniou N. Source: International Journal of Hematology. 2003 June; 77(5): 476-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841386&dopt=Abstract
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c-Myc overcomes cell cycle inhibition by CBFbeta-SMMHC, a myeloid leukemia oncoprotein. Author(s): Bernardin F, Yang Y, Civin CI, Friedman AD. Source: Cancer Biology & Therapy. 2002 September-October; 1(5): 492-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12496475&dopt=Abstract
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Combination of imatinib and established antileukemic treatment modalities for otherwise refractory BCR-ABL positive lymphoblastic leukemia. Author(s): Fruehauf S, Topaly J, Buss EC, Schad M, Goerner M, Zeller WJ, Ho AD. Source: Haematologica. 2002 December; 87(12): Ecr38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495909&dopt=Abstract
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Combination with an antisense oligonucleotide synergistically improves the antileukemic efficacy of erucylphospho-N,N,N-trimethylpropylammonium in chronic myeloid leukemia cell lines. Author(s): Konstantinov SM, Georgieva MC, Topashka-Ancheva M, Eibl H, Berger MR. Source: Molecular Cancer Therapeutics. 2002 August; 1(10): 877-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492121&dopt=Abstract
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Comparison of the gene expression profiles of monocytic versus granulocytic lineages of HL-60 leukemia cell differentiation by DNA microarray analysis. Author(s): Song JH, Kim JM, Kim SH, Kim HJ, Lee JJ, Sung MH, Hwang SY, Kim TS. Source: Life Sciences. 2003 August 15; 73(13): 1705-19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12875902&dopt=Abstract
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Complex karyotypes in childhood acute lymphoblastic leukemia: cytogenetic and molecular cytogenetic study of 21 cases. Author(s): Jarosova M, Holzerova M, Mihal V, Lakoma I, Divoky V, Blazek B, Pospisilova D, Hajduch M, Novak Z, Dusek L, Koptikova J, Poulsen TS, Indrak K. Source: Cancer Genetics and Cytogenetics. 2003 September; 145(2): 161-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12935929&dopt=Abstract
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Constitutional pericentric inversion of chromosome 9 and acute leukemia. Author(s): Keung YK, Knovich MA, Powell BL, Buss DH, Pettenati M. Source: Cancer Genetics and Cytogenetics. 2003 August; 145(1): 82-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885469&dopt=Abstract
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Constitutive phosphorylation of FKHR transcription factor as a prognostic variable in acute myeloid leukemia. Author(s): Cheong JW, Eom JI, Maeng HY, Lee ST, Hahn JS, Ko YW, Min YH. Source: Leukemia Research. 2003 December; 27(12): 1159-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921955&dopt=Abstract
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Core binding factor (CBF) acute myeloid leukemia: is molecular monitoring by RTPCR useful clinically? Author(s): Marcucci G, Caligiuri MA, Bloomfield CD. Source: European Journal of Haematology. 2003 September; 71(3): 143-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930314&dopt=Abstract
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Core binding factor genes and human leukemia. Author(s): Hart SM, Foroni L. Source: Haematologica. 2002 December; 87(12): 1307-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495904&dopt=Abstract
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Cryptic t(5;11)(q35;p15.5) in adult de novo acute myelocytic leukemia with normal karyotype. Author(s): Casas S, Aventin A, Nomdedeu J, Sierra J. Source: Cancer Genetics and Cytogenetics. 2003 September; 145(2): 183. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12935934&dopt=Abstract
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Cryptococcus neoformans var neoformans resistant to fluconazole in an HIV-negative patient with chronic lymphocytic leukemia. Author(s): Assing K, Birgens H, Arendrup M. Source: Clinical Microbiology and Infection : the Official Publication of the European Society of Clinical Microbiology and Infectious Diseases. 2003 May; 9(5): 441-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848761&dopt=Abstract
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Current treatment results of allogeneic bone marrow transplantation for acute myeloid and lymphoid leukemia. Author(s): Rodriguez TE, Stiff PJ. Source: Curr Hematol Rep. 2003 July; 2(4): 295-301. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901326&dopt=Abstract
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Cutaneous sarcoidlike lesions in B-cell chronic lymphocytic leukemia. Author(s): Bachmeyer C, Debs R, Aractingi S. Source: Journal of the American Academy of Dermatology. 2003 August; 49(2 Suppl Case Reports): S180-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894116&dopt=Abstract
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Cytogenetic and molecular analysis of an unusual case of acute promyelocytic leukemia with a t(15;17;17)(q22;q23;q21). Author(s): Tirado CA, Golembiewski-Ruiz V, Horvatinovich J, Moore JO, Buckley PJ, Stenzel TT, Goodman BK. Source: Cancer Genetics and Cytogenetics. 2003 August; 145(1): 31-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885460&dopt=Abstract
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Cytoplasmic tail of Moloney murine leukemia virus envelope protein influences the conformation of the extracellular domain: implications for mechanism of action of the R Peptide. Author(s): Aguilar HC, Anderson WF, Cannon PM. Source: Journal of Virology. 2003 January; 77(2): 1281-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12502845&dopt=Abstract
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De novo acute myeloblastic leukemia with trilineage abnormalities and a t(3;12) in a child. Author(s): Hazard E, Bastard C, Callat MP, Schneider P, Vannier JP. Source: Medical and Pediatric Oncology. 2003 June; 40(6): 397-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692813&dopt=Abstract
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Decision-making in the diagnosis and treatment of leukemia. Author(s): Shannon-Dorcy K, Wolfe V. Source: Semin Oncol Nurs. 2003 May; 19(2): 142-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830738&dopt=Abstract
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Defective expression of Bruton's tyrosine kinase in acute lymphoblastic leukemia. Author(s): Goodman PA, Wood CM, Vassilev AO, Mao C, Uckun FM. Source: Leukemia & Lymphoma. 2003 June; 44(6): 1011-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854903&dopt=Abstract
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Deletion 9q as the sole karyotypic abnormality in myelocytic disorders: a new case of myelodysplastic syndrome and its prognostic implications in acute myelocytic leukemia. Author(s): Wan TS, Ma ES, Lam CC, Chan LC, Lee KK, Au WY. Source: Cancer Genetics and Cytogenetics. 2003 September; 145(2): 184-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12935935&dopt=Abstract
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Deletion of 6q23 as sole abnormality in acute myelocytic leukemia. Author(s): Sundareshan TS, Prabhash K, Bapsy PP. Source: Cancer Genetics and Cytogenetics. 2003 May; 143(1): 87-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742161&dopt=Abstract
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Dendritic cell vaccination for patients with chronic myelogenous leukemia. Author(s): Takahashi T, Tanaka Y, Nieda M, Azuma T, Chiba S, Juji T, Shibata Y, Hirai H. Source: Leukemia Research. 2003 September; 27(9): 795-802. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804637&dopt=Abstract
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Dengue fever mimicking plasma cell leukemia. Author(s): Gawoski JM, Ooi WW. Source: Archives of Pathology & Laboratory Medicine. 2003 August; 127(8): 1026-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873179&dopt=Abstract
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Derivative (7)t(7;8)(q34;q21). a new additional cytogenetic abnormality in acute promyelocytic leukemia. Author(s): Vial JP, Mahon FX, Pigneux A, Notz A, Lacombe F, Reiffers J, Bilhou-Nabera C. Source: Cancer Genetics and Cytogenetics. 2003 January 1; 140(1): 78-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12550765&dopt=Abstract
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Detection by CT scan of Penicillium sp. lesions in a patient with B-precursor acute lymphoblastic leukemia. Author(s): Mancao MY, Figarola MS, Wilson FM, Manci EA. Source: Pediatric Radiology. 2003 January; 33(1): 66-8. Epub 2002 March 23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12497245&dopt=Abstract
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Detection of NPM/MLF1 fusion in t(3;5)-positive acute myeloid leukemia and myelodysplasia. Author(s): Arber DA, Chang KL, Lyda MH, Bedell V, Spielberger R, Slovak ML. Source: Human Pathology. 2003 August; 34(8): 809-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14506644&dopt=Abstract
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Determining the clinical course and outcome in chronic lymphocytic leukemia. Author(s): Rai KR, Chiorazzi N. Source: The New England Journal of Medicine. 2003 May 1; 348(18): 1797-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724486&dopt=Abstract
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Development of a novel surrogate virus for human T-cell leukemia virus type 1: inhibition of infection by osteoprotegerin. Author(s): Okuma K, Dalton KP, Buonocore L, Ramsburg E, Rose JK. Source: Journal of Virology. 2003 August; 77(15): 8562-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857926&dopt=Abstract
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Development of chronic myelocytic leukemia after chemotherapy for malignant fibrous histiocytoma. Author(s): Yamamura R, Yamane T, Aoyama Y, Nakamae H, Makita K, Shima E, Ohta K, Inoue T, Sakamoto H, Hino M. Source: Acta Haematologica. 2003; 109(3): 141-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714824&dopt=Abstract
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Development of hairy cell leukemia in a patient treated with cytoreductive agents for essential thrombocythemia. Author(s): Azagury M, Martelli JM, Morcelet M, Duboucher C, Flandrin G. Source: Leukemia & Lymphoma. 2003 June; 44(6): 1067-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854912&dopt=Abstract
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Development of large genital ulcer due to hydroxyurea treatment in a patient with chronic myeloid leukemia and Behcet's disease. Author(s): Karincaoglu Y, Kaya E, Esrefoglu M, Aydogdu I. Source: Leukemia & Lymphoma. 2003 June; 44(6): 1063-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854911&dopt=Abstract
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Diagnosis, treatment, and nursing care of acute leukemia. Author(s): Viele CS. Source: Semin Oncol Nurs. 2003 May; 19(2): 98-108. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830734&dopt=Abstract
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Diagnosis, treatment, and nursing care of patients with chronic leukemia. Author(s): Breed CD. Source: Semin Oncol Nurs. 2003 May; 19(2): 109-17. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830735&dopt=Abstract
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Diagnostic x rays, DNA repair genes and childhood acute lymphoblastic leukemia. Author(s): Infante-Rivard C. Source: Health Physics. 2003 July; 85(1): 60-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852472&dopt=Abstract
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Differences between the CD34+ and CD34- blast compartments in apoptosis resistance in acute myeloid leukemia. Author(s): van Stijn A, van der Pol MA, Kok A, Bontje PM, Roemen GM, Beelen RH, Ossenkoppele GJ, Schuurhuis GJ. Source: Haematologica. 2003 May; 88(5): 497-508. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745269&dopt=Abstract
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Differences in significance of drug resistance mechanisms between adult and childhood acute lymphoblastic leukemia. Author(s): Styczynski J, Wysocki M. Source: Haematologia. 2002; 32(4): 313-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803106&dopt=Abstract
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Different mechanisms lead to a karyotypically identical t(20;21) in myelodysplastic syndrome and in acute myelocytic leukemia. Author(s): Matteucci C, La Starza R, Crescenzi B, Romoli S, Santoro A, Magrin S, Lauria F, Coco FL, Martelli MF, Mecucci C. Source: Cancer Genetics and Cytogenetics. 2003 January 1; 140(1): 13-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12550752&dopt=Abstract
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Differential effects of staurosporine and its analogues on chemokine release by promyelocytic leukemia cell line NB-4. Author(s): Steube KG, Meyer C, Schupp P, Proksch P, Drexler HG. Source: Leukemia Research. 2003 October; 27(10): 957-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860017&dopt=Abstract
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Differential patterns of human cytomegalovirus gene expression in various T-cell lines carrying human T-cell leukemia-lymphoma virus type I: role of Tax-activated cellular transcription factors. Author(s): Beck Z, Bacsi A, Liu X, Ebbesen P, Andirko I, Csoma E, Konya J, Nagy E, Toth FD. Source: Journal of Medical Virology. 2003 September; 71(1): 94-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12858414&dopt=Abstract
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Discovery, characterization, and structure-activity relationships studies of proapoptotic polyphenols targeting B-cell lymphocyte/leukemia-2 proteins. Author(s): Kitada S, Leone M, Sareth S, Zhai D, Reed JC, Pellecchia M. Source: Journal of Medicinal Chemistry. 2003 September 25; 46(20): 4259-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13678404&dopt=Abstract
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Disseminated candidiasis in a patient with acute myelogenous leukemia. Author(s): Grabowski R, Dugan E. Source: Cutis; Cutaneous Medicine for the Practitioner. 2003 June; 71(6): 466-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839257&dopt=Abstract
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DNA microarray analysis of hematopoietic stem cell-like fractions from individuals with the M2 subtype of acute myeloid leukemia. Author(s): Oshima Y, Ueda M, Yamashita Y, Choi YL, Ota J, Ueno S, Ohki R, Koinuma K, Wada T, Ozawa K, Fujimura A, Mano H. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 1990-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513049&dopt=Abstract
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DNA microarrays for comparison of gene expression profiles between diagnosis and relapse in precursor-B acute lymphoblastic leukemia: choice of technique and purification influence the identification of potential diagnostic markers. Author(s): Staal FJ, van der Burg M, Wessels LF, Barendregt BH, Baert MR, van den Burg CM, van Huffel C, Langerak AW, van der Velden VH, Reinders MJ, van Dongen JJ. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1324-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835720&dopt=Abstract
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Donor leukocyte infusions in acute myelogenous leukemia. Author(s): Porter DL. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 June; 17(6): 1035-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764364&dopt=Abstract
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Dose reduction of coadministered 6-mercaptopurine decreases myelotoxicity following high-dose methotrexate in childhood leukemia. Author(s): Nygaard U, Schmiegelow K. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1344-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835723&dopt=Abstract
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Double jeopardy from a single translocation: deletions of the derivative chromosome 9 in chronic myeloid leukemia. Author(s): Huntly BJ, Bench A, Green AR. Source: Blood. 2003 August 15; 102(4): 1160-8. Epub 2003 May 01. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730117&dopt=Abstract
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Down syndrome and acute myeloid leukemia: the paradox of increased risk for leukemia and heightened sensitivity to chemotherapy. Author(s): Ravindranath Y. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 September 15; 21(18): 3385-7. Epub 2003 July 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885833&dopt=Abstract
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Downmodulation of ERK activity inhibits the proliferation and induces the apoptosis of primary acute myelogenous leukemia blasts. Author(s): Lunghi P, Tabilio A, Dall'Aglio PP, Ridolo E, Carlo-Stella C, Pelicci PG, Bonati A. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1783-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970778&dopt=Abstract
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Downregulation of c-Jun expression and cell cycle regulatory molecules in acute myeloid leukemia cells upon CD44 ligation. Author(s): Zada AA, Singh SM, Reddy VA, Elsasser A, Meisel A, Haferlach T, Tenen DG, Hiddemann W, Behre G. Source: Oncogene. 2003 April 17; 22(15): 2296-308. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12700665&dopt=Abstract
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Doxycycline induces apoptosis by way of caspase-3 activation with inhibition of matrix metalloproteinase in human T-lymphoblastic leukemia CCRF-CEM cells. Author(s): Iwasaki H, Inoue H, Mitsuke Y, Badran A, Ikegaya S, Ueda T. Source: The Journal of Laboratory and Clinical Medicine. 2002 December; 140(6): 382-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12486404&dopt=Abstract
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Durable remissions of myelodysplastic syndrome and acute myeloid leukemia after reduced-intensity allografting. Author(s): Taussig DC, Davies AJ, Cavenagh JD, Oakervee H, Syndercombe-Court D, Kelsey S, Amess JA, Rohatiner AZ, Lister TA, Barnett MJ. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3060-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915594&dopt=Abstract
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Dysplasia and high proliferation rate are common in acute myeloid leukemia with inv(16)(p13q22). Author(s): Sun X, Medeiros LJ, Lu D, Rassidakis GZ, Bueso-Ramos C. Source: American Journal of Clinical Pathology. 2003 August; 120(2): 236-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12931554&dopt=Abstract
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Economic evaluation of recombinant human granulocyte colony-stimulating factor in very high-risk childhood acute lymphoblastic leukemia. Author(s): Delorme J, Badin S, Le Corroller AG, Auvrignon AA, Auclerc MF, Gandemer V, Bordigoni P, Lamagnere JP, Demeocq F, Perel Y, Berthou C, Bauduer F, Pautard B, Vannier JP, Braguer D, Leblanc T, Leverger G, Baruchel A, Michel G. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 June; 25(6): 441-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794521&dopt=Abstract
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Effect of priming with granulocyte colony-stimulating factor on the outcome of chemotherapy for acute myeloid leukemia. Author(s): Lowenberg B, van Putten W, Theobald M, Gmur J, Verdonck L, Sonneveld P, Fey M, Schouten H, de Greef G, Ferrant A, Kovacsovics T, Gratwohl A, Daenen S, Huijgens P, Boogaerts M; Dutch-Belgian Hemato-Oncology Cooperative Group; Swiss Group for Clinical Cancer Research. Source: The New England Journal of Medicine. 2003 August 21; 349(8): 743-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930926&dopt=Abstract
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Effects of 9-beta-D-arabinofuranosylguanine on mitochondria in CEM T-lymphoblast leukemia cells. Author(s): Curbo S, Zhivotovsky B, Johansson M, Karlsson A. Source: Biochemical and Biophysical Research Communications. 2003 August 8; 307(4): 942-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12878202&dopt=Abstract
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Effects of age on prognosis with imatinib mesylate therapy for patients with Philadelphia chromosome-positive chronic myelogenous leukemia. Author(s): Cortes J, Talpaz M, O'Brien S, Giles F, Beth Rios M, Shan J, Faderl S, GarciaManero G, Ferrajoli A, Wierda W, Kantarjian H. Source: Cancer. 2003 September 15; 98(6): 1105-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973833&dopt=Abstract
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Effects of angiogenic regulators on in vitro proliferation and cytokine secretion by native human acute myelogenous leukemia blasts. Author(s): Bruserud O, Glenjen N, Ryningen A. Source: European Journal of Haematology. 2003 July; 71(1): 9-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801293&dopt=Abstract
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Effects of TNFalpha on the growth and sensitivity to cytosine arabinoside of blast progenitors in acute myelogenous leukemia with special reference to the role of NFkappaB. Author(s): Wu Z, Shen L, Inatomi Y, U M, Miyashita T, Toyama K, Miyauchi J. Source: Leukemia Research. 2003 November; 27(11): 1009-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12859994&dopt=Abstract
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Efficacy and safety of imatinib mesylate (Glivec) in combination with interferonalpha (IFN-alpha) in Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL). Author(s): Wassmann B, Scheuring U, Pfeifer H, Binckebanck A, Kabisch A, Lubbert M, Leimer L, Gschaidmeier H, Hoelzer D, Ottmann OG. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 1919-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513038&dopt=Abstract
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Efficacy and toxicity of low-dose melphalan in myelodysplastic syndromes and acute myeloid leukemia with multilineage dysplasia. Author(s): Robak T, Szmigielska-Kaplon A, Urbanska-Rys H, Chojnowski K, WrzesienKus A. Source: Neoplasma. 2003; 50(3): 172-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937849&dopt=Abstract
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ELL and EAF1 are Cajal body components that are disrupted in MLL-ELL leukemia. Author(s): Polak PE, Simone F, Kaberlein JJ, Luo RT, Thirman MJ. Source: Molecular Biology of the Cell. 2003 April; 14(4): 1517-28. Erratum In: Mol Biol Cell.2003 May; 14(5): Following Table of Contents. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686606&dopt=Abstract
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Elucidation of the mechanisms of hairy-cell localization in tissues and the process of the bone marrow fibrosis in hairy-cell leukemia. Author(s): Aziz KA. Source: Saudi Med J. 2003 July; 24(7): 715-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12883600&dopt=Abstract
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Emergence of Ph negative clones in chronic myeloid leukemia (CML) patients in complete cytogenetic remission after therapy with imatinib mesylate (STI). Author(s): Gozzetti A, Tozzuoli D, Crupi R, Gentili S, Bocchia M, Raspadori D, Lauria F. Source: European Journal of Haematology. 2003 October; 71(4): 313-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950245&dopt=Abstract
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Environmental factors contributing to the development of childhood leukemia in children with Down's syndrome. Author(s): Mejia-Arangure JM, Fajardo-Gutierrez A, Flores-Aguilar H, Martinez-Garcia MC, Salamanca-Gomez F, Palma-Padilla V, Paredes-Aguilera R, Bernaldez-Rios R, Ortiz-Fernandez A, Martinez-Avalos A, Gorodezky C. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1905-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970794&dopt=Abstract
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Eosinophilic colitis in a patient with acute myeloid leukemia after allogeneic bone marrow transplantation. Author(s): Ashida T, Shimada T, Kawanishi K, Miyatake J, Kanamaru A. Source: International Journal of Hematology. 2003 July; 78(1): 76-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894856&dopt=Abstract
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Epstein-Barr virus in concomitant gastric carcinoma and adult T-cell leukemia/lymphoma. Author(s): Daibata M, Nemoto Y, Takemoto S, Miyoshi I, Taguchi H. Source: The American Journal of Medicine. 2003 April 15; 114(6): 509-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727587&dopt=Abstract
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Eradication of Cryptosporidium in four children with acute lymphoblastic leukemia. Author(s): Trad O, Jumaa P, Uduman S, Nawaz A. Source: Journal of Tropical Pediatrics. 2003 April; 49(2): 128-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12729299&dopt=Abstract
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Erythematous facial plaques in a patient with leukemia. Neutrophilic eccrine hidradenitis. Author(s): Crawford GH, Chu AY, Halpern M, James WD. Source: Archives of Dermatology. 2003 April; 139(4): 531-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707104&dopt=Abstract
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Erythropoietin and chronic lymphocytic leukemia. Author(s): Mauro FR, Gentile M, Foa R. Source: Reviews in Clinical and Experimental Hematology. 2002; Suppl 1: 21-31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735212&dopt=Abstract
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Esophageal erosion as a possible bacterial entry site in an acute lymphoblastic leukemia patient with sepsis. Author(s): Ikegaya S, Yoshida A, Iwasaki H, Naiki H, Ueda T. Source: International Journal of Hematology. 2003 May; 77(4): 395-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774931&dopt=Abstract
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Establishment and characterization of new B-cell precursor leukemia cell line NALM35. Author(s): Matsuo Y, Drexler HG, Harashima A, Fujii N, Ishimaru F, Orita K. Source: Hum Cell. 2002 December; 15(4): 215-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12889857&dopt=Abstract
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Evaluating the volume ratio of bone marrow affected by fibrosis: a parameter crucial for the prognostic significance of marrow fibrosis in chronic myeloid leukemia. Author(s): Buesche G, Georgii A, Duensing A, Schmeil A, Schlue J, Kreipe HH. Source: Human Pathology. 2003 April; 34(4): 391-401. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733122&dopt=Abstract
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Evaluation of patient age as a risk assigment parameter in high risk acute lymphocytic leukemia. Author(s): Winchester L, Acevedo S, Guiven A, Pabon M, Montalvo F. Source: Bol Asoc Med P R. 2003 January-February; 95(1): 26-8, 33-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898748&dopt=Abstract
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Evidence for whole chromosome 6 loss and duplication of the remaining chromosome in acute lymphoblastic leukemia. Author(s): McEvoy CR, Morley AA, Firgaira FA. Source: Genes, Chromosomes & Cancer. 2003 July; 37(3): 321-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759931&dopt=Abstract
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Evidence of a graft-versus-leukemia effect in chronic lymphocytic leukemia after reduced-intensity conditioning and allogeneic stem-cell transplantation: the Cooperative German Transplant Study Group. Author(s): Schetelig J, Thiede C, Bornhauser M, Schwerdtfeger R, Kiehl M, Beyer J, Sayer HG, Kroger N, Hensel M, Scheffold C, Held TK, Hoffken K, Ho AD, Kienast J, Neubauer A, Zander AR, Fauser AA, Ehninger G, Siegert W; Cooperative German Transplant Study Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 15; 21(14): 2747-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860954&dopt=Abstract
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Evidence-based care for the neutropenic patient with leukemia. Author(s): Shelton BK. Source: Semin Oncol Nurs. 2003 May; 19(2): 133-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830737&dopt=Abstract
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Ex vivo purging of leukemia cells using tumor-necrosis-factor-related apoptosisinducing ligand in hematopoietic stem cell transplantation. Author(s): Lee NS, Cheong HJ, Kim SJ, Kim SE, Kim CK, Lee KT, Park SK, Baick SH, Hong DS, Park HS, Won JH. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1375-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835727&dopt=Abstract
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Expansion of CMV-specific CD8+CD45RA+CD27- T cells in B-cell chronic lymphocytic leukemia. Author(s): Mackus WJ, Frakking FN, Grummels A, Gamadia LE, De Bree GJ, Hamann D, Van Lier RA, Van Oers MH. Source: Blood. 2003 August 1; 102(3): 1057-63. Epub 2003 April 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12689926&dopt=Abstract
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Expansion of natural killer (NK) and natural killer-like T (NKT)-cell populations derived from patients with B-chronic lymphocytic leukemia (B-CLL): a potential source for cellular immunotherapy. Author(s): Guven H, Gilljam M, Chambers BJ, Ljunggren HG, Christensson B, Kimby E, Dilber MS. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 1973-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513047&dopt=Abstract
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Expression analysis of alpha-NAC and ANX2 in juvenile myelomonocytic leukemia using SMART polymerase chain reaction and “virtual Northern” hybridization. Author(s): Hammerle K, Shayan P, Niemeyer CM, Flotho C. Source: Cancer Genetics and Cytogenetics. 2003 April 15; 142(2): 149-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699894&dopt=Abstract
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Expression and functional reconstitution of IL-18 receptor in K562 leukemia cells. Author(s): Zhang B, Cao ZY, Wu KF, Lin YM. Source: Leukemia Research. 2003 October; 27(10): 971-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860020&dopt=Abstract
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Expression of bone morphogenetic proteins in acute promyelocytic leukemia before and after combined all trans-retinoic acid and cytotoxic treatment. Author(s): Grcevic D, Marusic A, Grahovac B, Jaksic B, Kusec R. Source: Leukemia Research. 2003 August; 27(8): 731-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801531&dopt=Abstract
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Expression of Fcgamma receptors type II (FcgammaRII) in chronic lymphocytic leukemia B cells. Author(s): Gamberale R, Geffner JR, Sanjurjo J, Fernandez-Calotti PX, Arrosagaray G, Sanchez Avalos J, Giordano M. Source: Blood. 2003 October 1; 102(7): 2698-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14504071&dopt=Abstract
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Expression of functional markers in acute lymphoblastic leukemia. Author(s): Oh EJ, Kahng J, Kim Y, Kim M, Lim J, Kang CS, Min WS, Cho B, Lee A, Lee KY, Kim WI, Shim SI, Han K. Source: Leukemia Research. 2003 October; 27(10): 903-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860010&dopt=Abstract
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Expression of IL-18 and its receptor in human leukemia cells. Author(s): Zhang B, Ma XT, Zheng GG, Li G, Rao Q, Wu KF. Source: Leukemia Research. 2003 September; 27(9): 813-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804640&dopt=Abstract
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Expression of LL-37/hCAP-18 gene in human leukemia cells. Author(s): Yang YH, Zheng GG, Li G, Zhang B, Song YH, Wu KF. Source: Leukemia Research. 2003 October; 27(10): 947-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860015&dopt=Abstract
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Expression of the antiapoptotic gene survivin in chronic myeloid leukemia. Author(s): Badran A, Yoshida A, Wano Y, Imamura S, Kawai Y, Tsutani H, Inuzuka M, Ueda T. Source: Anticancer Res. 2003 January-February; 23(1B): 589-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680151&dopt=Abstract
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Expression of the hemoglobin scavenger receptor (CD163/HbSR) as immunophenotypic marker of monocytic lineage in acute myeloid leukemia. Author(s): Walter RB, Bachli EB, Schaer DJ, Ruegg R, Schoedon G. Source: Blood. 2003 May 1; 101(9): 3755-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707228&dopt=Abstract
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Extended follow-up of long-term survivors of childhood acute lymphoblastic leukemia. Author(s): Pui CH, Cheng C, Leung W, Rai SN, Rivera GK, Sandlund JT, Ribeiro RC, Relling MV, Kun LE, Evans WE, Hudson MM. Source: The New England Journal of Medicine. 2003 August 14; 349(7): 640-9. Erratum In: N Engl J Med. 2003 September 25; 349(13): 1299. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917300&dopt=Abstract
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Extramedullary relapse in the pleura in acute promyelocytic leukemia. Author(s): Disel U, Yavuz S, Paydas S, Sahin B, Zeren H. Source: Leukemia & Lymphoma. 2003 January; 44(1): 189-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12691162&dopt=Abstract
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False leukemia-lymphoma cell lines: an update on over 500 cell lines. Author(s): Drexler HG, Dirks WG, Matsuo Y, MacLeod RA. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 February; 17(2): 416-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592342&dopt=Abstract
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Family history of autoimmune thyroid disease and childhood acute leukemia. Author(s): Perillat-Menegaux F, Clavel J, Auclerc MF, Baruchel A, Leverger G, Nelken B, Philippe N, Sommelet D, Vilmer E, Hemon D. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2003 January; 12(1): 60-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540505&dopt=Abstract
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Fatal Bacillus cereus sepsis following resolving neutropenic enterocolitis during the treatment of acute leukemia. Author(s): Ginsburg AS, Salazar LG, True LD, Disis ML. Source: American Journal of Hematology. 2003 March; 72(3): 204-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12605393&dopt=Abstract
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Fatal Pasteurella sepsis and hairy-cell leukemia. Author(s): Athar MK, Karim MS, Mannam S, Ahmed M. Source: American Journal of Hematology. 2003 April; 72(4): 285. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666145&dopt=Abstract
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FDA halts 27 gene therapy trials after illness: leukemia-like cases in 2 children in France prompt the action. Author(s): Pollack A. Source: Ny Times (Print). 2003 January 15; : A1, A17. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12647754&dopt=Abstract
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Fetal and neonatal leukemia. Author(s): Isaacs H Jr. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 May; 25(5): 348-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759620&dopt=Abstract
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Fever and respiratory distress in an 8-year-old boy receiving therapy for acute lymphoblastic leukemia. Author(s): Weitzman S, Manson D, Wilson G, Allen U. Source: The Journal of Pediatrics. 2003 June; 142(6): 714-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12838203&dopt=Abstract
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FGF-2 expression and its action in human leukemia and lymphoma cell lines. Author(s): Krejci P, Faitova J, Laurell H, Hampl A, Dvorak P. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 April; 17(4): 818-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12682649&dopt=Abstract
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Fingertip cellulitis after fingerstick for capillary microhematocrit measurement in a patient with chronic lymphocytic leukemia: an uncommom infectious complication. Author(s): Arellano-Rodrigo E, Rovira M, Cibeira MT, Abello D, Montserrat E. Source: Haematologica. 2002 December; 87(12): Ecr39. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495910&dopt=Abstract
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FISH, CGH, and SKY in the diagnosis of childhood acute lymphoblastic leukemia. Author(s): Mathew S, Raimondi SC. Source: Methods in Molecular Biology (Clifton, N.J.). 2003; 220: 213-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744216&dopt=Abstract
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FLAG-IDA in the treatment of refractory/relapsed acute myeloid leukemia: singlecenter experience. Author(s): Pastore D, Specchia G, Carluccio P, Liso A, Mestice A, Rizzi R, Greco G, Buquicchio C, Liso V. Source: Annals of Hematology. 2003 April; 82(4): 231-5. Epub 2003 March 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707726&dopt=Abstract
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Flow cytometric analysis of aneuploidy and S-phase fraction in chronic myeloid leukemia patients: role in early detection of accelerated phase. Author(s): Tripathi AK, Chaturvedi R, Ahmad R, Asim M, Sawlani KK, Singh MK, Tripathi P, Tekwani BL. Source: Leukemia Research. 2003 October; 27(10): 899-902. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860009&dopt=Abstract
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Flow cytometric immunophenotyping of acute lymphoblastic leukemia: is the time ready for consensus the guidelines? Author(s): Basso G, Lanza F, Orfao A, Bene M, Borowitz M, Campana D, Lacombe F, Ludwig WD, Porwitt-MacDonald A, Rothe G, Dworzac M; ALL Working Group. Source: J Biol Regul Homeost Agents. 2002 October-December; 16(4): 257-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12597641&dopt=Abstract
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FLT3 inhibition as tailored therapy for acute myeloid leukemia. Author(s): Martinelli G, Piccaluga PP, Lo Coco F. Source: Haematologica. 2003 January; 88(1): 4-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12551818&dopt=Abstract
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FLT3 internal tandem duplication in 234 children with acute myeloid leukemia: prognostic significance and relation to cellular drug resistance. Author(s): Zwaan CM, Meshinchi S, Radich JP, Veerman AJ, Huismans DR, Munske L, Podleschny M, Hahlen K, Pieters R, Zimmermann M, Reinhardt D, Harbott J, Creutzig U, Kaspers GJ, Griesinger F. Source: Blood. 2003 October 1; 102(7): 2387-94. Epub 2003 June 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816873&dopt=Abstract
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FLT3 mutations do not influence MDR-1 gene expression in acute myeloid leukemia. Author(s): Galimberti S, Rossi A, Palumbo GA, Morabito F, Guerrini F, Vincelli I, Fazzi R, Santini V, Petrini M. Source: Anticancer Res. 2003 July-August; 23(4): 3419-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926083&dopt=Abstract
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FLT3: ITDoes matter in leukemia. Author(s): Levis M, Small D. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1738-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970773&dopt=Abstract
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FLT3-TKD mutation in childhood acute myeloid leukemia. Author(s): Liang DC, Shih LY, Hung IJ, Yang CP, Chen SH, Jaing TH, Liu HC, Wang LY, Chang WH. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 May; 17(5): 883-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750701&dopt=Abstract
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Fludarabine plus cyclophosphamide for the treatment of advanced chronic lymphocytic leukemia. Author(s): Schiavone EM, De Simone M, Palmieri S, Annunziata M, Pocali B, Copia C, D'Amico MR, Vecchio LD, Ferrara F. Source: European Journal of Haematology. 2003 July; 71(1): 23-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801295&dopt=Abstract
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Fludarabine plus rituximab for untreated B-cell chronic lymphocytic leukemia. Author(s): Castagna L, Sarina B, Santoro A. Source: Blood. 2003 September 15; 102(6): 2309; Author Reply 2309-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12959942&dopt=Abstract
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Fludarabine-induced apoptosis of B chronic lymphocytic leukemia cells includes early cleavage of p27kip1 by caspases. Author(s): Sanhes L, Tang R, Delmer A, DeCaprio JA, Ajchenbaum-Cymbalista F. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 June; 17(6): 1104-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764376&dopt=Abstract
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Fludarabine-related myeloid leukemia. Author(s): Astrow AB. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 October 1; 21(19): 3709; Author Reply 3709-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512411&dopt=Abstract
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Fluorescence in situ hybridization analysis of aneuploidization patterns in monoclonal gammopathy of undetermined significance versus multiple myeloma and plasma cell leukemia. Author(s): Rasillo A, Tabernero MD, Sanchez ML, Perez de Andres M, Martin Ayuso M, Hernandez J, Moro MJ, Fernandez-Calvo J, Sayagues JM, Bortoluci A, San Miguel JF, Orfao A. Source: Cancer. 2003 February 1; 97(3): 601-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548602&dopt=Abstract
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Fluorescence in situ hybridization detection of AML-1/ETO rearrangement in a case of acute myelogenous leukemia with complicated cytogenetic abnormalities. Author(s): Obama K, Tara M, Niina K. Source: International Journal of Hematology. 2003 January; 77(1): 91-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12568306&dopt=Abstract
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Follow-up of minimal residual disease in acute childhood lymphoblastic leukemia by WT1 gene expression in the peripheral blood: the Hungarian experience. Author(s): Magyarosy E, Varga N, Timar J, Raso E. Source: Pediatric Hematology and Oncology. 2003 January-February; 20(1): 65-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687755&dopt=Abstract
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Frameshift mutations in caspase-5 and other target genes in leukemia and lymphoma cell lines having microsatellite instability. Author(s): Takeuchi S, Takeuchi N, Fermin AC, Taguchi H, Koeffler HP. Source: Leukemia Research. 2003 April; 27(4): 359-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531228&dopt=Abstract
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Free radical stress in chronic lymphocytic leukemia cells and its role in cellular sensitivity to ROS-generating anticancer agents. Author(s): Zhou Y, Hileman EO, Plunkett W, Keating MJ, Huang P. Source: Blood. 2003 May 15; 101(10): 4098-104. Epub 2003 January 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531810&dopt=Abstract
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Frequencies of the major subgroups of precursor B-cell acute lymphoblastic leukemia in Indian children differ from the West. Author(s): Siraj AK, Kamat S, Gutierrez MI, Banavali S, Timpson G, Sazawal S, Bhargava M, Advani S, Adde M, Magrath I, Bhatia K. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 June; 17(6): 1192-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764391&dopt=Abstract
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Frequency of ETV6/AML1 fusion in adult acute lymphoblastic leukemia. Author(s): Cuneo A, Agostini P, Vitale A, Foa R, Castoldi G. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 February; 17(2): 476-7; Author Reply 477. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592356&dopt=Abstract
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Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia. Author(s): Hughes TP, Kaeda J, Branford S, Rudzki Z, Hochhaus A, Hensley ML, Gathmann I, Bolton AE, van Hoomissen IC, Goldman JM, Radich JP; International Randomised Study of Interferon versus STI571 (IRIS) Study Group. Source: The New England Journal of Medicine. 2003 October 9; 349(15): 1423-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14534335&dopt=Abstract
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Friend virus-induced erythroleukemias: a unique and well-defined mouse model for the development of leukemia. Author(s): Lee CR, Cervi D, Truong AH, Li YJ, Sarkar A, Ben-David Y. Source: Anticancer Res. 2003 May-June; 23(3A): 2159-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894591&dopt=Abstract
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Function of the ABC transporters, P-glycoprotein, multidrug resistance protein and breast cancer resistance protein, in minimal residual disease in acute myeloid leukemia. Author(s): van der Pol MA, Broxterman HJ, Pater JM, Feller N, van der Maas M, Weijers GW, Scheffer GL, Allen JD, Scheper RJ, van Loevezijn A, Ossenkoppele GJ, Schuurhuis GJ. Source: Haematologica. 2003 February; 88(2): 134-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604403&dopt=Abstract
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Functional blocks in caspase activation pathways are common in leukemia and predict patient response to induction chemotherapy. Author(s): Schimmer AD, Pedersen IM, Kitada S, Eksioglu-Demiralp E, Minden MD, Pinto R, Mah K, Andreeff M, Kim Y, Suh WS, Reed JC. Source: Cancer Research. 2003 March 15; 63(6): 1242-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649183&dopt=Abstract
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Functional expression and release of ligands for the activating immunoreceptor NKG2D in leukemia. Author(s): Salih HR, Antropius H, Gieseke F, Lutz SZ, Kanz L, Rammensee HG, Steinle A. Source: Blood. 2003 August 15; 102(4): 1389-96. Epub 2003 April 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714493&dopt=Abstract
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Functional FAS promoter polymorphisms are associated with increased risk of acute myeloid leukemia. Author(s): Sibley K, Rollinson S, Allan JM, Smith AG, Law GR, Roddam PL, Skibola CF, Smith MT, Morgan GJ. Source: Cancer Research. 2003 August 1; 63(15): 4327-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907599&dopt=Abstract
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Fusion of an AF4-related gene, LAF4, to MLL in childhood acute lymphoblastic leukemia with t(2;11)(q11;q23). Author(s): Hiwatari M, Taki T, Taketani T, Taniwaki M, Sugita K, Okuya M, Eguchi M, Ida K, Hayashi Y. Source: Oncogene. 2003 May 8; 22(18): 2851-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743608&dopt=Abstract
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Galpha 12 activates Rho GTPase through tyrosine-phosphorylated leukemiaassociated RhoGEF. Author(s): Suzuki N, Nakamura S, Mano H, Kozasa T. Source: Proceedings of the National Academy of Sciences of the United States of America. 2003 January 21; 100(2): 733-8. Epub 2003 Jan 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515866&dopt=Abstract
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Gastric mucosa-associated lymphoid tissue lymphoma with adult T cell leukemia/lymphoma cell infiltration. case report. Author(s): Oda S, Ochiai T, Yasuda O, Harada N, Muta K, Okada N, Yao T, Takata M, Chijiiwa Y, Nawata H. Source: The American Journal of Gastroenterology. 2003 February; 98(2): 491-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12591074&dopt=Abstract
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GATA1 mutations in transient leukemia and acute megakaryoblastic leukemia of Down syndrome. Author(s): Hitzler JK, Cheung J, Li Y, Scherer SW, Zipursky A. Source: Blood. 2003 June 1; 101(11): 4301-4. Epub 2003 February 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12586620&dopt=Abstract
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G-CSF-primed haploidentical marrow transplantation without ex vivo T cell depletion: an excellent alternative for high-risk leukemia. Author(s): Ji SQ, Chen HR, Wang HX, Yan HM, Zhu L, Liu J, Xue M, Xun CQ. Source: Bone Marrow Transplantation. 2002 December; 30(12): 861-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12476277&dopt=Abstract
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Gemtuzumab ozogamicin in pediatric CD33-positive acute lymphoblastic leukemia: first clinical experiences and relation with cellular sensitivity to single agent calicheamicin. Author(s): Zwaan CM, Reinhardt D, Jurgens H, Huismans DR, Hahlen K, Smith OP, Biondi A, van Wering ER, Feingold J, Kaspers GJ. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 February; 17(2): 468-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592351&dopt=Abstract
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Gemtuzumab ozogamicin, fludarabine, cytarabine and cyclosporine combination regimen in patients with CD33+ primary resistant or relapsed acute myeloid leukemia. Author(s): Tsimberidou A, Cortes J, Thomas D, Garcia-Manero G, Verstovsek S, Faderl S, Albitar M, Kantarjian H, Estey E, Giles FJ. Source: Leukemia Research. 2003 October; 27(10): 893-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860008&dopt=Abstract
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Gemtuzumab ozogamicin: first clinical experiences in children with relapsed/refractory acute myeloid leukemia treated on compassionate-use basis. Author(s): Zwaan CM, Reinhardt D, Corbacioglu S, van Wering ER, Bokkerink JP, Tissing WJ, Samuelsson U, Feingold J, Creutzig U, Kaspers GJ. Source: Blood. 2003 May 15; 101(10): 3868-71. Epub 2003 January 23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12543868&dopt=Abstract
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Gemtuzumab ozogamicin: promise and challenge in patients with acute myeloid leukemia. Author(s): Giles FJ. Source: Expert Rev Anticancer Ther. 2002 December; 2(6): 630-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12503209&dopt=Abstract
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Gemtuzumab, fludarabine, cytarabine, and cyclosporine in patients with newly diagnosed acute myelogenous leukemia or high-risk myelodysplastic syndromes. Author(s): Tsimberidou A, Estey E, Cortes J, Thomas D, Faderl S, Verstovsek S, GarciaManero G, Keating M, Albitar M, O'Brien S, Kantarjian H, Giles F. Source: Cancer. 2003 March 15; 97(6): 1481-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12627513&dopt=Abstract
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Gene therapy. Second child in French trial is found to have leukemia. Author(s): Marshall E. Source: Science. 2003 January 17; 299(5605): 320. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531981&dopt=Abstract
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Gene transfer for generation of tumor and leukemia vaccines. Author(s): Dilloo D, Zibert A. Source: Methods in Molecular Biology (Clifton, N.J.). 2003; 215: 261-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12512305&dopt=Abstract
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Generation of immunostimulatory dendritic cells from the malignant clone in patients with juvenile myelomonocytic leukemia. Author(s): Nabarro S, Thrasher AJ, Kempski H, Amrolia P, Anderson J. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1910-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970796&dopt=Abstract
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Generation of leukemic dendritic cells from patients with acute myeloid leukemia. Author(s): Mohty M, Gaugler B, Olive D. Source: Methods in Molecular Biology (Clifton, N.J.). 2003; 215: 463-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12512320&dopt=Abstract
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Generation of the NUP98-TOP1 fusion transcript by the t(11;20) (p15;q11) in a case of acute monocytic leukemia. Author(s): Chen S, Xue Y, Chen Z, Guo Y, Wu Y, Pan J. Source: Cancer Genetics and Cytogenetics. 2003 January 15; 140(2): 153-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645654&dopt=Abstract
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Genetic reversion in an acute myelogenous leukemia cell line from a Fanconi anemia patient with biallelic mutations in BRCA2. Author(s): Ikeda H, Matsushita M, Waisfisz Q, Kinoshita A, Oostra AB, Nieuwint AW, De Winter JP, Hoatlin ME, Kawai Y, Sasaki MS, D'Andrea AD, Kawakami Y, Joenje H. Source: Cancer Research. 2003 May 15; 63(10): 2688-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750298&dopt=Abstract
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Genome-wide analysis of acute myeloid leukemia with normal karyotype reveals a unique pattern of homeobox gene expression distinct from those with translocationmediated fusion events. Author(s): Debernardi S, Lillington DM, Chaplin T, Tomlinson S, Amess J, Rohatiner A, Lister TA, Young BD. Source: Genes, Chromosomes & Cancer. 2003 June; 37(2): 149-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12696063&dopt=Abstract
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Genomic anatomy of the specific reciprocal translocation t(15;17) in acute promyelocytic leukemia. Author(s): Reiter A, Saussele S, Grimwade D, Wiemels JL, Segal MR, Lafage-Pochitaloff M, Walz C, Weisser A, Hochhaus A, Willer A, Reichert A, Buchner T, Lengfelder E, Hehlmann R, Cross NC. Source: Genes, Chromosomes & Cancer. 2003 February; 36(2): 175-88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508246&dopt=Abstract
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Genomic deletions on other chromosomes involved in variant t(9;22) chronic myeloid leukemia cases. Author(s): Albano F, Specchia G, Anelli L, Zagaria A, Storlazzi CT, Buquicchio C, Roberti MG, Liso V, Rocchi M. Source: Genes, Chromosomes & Cancer. 2003 April; 36(4): 353-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12619159&dopt=Abstract
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Genomic p16 abnormalities in the progression of chronic myeloid leukemia into blast crisis: a sequential study in 42 patients. Author(s): Hernandez-Boluda JC, Cervantes F, Colomer D, Vela MC, Costa D, Paz MF, Esteller M, Montserrat E. Source: Experimental Hematology. 2003 March; 31(3): 204-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12644017&dopt=Abstract
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Genotypes of the glutathione S-transferase superfamily do not correlate with outcome of childhood acute lymphoblastic leukemia. Author(s): Sala A, Lanciotti M, Valsecchi MG, di Michele P, Dufour C, Haupt R, Basso G, Rizzari C, Biondi A. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 May; 17(5): 981-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750715&dopt=Abstract
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Geographical correlation between ambient UVB level and mortality risk of leukemia in Japan. Author(s): Uehara M, Takahashi K, Hoshuyama T, Pan G, Feng Y. Source: Environmental Research. 2003 June; 92(2): 78-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854686&dopt=Abstract
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Global down-regulation of HOX gene expression in PML-RARalpha + acute promyelocytic leukemia identified by small-array real-time PCR. Author(s): Thompson A, Quinn MF, Grimwade D, O'Neill CM, Ahmed MR, Grimes S, McMullin MF, Cotter F, Lappin TR. Source: Blood. 2003 February 15; 101(4): 1558-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12560242&dopt=Abstract
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Granulocyte colony-stimulating factor receptor signaling defects from neutropenia to leukemia. Author(s): Corey SJ, Zhu QS. Source: Isr Med Assoc J. 2002 November; 4(11): 1032-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12489499&dopt=Abstract
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Granulocyte colony-stimulating factor reverses cytopenia and may permit cytogenetic responses in patients with chronic myeloid leukemia treated with imatinib mesylate. Author(s): Marin D, Marktel S, Foot N, Bua M, Goldman JM, Apperley JF. Source: Haematologica. 2003 February; 88(2): 227-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604417&dopt=Abstract
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Granulocyte-macrophage colony-stimulating factor (GM-CSF) induces antiapoptotic and proapoptotic signals in acute myeloid leukemia. Author(s): Faderl S, Harris D, Van Q, Kantarjian HM, Talpaz M, Estrov Z. Source: Blood. 2003 July 15; 102(2): 630-7. Epub 2003 March 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663443&dopt=Abstract
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Granzyme A mediates glucocorticoid-induced apoptosis in leukemia cells. Author(s): Yamada M, Hirasawa A, Shiojima S, Tsujimoto G. Source: The Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology. 2003 September; 17(12): 1712-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12958185&dopt=Abstract
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Gris1, a new common integration site in Graffi murine leukemia virus-induced leukemias: overexpression of a truncated cyclin D2 due to alternative splicing. Author(s): Denicourt C, Kozak CA, Rassart E. Source: Journal of Virology. 2003 January; 77(1): 37-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12477808&dopt=Abstract
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Growth suppression of pre-T acute lymphoblastic leukemia cells by inhibition of notch signaling. Author(s): Weng AP, Nam Y, Wolfe MS, Pear WS, Griffin JD, Blacklow SC, Aster JC. Source: Molecular and Cellular Biology. 2003 January; 23(2): 655-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12509463&dopt=Abstract
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Hairy cell leukemia and sarcoidosis: a case report and review of the literature. Author(s): Schiller G, Said J, Pal S. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 2057-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513061&dopt=Abstract
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Hairy cell leukemia: biology, clinical diagnosis, unusual manifestations and associated disorders. Author(s): Polliack A. Source: Reviews in Clinical and Experimental Hematology. 2002 December; 6(4): 366-88; Discussion 449-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823778&dopt=Abstract
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Height and weight in children treated for acute lymphoblastic leukemia: relationship to CNS treatment. Author(s): Dalton VK, Rue M, Silverman LB, Gelber RD, Asselin BL, Barr RD, Clavell LA, Hurwitz CA, Moghrabi A, Samson Y, Schorin M, Tarbell NJ, Sallan SE, Cohen LE. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 1; 21(15): 2953-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885815&dopt=Abstract
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Hematopoietic cell transplantation in the treatment of leukemia. Author(s): Devine H, DeMeyer E. Source: Semin Oncol Nurs. 2003 May; 19(2): 118-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830736&dopt=Abstract
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Hematopoietic growth factors and the future of therapeutic research on acute myeloid leukemia. Author(s): Schiffer CA. Source: The New England Journal of Medicine. 2003 August 21; 349(8): 727-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930923&dopt=Abstract
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Hepatocellular carcinoma of a short malignant transformation time in a patient with acute myeloblastic leukemia. Author(s): Mabed M, Aref S, Aladle DA. Source: Annals of Hematology. 2003 May; 82(5): 318-20. Epub 2003 April 23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709828&dopt=Abstract
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Hepatosplenic microabscesses in pediatric leukemia: a report of five cases. Author(s): Lin PC, Chang TT, Jang RC, Chiou SS. Source: Kaohsiung J Med Sci. 2003 July; 19(7): 368-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926524&dopt=Abstract
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Heterogeneity of the 7q36 breakpoints in the t(7;12) involving ETV6 in infant leukemia. Author(s): Tosi S, Hughes J, Scherer SW, Nakabayashi K, Harbott J, Haas OA, Cazzaniga G, Biondi A, Kempski H, Kearney L. Source: Genes, Chromosomes & Cancer. 2003 October; 38(2): 191-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939747&dopt=Abstract
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High frequency of p53 dysfunction and low level of VH mutation in chronic lymphocytic leukemia patients using the VH3-21 gene segment. Author(s): Lin K, Manocha S, Harris RJ, Matrai Z, Sherrington PD, Pettitt AR. Source: Blood. 2003 August 1; 102(3): 1145-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869492&dopt=Abstract
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High frequency of pro-B acute lymphoblastic leukemia in adults with secondary leukemia with 11q23 abnormalities. Author(s): Ishizawa S, Slovak ML, Popplewell L, Bedell V, Wrede JE, Carter NH, Snyder DS, Arber DA. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 June; 17(6): 1091-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764373&dopt=Abstract
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High prevalence of an IgG response against murine leukemia virus (MLV) in patients with psoriasis. Author(s): Moles JP, Hadi JC, Guilhou JJ. Source: Virus Research. 2003 August; 94(2): 97-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902038&dopt=Abstract
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High simian T-cell leukemia virus type 1 proviral loads combined with genetic stability as a result of cell-associated provirus replication in naturally infected, asymptomatic monkeys. Author(s): Gabet AS, Gessain A, Wattel E. Source: International Journal of Cancer. Journal International Du Cancer. 2003 October 20; 107(1): 74-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925959&dopt=Abstract
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High-penetrance mouse model of acute promyelocytic leukemia with very low levels of PML-RARalpha expression. Author(s): Westervelt P, Lane AA, Pollock JL, Oldfather K, Holt MS, Zimonjic DB, Popescu NC, DiPersio JF, Ley TJ. Source: Blood. 2003 September 1; 102(5): 1857-65. Epub 2003 May 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750176&dopt=Abstract
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High-resolution analysis of acquired genomic imbalances in bone marrow samples from chronic myeloid leukemia patients by use of multiple short DNA probes. Author(s): Reid AG, Tarpey PS, Nacheva EP. Source: Genes, Chromosomes & Cancer. 2003 July; 37(3): 282-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759926&dopt=Abstract
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Histone deacetylase inhibitor LAQ824 both lowers expression and promotes proteasomal degradation of Bcr-Abl and induces apoptosis of imatinib mesylatesensitive or -refractory chronic myelogenous leukemia-blast crisis cells. Author(s): Nimmanapalli R, Fuino L, Bali P, Gasparetto M, Glozak M, Tao J, Moscinski L, Smith C, Wu J, Jove R, Atadja P, Bhalla K. Source: Cancer Research. 2003 August 15; 63(16): 5126-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941844&dopt=Abstract
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Histone deacetylase inhibitors promote STI571-mediated apoptosis in STI571sensitive and -resistant Bcr/Abl+ human myeloid leukemia cells. Author(s): Yu C, Rahmani M, Almenara J, Subler M, Krystal G, Conrad D, Varticovski L, Dent P, Grant S. Source: Cancer Research. 2003 May 1; 63(9): 2118-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727828&dopt=Abstract
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HLA system affects the age-at-onset in chronic myeloid leukemia. Author(s): Oguz FS, Kalayoglu S, Diler AS, Tozkir H, Sargin D, Carin M, Dorak MT. Source: American Journal of Hematology. 2003 August; 73(4): 256-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879429&dopt=Abstract
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Hodgkin's type of Richter's syndrome in familial chronic lymphocytic leukemia treated with cladribine and cyclophosphamide. Author(s): Robak T, Szmigielska-Kaplon A, Smolewski P, Wawrzyniak E, Korycka A, Bartkowiak J, Kordek R. Source: Leukemia & Lymphoma. 2003 May; 44(5): 859-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802926&dopt=Abstract
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Homocysteine, pharmacogenetics, and neurotoxicity in children with leukemia. Author(s): Kishi S, Griener J, Cheng C, Das S, Cook EH, Pei D, Hudson M, Rubnitz J, Sandlund JT, Pui CH, Relling MV. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3084-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915598&dopt=Abstract
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Human cytotoxic T lymphocytes specific for Wilms' tumor antigen-1 inhibit engraftment of leukemia-initiating stem cells in non-obese diabetic-severe combined immunodeficient recipients. Author(s): Gao L, Xue SA, Hasserjian R, Cotter F, Kaeda J, Goldman JM, Dazzi F, Stauss HJ. Source: Transplantation. 2003 May 15; 75(9): 1429-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12792492&dopt=Abstract
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Human T cell leukemia virus type I-induced disease: pathways to cancer and neurodegeneration. Author(s): Barmak K, Harhaj E, Grant C, Alefantis T, Wigdahl B. Source: Virology. 2003 March 30; 308(1): 1-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706085&dopt=Abstract
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Human T-cell leukemia virus type 1 envelope glycoprotein gp46 interacts with cell surface heparan sulfate proteoglycans. Author(s): Pinon JD, Klasse PJ, Jassal SR, Welson S, Weber J, Brighty DW, Sattentau QJ. Source: Journal of Virology. 2003 September; 77(18): 9922-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941902&dopt=Abstract
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Human T-cell leukemia virus type 1 envelope-mediated syncytium formation can be activated in resistant Mammalian cell lines by a carboxy-terminal truncation of the envelope cytoplasmic domain. Author(s): Kim FJ, Manel N, Boublik Y, Battini JL, Sitbon M. Source: Journal of Virology. 2003 January; 77(2): 963-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12502812&dopt=Abstract
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Human T-cell leukemia virus type I and adult T-cell leukemia. Author(s): Matsuoka M. Source: Oncogene. 2003 August 11; 22(33): 5131-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910250&dopt=Abstract
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Hypermethylation of GpG islands in the promoter region of p15(INK4b) in acute promyelocytic leukemia represses p15(INK4b) expression and correlates with poor prognosis. Author(s): Teofili L, Martini M, Luongo M, Diverio D, Capelli G, Breccia M, Lo Coco F, Leone G, Larocca LM. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 May; 17(5): 919-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750706&dopt=Abstract
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Hypermethylation of the spleen tyrosine kinase promoter in T-lineage acute lymphoblastic leukemia. Author(s): Goodman PA, Burkhardt N, Juran B, Tibbles HE, Uckun FM. Source: Oncogene. 2003 April 24; 22(16): 2504-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12717427&dopt=Abstract
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Hypocellular acute promyelocytic leukemia with a tetraploid clone characterized by two t(15;17). Author(s): Kojima K, Imaoka M, Noguchi T, Narumi H, Uchida N, Sakai I, Yasukawa M, Fujita S. Source: Cancer Genetics and Cytogenetics. 2003 September; 145(2): 169-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12935930&dopt=Abstract
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Hypodiploidy of 37 chromosomes in an adult patient with acute lymphoblastic leukemia. Author(s): Das PK, Sharma P, Koutts J, Smith A. Source: Cancer Genetics and Cytogenetics. 2003 September; 145(2): 176-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12935932&dopt=Abstract
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Identification and characterization of a PU.1/Spi-B binding site in the bovine leukemia virus long terminal repeat. Author(s): Dekoninck A, Calomme C, Nizet S, de Launoit Y, Burny A, Ghysdael J, Van Lint C. Source: Oncogene. 2003 May 15; 22(19): 2882-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771939&dopt=Abstract
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Identification of a critical basic residue on the ecotropic murine leukemia virus receptor. Author(s): Qian Z, Donald R, Wang H, Chen Q, Albritton LM. Source: Journal of Virology. 2003 August; 77(15): 8596-601. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857932&dopt=Abstract
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Identification of a novel fusion gene, TTL, fused to ETV6 in acute lymphoblastic leukemia with t(12;13)(p13;q14), and its implication in leukemogenesis. Author(s): Qiao Y, Ogawa S, Hangaishi A, Yuji K, Izutsu K, Kunisato A, Imai Y, Wang L, Hosoya N, Nannya Y, Sato Y, Maki K, Mitani K, Hirai H. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 June; 17(6): 1112-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764377&dopt=Abstract
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Images in clinical medicine. Hyperleukocytosis in acute myeloid leukemia. Author(s): Mauro MJ. Source: The New England Journal of Medicine. 2003 August 21; 349(8): 767. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930929&dopt=Abstract
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Imatinib mesylate (STI-571) reduces Bcr-Abl-mediated vascular endothelial growth factor secretion in chronic myelogenous leukemia. Author(s): Ebos JM, Tran J, Master Z, Dumont D, Melo JV, Buchdunger E, Kerbel RS. Source: Molecular Cancer Research : Mcr. 2002 December; 1(2): 89-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12496355&dopt=Abstract
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Imatinib mesylate elicits positive clinical response in atypical chronic myeloid leukemia involving the platelet-derived growth factor receptor beta. Author(s): Garcia JL, Font de Mora J, Hernandez JM, Queizan JA, Gutierrez NC, Hernandez JM, San Miguel JF. Source: Blood. 2003 October 1; 102(7): 2699-700. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14504072&dopt=Abstract
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Imatinib mesylate for chronic myeloid leukemia: what do we really know? Author(s): Husereau D. Source: Issues Emerg Health Technol. 2002 December; (42): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492100&dopt=Abstract
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Imatinib mesylate noncompliance simulating chronic myeloid leukemia resistance. Author(s): Sandoval C, Giamelli J, Jayabose S. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 June; 25(6): 507-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794534&dopt=Abstract
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Immunohistochemical detection of VEGF in the bone marrow of patients with acute myeloid leukemia. Correlation between VEGF expression and the FAB category. Author(s): Ghannadan M, Wimazal F, Simonitsch I, Sperr WR, Mayerhofer M, Sillaber C, Hauswirth AW, Gadner H, Chott A, Horny HP, Lechner K, Valent P. Source: American Journal of Clinical Pathology. 2003 May; 119(5): 663-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760284&dopt=Abstract
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Immunophenotypic analysis of various blastic crises in chronic myeloid leukemia: correlations between CD7 expression and response to chemotherapy. Author(s): Hirose Y, Masaki Y, Shimoyama K, Fukushima T, Kawabata H, Ogawa N, Wano Y, Sugai S. Source: International Journal of Hematology. 2003 May; 77(4): 420-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774936&dopt=Abstract
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Immunoprofiling of cell lines derived from natural killer-cell and natural killer-like T-cell leukemia-lymphoma. Author(s): Matsuo Y, Drexler HG. Source: Leukemia Research. 2003 October; 27(10): 935-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860014&dopt=Abstract
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Impact of bone marrow morphology on multivariate risk classification in chronic myelogenous leukemia. Author(s): Kvasnicka HM, Thiele J, Schmitt-Graeff A, Diehl V, Niederle N, Schaefer HE. Source: Acta Haematologica. 2003; 109(1): 53-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12486326&dopt=Abstract
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In vitro chemosensitivity testing of selected myeloid cells in acute myeloid leukemia. Author(s): Mollgard L, Prenkert M, Smolowicz A, Paul C, Tidefelt U. Source: Leukemia & Lymphoma. 2003 May; 44(5): 783-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802914&dopt=Abstract
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In vitro sensitivity of hematopoietic progenitors to tiazofurin in refractory acute myeloid leukemia and in the blast crisis of chronic myeloid leukemia. Author(s): Colovic M, Sefer D, Bogdanovic A, Suvajdzic N, Jankovic G, Atkinson HD, Milenkovic P. Source: Cancer Letters. 2003 June 10; 195(2): 153-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767523&dopt=Abstract
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Inactivation of p16 gene in leukemia. Author(s): Wenming C, Jiazhi Z, Shuzhen T, Bai X, Jingzhong L. Source: Chinese Medical Sciences Journal = Chung-Kuo I Hsueh K'o Hsueh Tsa Chih / Chinese Academy of Medical Sciences. 1999 December; 14(4): 206-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894892&dopt=Abstract
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Incidence and prognostic significance of C-MPL expression in acute myeloid leukemia. Author(s): Chelvatheebam S, Langabeer SE, Linch DC, Hills RK, Greenwell P. Source: Leukemia Research. 2003 September; 27(9): 869-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804647&dopt=Abstract
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Inclusion of Moloney murine leukemia virus elements upstream of the transgene cassette in an E1-deleted adenovirus leads to an unusual genomic integration in epithelial cells. Author(s): Zheng C, O'Connell BC, Baum BJ. Source: Virology. 2003 September 1; 313(2): 460-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12954213&dopt=Abstract
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Increased age at diagnosis has a significantly negative effect on outcome in children with Down syndrome and acute myeloid leukemia: a report from the Children's Cancer Group Study 2891. Author(s): Gamis AS, Woods WG, Alonzo TA, Buxton A, Lange B, Barnard DR, Gold S, Smith FO; Children's Cancer Group Study 2891. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 September 15; 21(18): 3415-22. Epub 2003 July 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885836&dopt=Abstract
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Induced dendritic cell differentiation of chronic myeloid leukemia blasts is associated with down-regulation of BCR-ABL. Author(s): Lindner I, Kharfan-Dabaja MA, Ayala E, Kolonias D, Carlson LM, BeazerBarclay Y, Scherf U, Hnatyszyn JH, Lee KP. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 August 15; 171(4): 1780-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902478&dopt=Abstract
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Insertion of chromosome 11 in chromosome 4 resulting in a 5'MLL-3'AF4 fusion gene in a case of adult acute lymphoblastic leukemia. Author(s): Morel F, Le Bris MJ, Douet-Guilbert N, Duchemin J, Herry A, Le Calvez G, Marion V, Berthou C, De Braekeleer M. Source: Cancer Genetics and Cytogenetics. 2003 August; 145(1): 74-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885467&dopt=Abstract
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Insertion of MLL sequences into chromosome band 5q31 results in an MLL-AF5Q31 fusion and is a rare but recurrent abnormality associated with infant leukemia. Author(s): Deveney R, Chervinsky DS, Jani-Sait SN, Grossi M, Aplan PD. Source: Genes, Chromosomes & Cancer. 2003 July; 37(3): 326-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759932&dopt=Abstract
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Internal tandem duplication and Asp835 mutations of the FMS-like tyrosine kinase 3 (FLT3) gene in acute promyelocytic leukemia. Author(s): Shih LY, Kuo MC, Liang DC, Huang CF, Lin TL, Wu JH, Wang PN, Dunn P, Lai CL. Source: Cancer. 2003 September 15; 98(6): 1206-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973844&dopt=Abstract
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Interphase cytogenetic analysis in Argentinean B-cell chronic lymphocytic leukemia patients: association of trisomy 12 and del(13q14). Author(s): Chena C, Arrossagaray G, Scolnik M, Palacios MF, Slavutsky I. Source: Cancer Genetics and Cytogenetics. 2003 October 15; 146(2): 154-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14553950&dopt=Abstract
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Investigation of TT virus in the etiology of pediatric acute lymphoblastic leukemia. Author(s): Shiramizu B, Yu Q, Hu N, Yanagihara R, Nerurkar VR. Source: Pediatric Hematology and Oncology. 2002 December; 19(8): 543-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12487829&dopt=Abstract
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Involvement of the matrix and nucleocapsid domains of the bovine leukemia virus Gag polyprotein precursor in viral RNA packaging. Author(s): Wang H, Norris KM, Mansky LM. Source: Journal of Virology. 2003 September; 77(17): 9431-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915558&dopt=Abstract
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Iris and anterior chamber involvement in acute lymphoblastic leukemia. Author(s): Patel SV, Herman DC, Anderson PM, Al-Zein NJ, Buettner H. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 August; 25(8): 653-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902923&dopt=Abstract
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Is B-lineage acute lymphoblastic leukemia with a mature phenotype and l1 morphology a precursor B-lymphoblastic leukemia/lymphoma or Burkitt leukemia/lymphoma? Author(s): Li S, Lew G. Source: Archives of Pathology & Laboratory Medicine. 2003 October; 127(10): 1340-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14521459&dopt=Abstract
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Is chronic lymphocytic leukemia one disease? Author(s): Hamblin T. Source: Haematologica. 2002 December; 87(12): 1235-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495893&dopt=Abstract
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Is chronic lymphocytic leukemia one disease? Author(s): Dighiero G. Source: Haematologica. 2002 December; 87(12): 1233-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495892&dopt=Abstract
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Jak3 expression and genomic sequence in pediatric acute lymphoblastic leukemia. Author(s): Wood CM, Goodman PA, Uckun FM. Source: Leukemia & Lymphoma. 2002 December; 43(12): 2355-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12613524&dopt=Abstract
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JunB gene expression is inactivated by methylation in chronic myeloid leukemia. Author(s): Yang MY, Liu TC, Chang JG, Lin PM, Lin SF. Source: Blood. 2003 April 15; 101(8): 3205-11. Epub 2002 December 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12506033&dopt=Abstract
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Juvenile myelomonocytic leukemia. Author(s): Niemeyer CM, Kratz C. Source: Curr Treat Options Oncol. 2003 June; 4(3): 203-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718797&dopt=Abstract
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Kinetics of hematopoiesis in bone marrow cultures from patients with chronic myeloid leukemia: effect of recombinant cytokines in dexter-type long-term cultures. Author(s): Luna-Bautista F, Sanchez-Valle E, Ayala-Sanchez M, Morales-Polanco M, Meillon-Garcia L, Benitez-Bribiesca L, Mayani H. Source: Hematology (Amsterdam, Netherlands). 2003 June; 8(3): 155-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745649&dopt=Abstract
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KRN5500: a novel therapeutic agent with in vitro activity against human B-cell chronic lymphocytic leukemia cells mediates cytotoxicity via the intrinsic pathway of apoptosis. Author(s): Byrd JC, Lucas DM, Mone AP, Kitner JB, Drabick JJ, Grever MR. Source: Blood. 2003 June 1; 101(11): 4547-50. Epub 2003 February 20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12595316&dopt=Abstract
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Lamivudine resistance in human T-cell leukemia virus type 1 may be due to a polymorphism at codon 118 (V-->I) of the reverse transcriptase. Author(s): Toro C, Rodes B, Mendoza C, Soriano V. Source: Antimicrobial Agents and Chemotherapy. 2003 May; 47(5): 1774; Author Reply 1774-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709359&dopt=Abstract
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Large diversity in transport-mediated methotrexate resistance in human leukemia cell line CCRF-CEM established in a high concentration of leucovorin. Author(s): Asai S, Miyachi H, Kobayashi H, Takemura Y, Ando Y. Source: Cancer Science. 2003 February; 94(2): 210-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12708499&dopt=Abstract
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Latency of viral expression in vivo is not related to CpG methylation in the U3 region and part of the R region of the long terminal repeat of bovine leukemia virus. Author(s): Tajima S, Tsukamoto M, Aida Y. Source: Journal of Virology. 2003 April; 77(7): 4423-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634400&dopt=Abstract
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Leukemia and lymphoma of natural killer lineage cells. Author(s): Oshimi K. Source: International Journal of Hematology. 2003 July; 78(1): 18-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894846&dopt=Abstract
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Leukemia and myelopathy: the persistent mystery of pathogenesis by HTLV-I/II. Author(s): Rosenblatt J, Harrington WJ Jr. Source: Cancer Investigation. 2003 April; 21(2): 323-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743997&dopt=Abstract
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Leukemia cutis (chronic lymphocytic leukemia-low grade B cell). Author(s): Schmults CA. Source: Dermatology Online Journal [electronic Resource]. 2002 October; 8(2): 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546769&dopt=Abstract
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Leukemia in severe congenital neutropenia: defective proteolysis suggests new pathways to malignancy and opportunities for therapy. Author(s): Horwitz M, Li FQ, Albani D, Duan Z, Person RE, Meade-White K, Benson KF. Source: Cancer Investigation. 2003; 21(4): 579-87. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14533448&dopt=Abstract
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Leukemia in twins: lessons in natural history. Author(s): Greaves MF, Maia AT, Wiemels JL, Ford AM. Source: Blood. 2003 October 1; 102(7): 2321-33. Epub 2003 June 05. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791663&dopt=Abstract
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Leukemia inhibitory factor (LIF), cardiotrophin-1, and oncostatin M share structural binding determinants in the immunoglobulin-like domain of LIF receptor. Author(s): Plun-Favreau H, Perret D, Diveu C, Froger J, Chevalier S, Lelievre E, Gascan H, Chabbert M. Source: The Journal of Biological Chemistry. 2003 July 18; 278(29): 27169-79. Epub 2003 April 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707269&dopt=Abstract
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Leukemia inhibitory factor regulates prolactin secretion in prolactinoma and lactotroph cells. Author(s): Ben-Shlomo A, Miklovsky I, Ren SG, Yong WH, Heaney AP, Culler MD, Melmed S. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 February; 88(2): 858-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574225&dopt=Abstract
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Leukemia-related transcription factor TEL accelerates differentiation of Friend erythroleukemia cells. Author(s): Waga K, Nakamura Y, Maki K, Arai H, Yamagata T, Sasaki K, Kurokawa M, Hirai H, Mitani K. Source: Oncogene. 2003 January 9; 22(1): 59-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527908&dopt=Abstract
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Leukemic dissemination within a glioblastoma in a patient with chronic lymphoid leukemia. Author(s): Bouillot S, Vignes JR, Guerin J, Dubus P, Vital A. Source: Clin Neuropathol. 2003 January-February; 22(1): 10-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12617188&dopt=Abstract
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Leukemic infiltration of the urinary bladder presenting as uncontrollable gross hematuria in a child with acute lymphoblastic leukemia. Author(s): Chang CY, Chiou TJ, Hsieh YL, Cheng SN. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 September; 25(9): 735-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12972811&dopt=Abstract
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Levels of the soluble, 55-kilodalton isoform of tumor necrosis factor receptor in bone marrow are correlated with the clinical outcome of children with acute lymphoblastic leukemia in first recurrence. Author(s): Wu S, Korte A, Gessner R, Henze G, Seeger K. Source: Cancer. 2003 August 1; 98(3): 625-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879482&dopt=Abstract
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Lineage specific treatment of adult patients with acute lymphoblastic leukemia in first remission with anti-B4-blocked ricin or high-dose cytarabine: Cancer and Leukemia Group B Study 9311. Author(s): Szatrowski TP, Dodge RK, Reynolds C, Westbrook CA, Frankel SR, Sklar J, Stewart CC, Hurd DD, Kolitz JE, Velez-Garcia E, Stone RM, Bloomfield CD, Schiffer CA, Larson RA. Source: Cancer. 2003 March 15; 97(6): 1471-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12627512&dopt=Abstract
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Localized lymphoid relapse in the pancreas following allogeneic hematopoietic stem cell transplant for chronic myelogenous leukemia. Author(s): Rossetti JM, Lister J, Shadduck RK, Bloom E, Geyer SJ, Caushaj PF, Homann J, Papasavas P, Cedar M. Source: Leukemia & Lymphoma. 2003 June; 44(6): 1071-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854913&dopt=Abstract
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Localized relapse in bone marrow in a posttransplantation patient with t(6;9) acute myeloid leukemia. Author(s): Maeda T, Kosugi S, Ujiie H, Osumi K, Fukui T, Yoshida H, Kashiwagi H, Ishikawa J, Tomiyama Y, Matsuzawa Y. Source: International Journal of Hematology. 2003 June; 77(5): 522-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841393&dopt=Abstract
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Locally invasive auricular aspergillosis after ear piercing in a neutropenic patient with leukemia. Author(s): Kontoyiannis DP, Chagua MR, Ramirez I, Prieto V. Source: American Journal of Hematology. 2003 August; 73(4): 296-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879439&dopt=Abstract
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Long-term outcome with pentostatin treatment in hairy cell leukemia patients. A French retrospective study of 238 patients. Author(s): Maloisel F, Benboubker L, Gardembas M, Coiffier B, Divine M, Sebban C, Blanc M, Abgrall JF, Lederlin P, Harousseau JL, Blaise AM, Grosbois B, Morice P, Ghandour C, Castaigne S. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 January; 17(1): 45-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529659&dopt=Abstract
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Long-term study of the clinical significance of loss of heterozygosity in childhood acute lymphoblastic leukemia. Author(s): Takeuchi S, Tsukasaki K, Bartram CR, Seriu T, Zimmermann M, Schrappe M, Takeuchi N, Park S, Taguchi H, Koeffler HP. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 January; 17(1): 149-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529672&dopt=Abstract
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Loss of folylpoly-gamma-glutamate synthetase activity is a dominant mechanism of resistance to polyglutamylation-dependent novel antifolates in multiple human leukemia sublines. Author(s): Liani E, Rothem L, Bunni MA, Smith CA, Jansen G, Assaraf YG. Source: International Journal of Cancer. Journal International Du Cancer. 2003 February 20; 103(5): 587-99. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12494465&dopt=Abstract
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Loss of imprinting of IGF-II gene in children with acute lymphoblastic leukemia. Author(s): Vorwerk P, Wex H, Bessert C, Hohmann B, Schmidt U, Mittler U. Source: Leukemia Research. 2003 September; 27(9): 807-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804639&dopt=Abstract
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Loss of multidrug resistance protein 1 expression and folate efflux activity results in a highly concentrative folate transport in human leukemia cells. Author(s): Assaraf YG, Rothem L, Hooijberg JH, Stark M, Ifergan I, Kathmann I, Dijkmans BA, Peters GJ, Jansen G. Source: The Journal of Biological Chemistry. 2003 February 28; 278(9): 6680-6. Epub 2002 December 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12486126&dopt=Abstract
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Low incidence of secondary myelodysplasia and acute myeloid leukemia after highdose chemotherapy as adjuvant therapy for breast cancer patients: a study by the Solid Tumors Working Party of the European Group for Blood and Marrow Transplantation. Author(s): Kroger N, Zander AR, Martinelli G, Ferrante P, Moraleda JM, Da Prada GA, Demirer T, Socie G, Rosti G; European Group for Blood and Marrow Transplantation. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 April; 14(4): 554-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649100&dopt=Abstract
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Lymphocyte recovery after allogeneic bone marrow transplantation predicts risk of relapse in acute lymphoblastic leukemia. Author(s): Kumar S, Chen MG, Gastineau DA, Gertz MA, Inwards DJ, Lacy MQ, Tefferi A, Litzow MR. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1865-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970788&dopt=Abstract
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Lymphocytic infiltrates and subclinical epithelial tumor extension in patients with chronic leukemia and solid-organ transplantation. Author(s): Mehrany K, Byrd DR, Roenigk RK, Weenig RH, Phillips PK, Nguyen TH, Otley CC. Source: Dermatologic Surgery : Official Publication for American Society for Dermatologic Surgery [et Al.]. 2003 February; 29(2): 129-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562340&dopt=Abstract
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Lymphoid blast crisis of chronic myelogenous leukemia occurring more than 11 years after receiving an allogeneic bone marrow transplant for chronic myelogenous leukemia in myeloid blast crisis at onset. Author(s): Fukuno K, Tsurumi H, Yamada T, Oyama M, Matsuyama T, Terakura S, Kodera Y, Moriwaki H. Source: Bone Marrow Transplantation. 2003 February; 31(3): 211-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12621483&dopt=Abstract
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Lymphoid disorders other than common acute lymphoblastic leukemia: background. Author(s): Swansbury J. Source: Methods in Molecular Biology (Clifton, N.J.). 2003; 220: 93-110. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744209&dopt=Abstract
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Lymphoma- and leukemia-associated chromosomal translocations in healthy individuals. Author(s): Janz S, Potter M, Rabkin CS. Source: Genes, Chromosomes & Cancer. 2003 March; 36(3): 211-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12557221&dopt=Abstract
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Macrocephaly and epidural involvement of T-cell acute lymphoblastic leukemia. Author(s): Jaing TH, Hung PC, Hung IJ, Wang HS, Wang CJ. Source: Pediatric Neurology. 2002 November; 27(5): 401-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12504211&dopt=Abstract
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Magnetic resonance abnormalities of bone marrow in a case of acute lymphoblastic leukemia. Author(s): Lu CS, Huang IA, Wang CJ, Lo WC, Jaing TH. Source: Acta Paediatr Taiwan. 2003 March-April; 44(2): 109-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12845855&dopt=Abstract
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Management of advanced chronic lymphocytic leukemia. Author(s): Cao TM, Coutre SE. Source: Curr Hematol Rep. 2003 January; 2(1): 65-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901156&dopt=Abstract
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Management of chronic lymphocytic leukemia: a changing field. Author(s): Keating MJ. Source: Reviews in Clinical and Experimental Hematology. 2002 December; 6(4): 350-65; Discussion 449-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823777&dopt=Abstract
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Management of molecular-targeted therapy for chronic myelogenous leukemia. Author(s): Ault P, Kaled S, Rios MB. Source: Journal of the American Academy of Nurse Practitioners. 2003 July; 15(7): 292-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12929249&dopt=Abstract
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Management of pregnancy-associated acute leukemia. Author(s): Su WL, Liu JY, Kao WY. Source: Eur J Gynaecol Oncol. 2003; 24(3-4): 251-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807234&dopt=Abstract
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Maternal herpesvirus infections and risk of acute lymphoblastic leukemia in the offspring. Author(s): Lehtinen M, Koskela P, Ogmundsdottir HM, Bloigu A, Dillner J, Gudnadottir M, Hakulinen T, Kjartansdottir A, Kvarnung M, Pukkala E, Tulinius H, Lehtinen T. Source: American Journal of Epidemiology. 2003 August 1; 158(3): 207-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882942&dopt=Abstract
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Maternal occupational exposure to extremely low frequency magnetic fields during pregnancy and childhood leukemia. Author(s): Infante-Rivard C, Deadman JE. Source: Epidemiology (Cambridge, Mass.). 2003 July; 14(4): 437-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843769&dopt=Abstract
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Medulloblastoma as a secondary malignancy after radiotherapy-free treatment for acute lymphoblastic leukemia. Author(s): Schiavetti A, Clerico A, De Pasquale MD, Bernardini L, Moleti ML. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 July; 25(7): 562-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847325&dopt=Abstract
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Megakaryoblastic leukemia 1, a potent transcriptional coactivator for serum response factor (SRF), is required for serum induction of SRF target genes. Author(s): Cen B, Selvaraj A, Burgess RC, Hitzler JK, Ma Z, Morris SW, Prywes R. Source: Molecular and Cellular Biology. 2003 September; 23(18): 6597-608. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12944485&dopt=Abstract
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Methotrexate-related neurotoxicity in the treatment of childhood acute lymphoblastic leukemia. Author(s): Shuper A, Stark B, Kornreich L, Cohen IJ, Avrahami G, Yaniv I. Source: Isr Med Assoc J. 2002 November; 4(11): 1050-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12489505&dopt=Abstract
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Methylation of p15INK4B is common, is associated with deletion of genes on chromosome arm 7q and predicts a poor prognosis in therapy-related myelodysplasia and acute myeloid leukemia. Author(s): Christiansen DH, Andersen MK, Pedersen-Bjergaard J. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1813-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970781&dopt=Abstract
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Minimal residual disease in chronic myeloid leukemia. Author(s): Lowenberg B. Source: The New England Journal of Medicine. 2003 October 9; 349(15): 1399-401. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14534331&dopt=Abstract
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Mismatch extension during strong stop strand transfer and minimal homology requirements for replicative template switching during Moloney murine leukemia virus replication. Author(s): Marr SF, Telesnitsky A. Source: Journal of Molecular Biology. 2003 July 18; 330(4): 657-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850138&dopt=Abstract
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MLL AT-hook sequence is strongly conserved in infant acute leukemia with or without MLL gene rearrangement. Author(s): Macrini CM, Pombo-de-Oliveira MS, Ford AM, Alves G. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1432-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835743&dopt=Abstract
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MLL/SEPTIN6 chimeric transcript from inv ins(X;11)(q24;q23q13) in acute monocytic leukemia: report of a case and review of the literature. Author(s): Kim HJ, Ki CS, Park Q, Koo HH, Yoo KH, Kim EJ, Kim SH. Source: Genes, Chromosomes & Cancer. 2003 September; 38(1): 8-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12874781&dopt=Abstract
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Model studies of cyclophosphamide resistance in human myeloid leukemia. Author(s): Andersson BS, Murray D. Source: Cancer Treat Res. 2002; 112: 211-35. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12487104&dopt=Abstract
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Molecular biology of leukemia. Author(s): Wujcik D. Source: Semin Oncol Nurs. 2003 May; 19(2): 83-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830732&dopt=Abstract
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Molecular differences between small and large cells in patients with chronic lymphocytic leukemia. Author(s): Lee JN, Giles F, Huh YO, Manshouri T, O'Brien S, Kantarjian HM, Keating MJ, Albitar M. Source: European Journal of Haematology. 2003 October; 71(4): 235-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950231&dopt=Abstract
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Molecular evidence for transferrin receptor 2 expression in all FAB subtypes of acute myeloid leukemia. Author(s): Kollia P, Samara M, Stamatopoulos K, Belessi C, Stavroyianni N, Tsompanakou A, Athanasiadou A, Vamvakopoulos N, Laoutaris N, Anagnostopoulos A, Fassas A. Source: Leukemia Research. 2003 December; 27(12): 1101-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921947&dopt=Abstract
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Molecular mechanisms of hyperthermia- and cisplatin-induced cytotoxicity in T cell leukemia. Author(s): Mauz-Korholz C, Dietzsch S, Schippel P, Banning U, Korholz D. Source: Anticancer Res. 2003 May-June; 23(3B): 2643-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894552&dopt=Abstract
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Molecular monitoring in chronic myeloid leukemia patients who achieve complete cytogenetic remission on imatinib. Author(s): Lin F, Drummond M, O'Brien S, Cervantes F, Goldman J, Kaeda J. Source: Blood. 2003 August 1; 102(3): 1143. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869491&dopt=Abstract
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Molecular targets in acute myelogenous leukemia. Author(s): Stirewalt DL, Meshinchi S, Radich JP. Source: Blood Reviews. 2003 March; 17(1): 15-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490207&dopt=Abstract
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Monoclonal antibody therapy in acute myeloid leukemia. Author(s): Feldman EJ. Source: Curr Hematol Rep. 2003 January; 2(1): 73-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901157&dopt=Abstract
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Morphologic dysplasia in acute myeloid leukemia: importance of granulocytic dysplasia. Author(s): Bennett JM. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 1; 21(15): 3004; Author Reply 3004-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885828&dopt=Abstract
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Multiple complete remissions in a patient with acute myeloid leukemia (M4eo) with low-dose cytosine arabinoside and all-trans retinoic acid. Author(s): Jantunen E, Mahlamaki E, Heinonen K, Nousiainen T. Source: Leukemia & Lymphoma. 2003 May; 44(5): 883-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802931&dopt=Abstract
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Mutant p53 in bone marrow stromal cells increases VEGF expression and supports leukemia cell growth. Author(s): Narendran A, Ganjavi H, Morson N, Connor A, Barlow JW, Keystone E, Malkin D, Freedman MH. Source: Experimental Hematology. 2003 August; 31(8): 693-701. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901974&dopt=Abstract
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Myelogenous leukemia cutis resembling stasis dermatitis. Author(s): Chang HY, Wong KM, Bosenberg M, McKee PH, Haynes HA. Source: Journal of the American Academy of Dermatology. 2003 July; 49(1): 128-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833025&dopt=Abstract
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Myeloid/natural killer cell precursor acute leukemia accompanied by homozygous protein C deficiency. Author(s): Shimamoto T, Nakajima A, Katagiri T, Ito Y, Ohyashiki K. Source: International Journal of Hematology. 2003 August; 78(2): 149-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953810&dopt=Abstract
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N-(4-Hydroxylphenyl)retinamide (fenretinide, 4-HPR), a retinoid compound with antileukemic and proapoptotic activity in acute lymphoblastic leukemia (ALL). Author(s): Faderl S, Lotan R, Kantarjian HM, Harris D, Van Q, Estrov Z. Source: Leukemia Research. 2003 March; 27(3): 259-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12537979&dopt=Abstract
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NADPH-dependent reductases and polyol formation in human leukemia cell lines. Author(s): Sato S, Secchi EF, Sakurai S, Ohta N, Fukase S, Lizak MJ. Source: Chemico-Biological Interactions. 2003 February 1; 143-144: 363-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604223&dopt=Abstract
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Natural killer resistance of a drug-resistant leukemia cell line, mediated by upregulation of HLA class I expression. Author(s): Classen CF, Falk CS, Friesen C, Fulda S, Herr I, Debatin KM. Source: Haematologica. 2003 May; 88(5): 509-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745270&dopt=Abstract
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Naturally occurring substitutions of the human T-cell leukemia virus type 1 3' LTR influence strand-transfer reaction. Author(s): Leclercq I, Mortreux F, Rabaaoui S, Jonsson CB, Wattel E. Source: Journal of Virological Methods. 2003 May; 109(2): 105-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12711052&dopt=Abstract
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Nephrotic syndrome with crescent formation and massive IgA deposition following allogeneic bone marrow transplantation for natural killer cell leukemia/lymphoma. Author(s): Kimura S, Horie A, Hiki Y, Yamamoto C, Suzuki S, Kuroda J, Deguchi M, Kato G, Karasuno T, Hiraoka A, Yoshikawa T, Maekawa T. Source: Blood. 2003 May 15; 101(10): 4219-21. Epub 2003 January 23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12543867&dopt=Abstract
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Neuroimaging in pediatric leukemia and lymphoma: differential diagnosis. Author(s): Vazquez E, Lucaya J, Castellote A, Piqueras J, Sainz P, Olive T, SanchezToledo J, Ortega JJ. Source: Radiographics : a Review Publication of the Radiological Society of North America, Inc. 2002 November-December; 22(6): 1411-28. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12432112&dopt=Abstract
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Neurologic complications of leukemia. Author(s): Demopoulos A, DeAngelis LM. Source: Current Opinion in Neurology. 2002 December; 15(6): 691-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12447107&dopt=Abstract
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New advances in the treatment of acute promyelocytic leukemia. Author(s): Douer D. Source: International Journal of Hematology. 2002 August; 76 Suppl 2: 179-87. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12430923&dopt=Abstract
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New developments in antibody therapy for acute myeloid leukemia. Author(s): Tomblyn MR, Tallman MS. Source: Seminars in Oncology. 2003 August; 30(4): 502-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939719&dopt=Abstract
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New highly sensitive fluorescence in situ hybridization method to detect PML/RARA fusion in acute promyelocytic leukemia. Author(s): Brockman SR, Paternoster SF, Ketterling RP, Dewald GW. Source: Cancer Genetics and Cytogenetics. 2003 September; 145(2): 144-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12935927&dopt=Abstract
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New strategies for prevention and treatment of graft-versus-host disease and for induction of graft-versus-leukemia effects. Author(s): Deeg HJ. Source: International Journal of Hematology. 2003 January; 77(1): 15-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12568295&dopt=Abstract
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New targets for therapy in acute myeloid leukemia. Author(s): Appelbaum FR. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 March; 17(3): 492-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12646936&dopt=Abstract
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New vessel formation and aberrant VEGF/VEGFR signaling in acute leukemia: does it matter? Author(s): de Bont ES, Neefjes VM, Rosati S, Vellenga E, Kamps WA. Source: Leukemia & Lymphoma. 2002 October; 43(10): 1901-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12481883&dopt=Abstract
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Nonmyeloablative allogeneic stem cell transplantation for acute leukemia. Author(s): Laport GG. Source: Curr Hematol Rep. 2003 January; 2(1): 49-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901154&dopt=Abstract
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Non-myeloablative conditioning before allogeneic stem cell transplantation in adult acute lymphoblastic leukemia. Author(s): Gokbuget N, Hoelzer D. Source: Haematologica. 2003 May; 88(5): 484-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745266&dopt=Abstract
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Normal intrinsic Th1/Th2 balance in patients with chronic phase chronic myeloid leukemia not treated with interferon-alpha or imatinib. Author(s): Kiani A, Habermann I, Schake K, Neubauer A, Rogge L, Ehninger G. Source: Haematologica. 2003 July; 88(7): 754-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857553&dopt=Abstract
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Normalization of previously shortened telomere length under treatment with imatinib argues against a preexisting telomere length deficit in normal hematopoietic stem cells from patients with chronic myeloid leukemia. Author(s): Brummendorf TH, Ersoz I, Hartmann U, Balabanov S, Wolke H, Paschka P, Lahaye T, Berner B, Bartolovic K, Kreil S, Berger U, Gschaidmeier H, Bokemeyer C, Hehlmann R, Dietz K, Lansdorp PM, Kanz L, Hochhaus A. Source: Annals of the New York Academy of Sciences. 2003 May; 996: 26-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12799279&dopt=Abstract
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Notch ligands, Delta-1 and Delta-4 suppress the self-renewal capacity and long-term growth of two myeloblastic leukemia cell lines. Author(s): Tohda S, Murata-Ohsawa M, Sakano S, Nara N. Source: International Journal of Oncology. 2003 May; 22(5): 1073-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684674&dopt=Abstract
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Notch, a unifying target in T-cell acute lymphoblastic leukemia? Author(s): Screpanti I, Bellavia D, Campese AF, Frati L, Gulino A. Source: Trends in Molecular Medicine. 2003 January; 9(1): 30-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12524208&dopt=Abstract
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Novel B-cell acute lymphoblastic leukemia sister cell lines BALM 19-23 and BALM-26 with interclonal proliferative and phenotypic heterogeneity from a patient with hypercalcemia. Author(s): Matsuo Y, Drexler HG, Kojima K, Sugimoto A, Harashima A, Okochi A, Hara M, Orita K. Source: Hum Cell. 2002 September; 15(3): 160-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12703546&dopt=Abstract
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Novel clonal der(8)t(8;14)(p11;q11),del(9)(q13q22) and t(14;22) (q13;q13) in a patient with fulminant adult T-cell leukemia/lymphoma. Author(s): Yeh SP, Yu MT, Chow KC, Lai LY, Chiu CF. Source: Cancer Genetics and Cytogenetics. 2002 November; 139(1): 34-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12547155&dopt=Abstract
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Novel constitutional t(2;12)(q21;q22) in a patient with t(9;22)-negative chronic myelocytic leukemia. Author(s): Kramer A, Fruehauf S, Ho AD, Hager HD, Bartram CR, Hochhaus A. Source: Cancer Genetics and Cytogenetics. 2003 April 15; 142(2): 162-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699897&dopt=Abstract
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Novel dic(16;18)(q11;p11) in two cases of Philadelphia chromosome positive acute Bcell lymphoblastic leukemia. Author(s): Domingo-Domenech E, Boque C, Aventin A, Calasanz MJ, Valiente A, PerezEquiza K, Domingo-Claros A, Granena A. Source: Cancer Genetics and Cytogenetics. 2002 November; 139(1): 63-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12547162&dopt=Abstract
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Novel SWI/SNF chromatin-remodeling complexes contain a mixed-lineage leukemia chromosomal translocation partner. Author(s): Nie Z, Yan Z, Chen EH, Sechi S, Ling C, Zhou S, Xue Y, Yang D, Murray D, Kanakubo E, Cleary ML, Wang W. Source: Molecular and Cellular Biology. 2003 April; 23(8): 2942-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665591&dopt=Abstract
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Novel targeted and immunotherapeutic strategies in chronic myeloid leukemia. Author(s): Schwartz J, Pinilla-Ibarz J, Yuan RR, Scheinberg DA. Source: Semin Hematol. 2003 January; 40(1): 87-96. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563615&dopt=Abstract
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Novel translocation in acute megakaryoblastic leukemia (AML-M7). Author(s): Toretsky JA, Everly EM, Padilla-Nash HM, Chen A, Abruzzo LV, Eskenazi AE, Frantz C, Ried T, Stamberg J. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 May; 25(5): 396-402. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759627&dopt=Abstract
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NUP98 is fused to adducin 3 in a patient with T-cell acute lymphoblastic leukemia and myeloid markers, with a new translocation t(10;11)(q25;p15). Author(s): Lahortiga I, Vizmanos JL, Agirre X, Vazquez I, Cigudosa JC, Larrayoz MJ, Sala F, Gorosquieta A, Perez-Equiza K, Calasanz MJ, Odero MD. Source: Cancer Research. 2003 June 15; 63(12): 3079-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810632&dopt=Abstract
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Nutrition and acute leukemia in adults: relation to remission rate and survival. Author(s): Cederholm T, Eriksson K, Palmblad J. Source: Haematologia. 2002; 32(4): 405-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803115&dopt=Abstract
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Obesity in adult survivors of childhood acute lymphoblastic leukemia: a report from the Childhood Cancer Survivor Study. Author(s): Oeffinger KC, Mertens AC, Sklar CA, Yasui Y, Fears T, Stovall M, Vik TA, Inskip PD, Robison LL; Childhood Cancer Survivor Study. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 April 1; 21(7): 1359-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663727&dopt=Abstract
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Occurrence of additional chromosome aberrations in chronic myeloid leukemia patients treated with imatinib mesylate. Author(s): Schoch C, Haferlach T, Kern W, Schnittger S, Berger U, Hehlmann R, Hiddemann W, Hochhaus A. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 February; 17(2): 461-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592348&dopt=Abstract
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Occurrence of an MLL/LAF4 fusion gene caused by the insertion ins(11;2)(q23;q11.2q11.2) in an infant with acute lymphoblastic leukemia. Author(s): Bruch J, Wilda M, Teigler-Schlegel A, Harbott J, Borkhardt A, Metzler M. Source: Genes, Chromosomes & Cancer. 2003 May; 37(1): 106-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12661012&dopt=Abstract
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Off-pump coronary artery bypass grafting in a patient with chronic myelomonocytic leukemia. Author(s): Ito K, Kawachi H, Nishiyama K, Yaku H, Kitamura N. Source: Japanese Heart Journal. 2003 May; 44(3): 435-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12825811&dopt=Abstract
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Ongoing in vivo immunoglobulin class switch DNA recombination in chronic lymphocytic leukemia B cells. Author(s): Cerutti A, Zan H, Kim EC, Shah S, Schattner EJ, Schaffer A, Casali P. Source: Journal of Immunology (Baltimore, Md. : 1950). 2002 December 1; 169(11): 6594603. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12444172&dopt=Abstract
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Oral arsenic trioxide in the treatment of relapsed acute promyelocytic leukemia. Author(s): Au WY, Kumana CR, Kou M, Mak R, Chan GC, Lam CW, Kwong YL. Source: Blood. 2003 July 1; 102(1): 407-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12814916&dopt=Abstract
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Orbital granulocytic sarcoma: an unusual presentation of acute myelocytic leukemia. Author(s): Stein-Wexler R, Wootton-Gorges SL, West DC. Source: Pediatric Radiology. 2003 February; 33(2): 136-9. Epub 2002 November 12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12557072&dopt=Abstract
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Osteonecrosis: An emerging complication of intensive chemotherapy for childhood acute lymphoblastic leukemia. Author(s): Arico M, Boccalatte MF, Silvestri D, Barisone E, Messina C, Chiesa R, Santoro N, Tamaro P, Lippi A, Gallisai D, Basso G, De Rossi G; Associazione Italiana di Ematologia ed Oncologia Pediatrica. Source: Haematologica. 2003 July; 88(7): 747-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857552&dopt=Abstract
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Osteosarcoma after bone marrow transplantation for acute lymphoblastic leukemia. Author(s): Asai T, Myoui A, Fujimoto T, Hara J, Aozasa K, Yoshikawa H. Source: International Journal of Clinical Oncology / Japan Society of Clinical Oncology. 2002 October; 7(5): 318-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12402067&dopt=Abstract
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Overview of bladder cancer trials in the Cancer and Leukemia Group B. Author(s): Small EJ, Halabi S, Dalbagni G, Pruthi R, Phillips G, Edelman M, Bajorin D; Cancer and Leukemia Group B. Source: Cancer. 2003 April 15; 97(8 Suppl): 2090-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673701&dopt=Abstract
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OX40 signaling renders adult T-cell leukemia cells resistant to Fas-induced apoptosis. Author(s): Kunitomi A, Hori T, Maeda M, Uchiyama T. Source: International Journal of Hematology. 2002 October; 76(3): 260-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12416737&dopt=Abstract
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p21(Waf1/Cip1/Sdi1) prevents apoptosis as well as stimulates growth in cells transformed or immortalized by human T-cell leukemia virus type 1-encoded tax. Author(s): Kawata S, Ariumi Y, Shimotohno K. Source: Journal of Virology. 2003 July; 77(13): 7291-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12805427&dopt=Abstract
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Pancreatic pseudocyst complicating treatment of acute lymphoblastic leukemia. Author(s): Tomar S, Bakhshi S, Kabra SK, Arya LS. Source: Indian Pediatrics. 2003 July; 40(7): 670-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12881625&dopt=Abstract
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Pathologic quiz case: chronic anemia with red cell aplasia and lymphocytosis in a middle-aged man. T-cell large granular lymphocyte leukemia. Author(s): Lee PS, Hwang WS. Source: Archives of Pathology & Laboratory Medicine. 2002 December; 126(12): 1549-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12503585&dopt=Abstract
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Pathophysiology-directed therapy for acute hypoxemic respiratory failure in acute myeloid leukemia with hyperleukocytosis. Author(s): Schmidt JE, Tamburro RF, Sillos EM, Hill DA, Ribeiro RC, Razzouk BI. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 July; 25(7): 569-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847327&dopt=Abstract
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Persistence of TEL-AML1 transcript in acute lymphoblastic leukemia in long-term remission. Author(s): Endo C, Oda M, Nishiuchi R, Seino Y. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2003 June; 45(3): 275-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828580&dopt=Abstract
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Ph1-positive acute lymphoblastic leukemia in a patient with a germline MEN1 gene mutation. Author(s): Ichikawa N, Kobayashi H, Saito H. Source: International Journal of Hematology. 2003 August; 78(2): 171-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953815&dopt=Abstract
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Phase I and pharmacodynamic study of Triapine, a novel ribonucleotide reductase inhibitor, in patients with advanced leukemia. Author(s): Giles FJ, Fracasso PM, Kantarjian HM, Cortes JE, Brown RA, Verstovsek S, Alvarado Y, Thomas DA, Faderl S, Garcia-Manero G, Wright LP, Samson T, Cahill A, Lambert P, Plunkett W, Sznol M, DiPersio JF, Gandhi V. Source: Leukemia Research. 2003 December; 27(12): 1077-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921943&dopt=Abstract
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Phase II study of cladribine (2-chlorodeoxyadenosine) in relapsed or refractory adult T-cell leukemia-lymphoma. Author(s): Tobinai K, Uike N, Saburi Y, Chou T, Etoh T, Masuda M, Kawano F, Matsuoka M, Taguchi H, Makino T, Asano Y, Tamura K, Ohashi Y; Cladribine/ATL Study Group, Japan. Source: International Journal of Hematology. 2003 June; 77(5): 512-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841391&dopt=Abstract
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Phase II study of cladribine and cyclophosphamide in patients with chronic lymphocytic leukemia and prolymphocytic leukemia. Author(s): Montillo M, Tedeschi A, O'Brien S, Di Raimondo F, Lerner S, Ferrajoli A, Morra E, Keating MJ. Source: Cancer. 2003 January 1; 97(1): 114-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12491512&dopt=Abstract
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Phase II study of troxacitabine, a novel dioxolane nucleoside analog, in patients with untreated or imatinib mesylate-resistant chronic myelogenous leukemia in blastic phase. Author(s): Giles FJ, Feldman EJ, Roboz GJ, Larson RA, Mamus SW, Cortes JE, Verstovsek S, Faderl S, Talpaz M, Beran M, Albitar M, O'Brien SM, Kantarjian HM. Source: Leukemia Research. 2003 December; 27(12): 1091-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921945&dopt=Abstract
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Phenotypic heterogeneity of B cells in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma. Author(s): Kampalath B, Barcos MP, Stewart C. Source: American Journal of Clinical Pathology. 2003 June; 119(6): 824-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12817430&dopt=Abstract
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Philadelphia-negative acute lymphoblastic leukemia developing in a CML patient in imatinib mesylate-induced complete cytogenetic remission. Author(s): Cherrier-De Wilde S, Rack K, Vannuffel P, Delannoy A, Hagemeijer A. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 2046-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513056&dopt=Abstract
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Pilot study of gemtuzumab ozogamicin, liposomal daunorubicin, cytarabine and cyclosporine regimen in patients with refractory acute myelogenous leukemia. Author(s): Apostolidou E, Cortes J, Tsimberidou A, Estey E, Kantarjian H, Giles FJ. Source: Leukemia Research. 2003 October; 27(10): 887-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860007&dopt=Abstract
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Pilot study of Mylotarg, idarubicin and cytarabine combination regimen in patients with primary resistant or relapsed acute myeloid leukemia. Author(s): Alvarado Y, Tsimberidou A, Kantarjian H, Cortes J, Garcia-Manero G, Faderl S, Thomas D, Estey E, Giles FJ. Source: Cancer Chemotherapy and Pharmacology. 2003 January; 51(1): 87-90. Epub 2002 November 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12497211&dopt=Abstract
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Plasma vascular endothelial growth factor levels have prognostic significance in patients with acute myeloid leukemia but not in patients with myelodysplastic syndromes. Author(s): Aguayo A, Kantarjian HM, Estey EH, Giles FJ, Verstovsek S, Manshouri T, Gidel C, O'Brien S, Keating MJ, Albitar M. Source: Cancer. 2002 November 1; 95(9): 1923-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12404286&dopt=Abstract
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Plasmapheresis as treatment for transient iatrogenic severe hyperlipidemia in a child with leukemia. Author(s): Kropshofer G, Wehl G, Hogler W, Meister B, Heitger A, Nussbaumer W. Source: Medical and Pediatric Oncology. 2003 August; 41(2): 177. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12825232&dopt=Abstract
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Practical aspects of the treatment of chronic myelogenous leukemia with imatinib mesylate. Author(s): Zonder JA, Schiffer CA. Source: Curr Hematol Rep. 2003 January; 2(1): 57-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901155&dopt=Abstract
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Prediction of initial cytogenetic response for subsequent major and complete cytogenetic response to imatinib mesylate therapy in patients with Philadelphia chromosome-positive chronic myelogenous leukemia. Author(s): Drummond MW, Holyoake TL. Source: Cancer. 2003 October 15; 98(8): 1776-7; Author Reply 1777-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14534900&dopt=Abstract
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Preliminary results of evaluation of progress in chemotherapy for childhood leukemia patients employing Fourier-transform infrared microspectroscopy and cluster analysis. Author(s): Ramesh J, Huleihel M, Mordehai J, Moser A, Erukhimovich V, Levi C, Kapelushnik J, Mordechai S. Source: The Journal of Laboratory and Clinical Medicine. 2003 June; 141(6): 385-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819636&dopt=Abstract
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Preparation and characterization for bispecific antibodies of anti-CD3 x anti-idiotype to B cell lymphocytic leukemia. Author(s): Shen G, Zhang Y, Zhu H, Yang J, Wang X. Source: J Tongji Med Univ. 1999; 19(3): 166-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840886&dopt=Abstract
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Preponderant mitotic activity of nonleukemic cells plays an important role in failures to detect abnormal clone in childhood acute lymphoblastic leukemia. Author(s): Wu SQ, Weinberg KI, Joo WJ, Quinn JJ, Franklin J, Siegel SE, Gaynon PS. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 July; 25(7): 520-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847317&dopt=Abstract
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Prognostic implications of t(10;11) translocations in childhood acute myelogenous leukemia: a report from the Children's Cancer Group. Author(s): Casillas JN, Woods WG, Hunger SP, McGavran L, Alonzo TA, Feig SA; Children's Cancer Group. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 August; 25(8): 594-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902910&dopt=Abstract
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Prognostic implications of the presence of FLT3 mutations in patients with acute myeloid leukemia. Author(s): Kottaridis PD, Gale RE, Linch DC. Source: Leukemia & Lymphoma. 2003 June; 44(6): 905-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854887&dopt=Abstract
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Prognostic significance of CD7+CD56+ phenotype and chromosome 5 abnormalities for acute myeloid leukemia M0. Author(s): Suzuki R, Murata M, Kami M, Ohtake S, Asou N, Kodera Y, Tomonaga M, Masaki Y, Kusumoto S, Takeuchi J, Matsuda S, Hirai H, Yorimitsu S, Hamajima N, Seto M, Shimoyama M, Ohno R, Morishima Y, Nakamura S. Source: International Journal of Hematology. 2003 June; 77(5): 482-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841387&dopt=Abstract
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Prognostic significance of trisomy 4 as the sole cytogenetic abnormality in acute myeloid leukemia. Author(s): Gupta V, Minden MD, Yi QL, Brandwein J, Chun K. Source: Leukemia Research. 2003 November; 27(11): 983-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12859991&dopt=Abstract
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Progressive multifocal leukoencephalopathy in a patient with chronic myelogenous leukemia. Author(s): Swamy PA, Nardino R. Source: Conn Med. 2003 May; 67(5): 263-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802840&dopt=Abstract
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Prolonged molecular remission after arsenic trioxide and all-trans retinoic acid for acute promyelocytic leukemia relapsed after allogeneic stem cell transplantation. Author(s): Grigg A, Kimber R, Szer J. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1916-7; Author Reply 1918. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970801&dopt=Abstract
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Pseudotumor cerebri induced by all-trans retinoic acid treatment of acute promyelocytic leukemia. Author(s): Colucciello M. Source: Archives of Ophthalmology. 2003 July; 121(7): 1064-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860824&dopt=Abstract
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Pulmonary alveolar proteinosis in a patient with acute lymphoid leukemia regression after G-CSF therapy. Author(s): Pamuk GE, Turgut B, Vural O, Demir M, Hatipoglu O, Unlu E, Altaner S, Gerenli M, Cakir B. Source: Leukemia & Lymphoma. 2003 May; 44(5): 871-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802928&dopt=Abstract
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Qualitative and quantitative analysis of human herpesviruses in chronic and acute B cell lymphocytic leukemia and in multiple myeloma. Author(s): Hermouet S, Sutton CA, Rose TM, Greenblatt RJ, Corre I, Garand R, Neves AM, Bataille R, Casey JW. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 January; 17(1): 185-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529677&dopt=Abstract
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Quality of life in patients with newly diagnosed chronic phase chronic myeloid leukemia on imatinib versus interferon alfa plus low-dose cytarabine: results from the IRIS Study. Author(s): Hahn EA, Glendenning GA, Sorensen MV, Hudgens SA, Druker BJ, Guilhot F, Larson RA, O'Brien SG, Dobrez DG, Hensley ML, Cella D; IRIS Investigators. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 1; 21(11): 2138-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775739&dopt=Abstract
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Quantitative comparison of the expression of EVI1 and its presumptive antagonist, MDS1/EVI1, in patients with myeloid leukemia. Author(s): Vinatzer U, Mannhalter C, Mitterbauer M, Gruener H, Greinix H, Schmidt HH, Fonatsch C, Wieser R. Source: Genes, Chromosomes & Cancer. 2003 January; 36(1): 80-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461752&dopt=Abstract
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Quantitative intra-individual monitoring of BCR-ABL transcript levels in archival bone marrow trephines of patients with chronic myeloid leukemia. Author(s): Bock O, Lehmann U, Kreipe H. Source: The Journal of Molecular Diagnostics : Jmd. 2003 February; 5(1): 54-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552081&dopt=Abstract
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Quantitative PCR identifies a minimal deleted region of 120 kb extending from the Philadelphia chromosome ABL translocation breakpoint in chronic myeloid leukemia with poor outcome. Author(s): Kolomietz E, Marrano P, Yee K, Thai B, Braude I, Kolomietz A, Chun K, Minkin S, Kamel-Reid S, Minden M, Squire JA. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1313-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835719&dopt=Abstract
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Quantitative polymerase chain reaction monitoring of BCR-ABL during therapy with imatinib mesylate (STI571; gleevec) in chronic-phase chronic myelogenous leukemia. Author(s): Kantarjian HM, Talpaz M, Cortes J, O'Brien S, Faderl S, Thomas D, Giles F, Rios MB, Shan J, Arlinghaus R. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2003 January; 9(1): 160-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12538464&dopt=Abstract
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Quantitative real-time RT-PCR analysis of PML-RAR alpha mRNA in acute promyelocytic leukemia: assessment of prognostic significance in adult patients from intergroup protocol 0129. Author(s): Gallagher RE, Yeap BY, Bi W, Livak KJ, Beaubier N, Rao S, Bloomfield CD, Appelbaum FR, Tallman MS, Slack JL, Willman CL. Source: Blood. 2003 April 1; 101(7): 2521-8. Epub 2002 December 05. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12468436&dopt=Abstract
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Quinine as a multidrug resistance inhibitor: a phase 3 multicentric randomized study in adult de novo acute myelogenous leukemia. Author(s): Solary E, Drenou B, Campos L, de Cremoux P, Mugneret F, Moreau P, Lioure B, Falkenrodt A, Witz B, Bernard M, Hunault-Berger M, Delain M, Fernandes J, Mounier C, Guilhot F, Garnache F, Berthou C, Kara-Slimane F, Harousseau JL; Groupe Ouest Est Leucemies Aigues Myeloblastiques. Source: Blood. 2003 August 15; 102(4): 1202-10. Epub 2003 March 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663440&dopt=Abstract
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Race and outcome in childhood acute lymphoblastic leukemia. Author(s): Carroll WL. Source: Jama : the Journal of the American Medical Association. 2003 October 15; 290(15): 2061-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14559962&dopt=Abstract
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Rapid improvement of disseminated intravascular coagulation by donor leukocyte infusions in a patient with promyelocytic crisis of chronic myelogenous leukemia after reduced-intensity stem cell transplantation from an HLA 2-antigen-mismatched mother. Author(s): Matsue K, Yamada K, Takeuchi M, Tabayashi T. Source: International Journal of Hematology. 2003 May; 77(4): 408-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774933&dopt=Abstract
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Rate of death due to leukemia/lymphoma in patients with rheumatoid arthritis. Author(s): Wolfe F, Fries JF. Source: Arthritis and Rheumatism. 2003 September; 48(9): 2694-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13130492&dopt=Abstract
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Re: “anthropometric characteristics, physical activity, and risk of non-Hodgkin's lymphoma subtypes and B-cell chronic lymphocytic leukemia: a prospective study”. Author(s): Groves FD, Lazarchick JS. Source: American Journal of Epidemiology. 2003 July 15; 158(2): 190. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851233&dopt=Abstract
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Rearrangement of the MLL gene and a region proximal to the RARalpha gene in a case of acute myelocytic leukemia M5 with a t(11;17)(q23;q21). Author(s): Dube S, Fetni R, Hazourli S, Champagne M, Lemieux N. Source: Cancer Genetics and Cytogenetics. 2003 August; 145(1): 54-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885463&dopt=Abstract
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Recent advances in pediatric acute lymphoblastic and myeloid leukemia. Author(s): Ravindranath Y. Source: Current Opinion in Oncology. 2003 January; 15(1): 23-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490758&dopt=Abstract
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Recent advances in the treatment of infant acute myeloid leukemia. Author(s): Ishii E, Kawasaki H, Isoyama K, Eguchi-Ishimae M, Eguchi M. Source: Leukemia & Lymphoma. 2003 May; 44(5): 741-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802909&dopt=Abstract
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Reconstitution of CD40 and CD80 in dendritic cells generated from blasts of patients with acute myeloid leukemia. Author(s): Li L, Schmitt A, Reinhardt P, Greiner J, Ringhoffer M, Vaida B, Bommer M, Vollmer M, Wiesneth M, Dohner H, Schmitt M. Source: Cancer Immunity [electronic Resource] : a Journal of the Academy of Cancer Immunology. 2003 July 16; 3: 8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12862419&dopt=Abstract
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Reconstitution of innate immunity in B-chronic lymphocytic leukemia: time to reconsider the possibilities. Author(s): Lee YK, Kay NE. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 1945-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513043&dopt=Abstract
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Reduced folate carrier and dihydrofolate reductase expression in acute lymphocytic leukemia may predict outcome: a Children's Cancer Group Study. Author(s): Levy AS, Sather HN, Steinherz PG, Sowers R, La M, Moscow JA, Gaynon PS, Uckun FM, Bertino JR, Gorlick R; Children's Cancer Group Study. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 September; 25(9): 688-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12972803&dopt=Abstract
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Refining prognostic factors in chronic lymphocytic leukemia. Author(s): Bosch F, Montserrat E. Source: Reviews in Clinical and Experimental Hematology. 2002 December; 6(4): 335-49; Discussion 449-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823776&dopt=Abstract
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Regulation of FcepsilonRI-mediated signaling by an adaptor protein STAP-2/BSK in rat basophilic leukemia RBL-2H3 cells. Author(s): Yamamoto T, Yumioka T, Sekine Y, Sato N, Minoguchi M, Yoshimura A, Matsuda T. Source: Biochemical and Biophysical Research Communications. 2003 July 4; 306(3): 76773. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810085&dopt=Abstract
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Relationship between cyclin D1 and p21(Waf1/Cip1) during differentiation of human myeloid leukemia cell lines. Author(s): Ullmannova V, Stockbauer P, Hradcova M, Soucek J, Haskovec C. Source: Leukemia Research. 2003 December; 27(12): 1115-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921950&dopt=Abstract
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Replication-competent hybrids between murine leukemia virus and foamy virus. Author(s): Shikova-Lekova E, Lindemann D, Pietschmann T, Juretzek T, Rudolph W, Herchenroder O, Gelderblom HR, Rethwilm A. Source: Journal of Virology. 2003 July; 77(13): 7677-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12805469&dopt=Abstract
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Residual disease in chronic myeloid leukemia after induction of molecular remission. Author(s): Lange T, Niederwieser DW, Deininger MW. Source: The New England Journal of Medicine. 2003 October 9; 349(15): 1483-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14534349&dopt=Abstract
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Resistance of Philadelphia-chromosome positive leukemia towards the kinase inhibitor imatinib (STI571, Glivec): a targeted oncoprotein strikes back. Author(s): von Bubnoff N, Peschel C, Duyster J. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 May; 17(5): 829-38. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750693&dopt=Abstract
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Resistance to glucocorticoid-induced apoptosis in lymphoblastic leukemia. Author(s): Kofler R, Schmidt S, Kofler A, Ausserlechner MJ. Source: The Journal of Endocrinology. 2003 July; 178(1): 19-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12844332&dopt=Abstract
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Resolution of fungemia due to Fusarium species in a patient with acute leukemia treated with caspofungin. Author(s): Apostolidis J, Bouzani M, Platsouka E, Belasiotou H, Stamouli M, Harhalakis N, Boutati EI, Paniara O, Nikiforakis E. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2003 May 15; 36(10): 1349-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746788&dopt=Abstract
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Response to imatinib in patients who relapse after allogeneic stem cell transplantation for chronic myeloid leukemia. Author(s): Bacigalupo A. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1722. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970770&dopt=Abstract
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Response to imatinib in patients who relapse after allogeneic stem cell transplantation for chronic myeloid leukemia. Author(s): Olavarria E, Ottmann OG, Deininger M, Clark RE, Bandini G, Byrne J, Lipton J, Vitek A, Michallet M, Siegert W, Ullmann A, Wassmann B, Niederwieser D, Fischer T; Chronic Leukaemia Working Party of the European Group of Bone and Marrow Transplantation (EBMT). Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1707-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970768&dopt=Abstract
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Response to STI571 in chronic myelomonocytic leukemia with platelet derived growth factor beta receptor involvement: a new case report. Author(s): Pitini V, Arrigo C, Teti D, Barresi G, Righi M, Alo G. Source: Haematologica. 2003 May; 88(5): Ecr18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745287&dopt=Abstract
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Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia. Author(s): Kantarjian HM, O'Brien S, Cortes J, Giles FJ, Faderl S, Issa JP, Garcia-Manero G, Rios MB, Shan J, Andreeff M, Keating M, Talpaz M. Source: Cancer. 2003 August 1; 98(3): 522-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879469&dopt=Abstract
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Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders. Author(s): Cortes J, Giles F, O'Brien S, Thomas D, Albitar M, Rios MB, Talpaz M, GarciaManero G, Faderl S, Letvak L, Salvado A, Kantarjian H. Source: Cancer. 2003 June 1; 97(11): 2760-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767088&dopt=Abstract
170 Leukemia
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Results of therapy for acute lymphoblastic leukemia in black and white children. Author(s): Pui CH, Sandlund JT, Pei D, Rivera GK, Howard SC, Ribeiro RC, Rubnitz JE, Razzouk BI, Hudson MM, Cheng C, Raimondi SC, Behm FG, Downing JR, Relling MV, Evans WE. Source: Jama : the Journal of the American Medical Association. 2003 October 15; 290(15): 2001-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14559953&dopt=Abstract
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Retinoic acid and steroid in acute promyelocytic leukemia. Author(s): Hicsonmez G. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 June; 17(6): 1203. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764396&dopt=Abstract
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Retinoid target genes in acute promyelocytic leukemia. Author(s): Pitha-Rowe I, Petty WJ, Kitareewan S, Dmitrovsky E. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1723-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970771&dopt=Abstract
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Risk classification at the time of diagnosis differentially affects the level of residual disease in children with B-precursor acute lymphoblastic leukemia after completion of therapy. Author(s): Okcu MF, Roberts WM, Johnston DA, Ouspenskaia MV, Papusha VZ, Brandt MA, Zipf TF. Source: Leukemia Research. 2003 August; 27(8): 743-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12801533&dopt=Abstract
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Risk of acute leukemia following epirubicin-based adjuvant chemotherapy: a report from the National Cancer Institute of Canada Clinical Trials Group. Author(s): Crump M, Tu D, Shepherd L, Levine M, Bramwell V, Pritchard K. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3066-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915595&dopt=Abstract
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Rituximab in B-cell chronic lymphocytic leukemia. Author(s): Lin TS, Lucas MS, Byrd JC. Source: Seminars in Oncology. 2003 August; 30(4): 483-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939717&dopt=Abstract
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Safety of lumbar puncture for adults with acute leukemia and restrictive prophylactic platelet transfusion. Author(s): Vavricka SR, Walter RB, Irani S, Halter J, Schanz U. Source: Annals of Hematology. 2003 September; 82(9): 570-3. Epub 2003 August 02. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12904898&dopt=Abstract
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Screening and quantification of multiple chromosome translocations in human leukemia. Author(s): Shi RZ, Morrissey JM, Rowley JD. Source: Clinical Chemistry. 2003 July; 49(7): 1066-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816902&dopt=Abstract
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Seasonal variations in the onset of childhood leukemia/lymphoma: April 1996 to March 2000, Shiraz, Iran. Author(s): Karimi M, Yarmohammadi H. Source: Hematological Oncology. 2003 June; 21(2): 51-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802809&dopt=Abstract
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Secondary myelodysplastic syndrome after treatment for promyelocytic leukemia: clinical and genetic features of two cases. Author(s): Panizo C, Patino A, Lecumberri R, Calasanz MJ, Odero MD, Bendandi M, Rocha E. Source: Cancer Genetics and Cytogenetics. 2003 June; 143(2): 178-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781455&dopt=Abstract
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Secondary myelodysplastic syndrome and leukemia following 131Imetaiodobenzylguanidine therapy for relapsed neuroblastoma. Author(s): Weiss B, Vora A, Huberty J, Hawkins RA, Matthay KK. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 July; 25(7): 543-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847321&dopt=Abstract
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Selection of oligonucleotide aptamers with enhanced uptake and activation of human leukemia B cells. Author(s): Wu CC, Castro JE, Motta M, Cottam HB, Kyburz D, Kipps TJ, Corr M, Carson DA. Source: Human Gene Therapy. 2003 June 10; 14(9): 849-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828856&dopt=Abstract
172 Leukemia
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Selective cytotoxic mechanism of GTP-14564, a novel tyrosine kinase inhibitor in leukemia cells expressing a constitutively active Fms-like tyrosine kinase 3 (FLT3). Author(s): Murata K, Kumagai H, Kawashima T, Tamitsu K, Irie M, Nakajima H, Suzu S, Shibuya M, Kamihira S, Nosaka T, Asano S, Kitamura T. Source: The Journal of Biological Chemistry. 2003 August 29; 278(35): 32892-8. Epub 2003 June 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12815052&dopt=Abstract
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Serial minimal residual disease (MRD) analysis as a predictor of response duration in Philadelphia-positive acute lymphoblastic leukemia (Ph+ALL) during imatinib treatment. Author(s): Scheuring UJ, Pfeifer H, Wassmann B, Bruck P, Gehrke B, Petershofen EK, Gschaidmeier H, Hoelzer D, Ottmann OG. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1700-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970767&dopt=Abstract
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Severe megakaryocytic dysplasia in a case of myelodysplasia progressing to acute megakaryocytic leukemia presenting with dic(1;16)(q21;p13.3) and t(1;22)(p13;q13). Author(s): Ghosh K, Vundinti BR, Kerketta L, Madkaikar M, Mohanty D, Jijina F. Source: Cancer Genetics and Cytogenetics. 2003 October 15; 146(2): 176-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14553955&dopt=Abstract
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Simple rules underlying gene expression profiles of more than six subtypes of acute lymphoblastic leukemia (ALL) patients. Author(s): Li J, Liu H, Downing JR, Yeoh AE, Wong L. Source: Bioinformatics (Oxford, England). 2003 January; 19(1): 71-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499295&dopt=Abstract
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Simultaneous novel BCR-ABL gene mutation and increased expression of BCR-ABL mRNA caused clinical resistance to STI571 in double-Ph-positive acute biphenotypic leukemia. Author(s): Inami M, Inokuchi K, Nakayama K, Tamura H, Shimada T, Dan K. Source: International Journal of Hematology. 2003 August; 78(2): 173-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953816&dopt=Abstract
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Simultaneous occurrence of chronic myeloid leukemia and multiple myeloma: evaluation by FISH analysis and in vitro expansion of bone marrow cells. Author(s): Schwarzmeier JD, Shehata M, Ackermann J, Hilgarth M, Kaufmann H, Drach J. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1426-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835740&dopt=Abstract
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Size and composition of T-cell receptor delta (TCRD) junctional sequences are not predictive of the sensitivity of clonospecific oligonucleotides designed for detection of minimal residual disease in acute lymphoblastic leukemia. Author(s): Seriu T, Stark Y, Erz D, Bartram CR. Source: International Journal of Hematology. 2003 May; 77(4): 371-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774926&dopt=Abstract
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Slower molecular response to treatment predicts poor outcome in patients with TEL/AML1 positive acute lymphoblastic leukemia: prospective real-time quantitative reverse transcriptase-polymerase chain reaction study. Author(s): Madzo J, Zuna J, Muzikova K, Kalinova M, Krejci O, Hrusak O, Otova B, Stary J, Trka J. Source: Cancer. 2003 January 1; 97(1): 105-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12491511&dopt=Abstract
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Small-molecule inhibitors of signal transduction pathways in leukemia therapeutics: how to assess selectivity for malignant signals. Author(s): White MK. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1759-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970775&dopt=Abstract
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Soluble hepatocyte growth factor (sHGF) and vascular endothelial growth factor (sVEGF) in adult acute myeloid leukemia: relationship to disease characteristics. Author(s): Aref S, Mabed M, Sakrana M, Goda T, El-Sherbiny M. Source: Hematology (Amsterdam, Netherlands). 2002 October; 7(5): 273-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850814&dopt=Abstract
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Specific protein redirection as a transcriptional therapy approach for t(8;21) leukemia. Author(s): Steffen B, Serve H, Berdel WE, Agrawal S, Linggi B, Buchner T, Hiebert SW, Muller-Tidow C. Source: Proceedings of the National Academy of Sciences of the United States of America. 2003 July 8; 100(14): 8448-53. Epub 2003 June 20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12819347&dopt=Abstract
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Splenic histopathological patterns in chronic myelomonocytic leukemia with clinical correlations: reinforcement of the heterogeneity of the syndrome. Author(s): Steensma DP, Tefferi A, Li CY. Source: Leukemia Research. 2003 September; 27(9): 775-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804634&dopt=Abstract
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Spontaneous death of bone marrow and peripheral blood cells during remission of acute lymphoblastic leukemia in children. Author(s): Kaznacheev KS, Vladimirskaya EB. Source: Bulletin of Experimental Biology and Medicine. 2002 November; 134(5): 474-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802456&dopt=Abstract
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Src family kinase-independent signal transduction and gene induction by leukemia inhibitory factor. Author(s): Laszlo GS, Nathanson NM. Source: The Journal of Biological Chemistry. 2003 July 25; 278(30): 27750-7. Epub 2003 May 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764151&dopt=Abstract
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Stenotrophomonas maltophilia infection related mortality during induction in childhood acute lymphoblastic leukemia. Author(s): Abbas AA, Fryer CJ, Felimban SK, Yousef AA, Fayea NY, Osoba O. Source: Medical and Pediatric Oncology. 2003 July; 41(1): 93-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764762&dopt=Abstract
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Successful reduced-intensity stem cell transplantation from an HLA haploidentical 3loci-mismatched donor on the basis of fetomaternal microchimerism in a patient with advanced acute myeloid leukemia. Author(s): Uoshima N, Kamitsuji Y, Maruya E, Saji H. Source: International Journal of Hematology. 2003 July; 78(1): 69-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894854&dopt=Abstract
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Sudden onset of the blastic phase of chronic myelogenous leukemia: patterns and implications. Author(s): Kantarjian H, O'Brien S, Cortes J, Giles F, Thomas D, Kornblau S, Shan J, Beth Rios M, Keating M, Freireich E, Talpaz M. Source: Cancer. 2003 July 1; 98(1): 81-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12833459&dopt=Abstract
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Suppression of leukemia inhibitor factor in lymphoid tissue in primary HIV infection: absence of HIV replication in gp130-positive cells. Author(s): Tjernlund A, Fleener Z, Behbahani H, Connick E, Sonnerborg A, Brostrom C, Goh LE, Spetz AL, Patterson BK, Andersson J. Source: Aids (London, England). 2003 June 13; 17(9): 1303-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12799551&dopt=Abstract
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Survival variability by race and ethnicity in childhood acute lymphoblastic leukemia. Author(s): Kadan-Lottick NS, Ness KK, Bhatia S, Gurney JG. Source: Jama : the Journal of the American Medical Association. 2003 October 15; 290(15): 2008-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14559954&dopt=Abstract
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Survival-weighted health profile for long-term survivors of acute myelogenous leukemia. Author(s): Hsu C, Wang JD, Hwang JS, Tien HF, Chang SM, Cheng AL, Chen YC, Tang JL. Source: Quality of Life Research : an International Journal of Quality of Life Aspects of Treatment, Care and Rehabilitation. 2003 August; 12(5): 503-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13677495&dopt=Abstract
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Susceptibility of human T cell leukemia virus type I to nucleoside reverse transcriptase inhibitors. Author(s): Hill SA, Lloyd PA, McDonald S, Wykoff J, Derse D. Source: The Journal of Infectious Diseases. 2003 August 1; 188(3): 424-7. Epub 2003 July 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870124&dopt=Abstract
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t(4;11)(q21;p15), including one complex translocation t(1;4;11)(p32;q21;p15), in adult Tcell acute lymphoblastic leukemia. Author(s): Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Le Calvez G, Marion V, Berthou C, De Braekeleer M. Source: Leukemia Research. 2003 October; 27(10): 965-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860018&dopt=Abstract
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t(5;14)/HOX11L2-positive T-cell acute lymphoblastic leukemia. A collaborative study of the Groupe Francais de Cytogenetique Hematologique (GFCH). Author(s): Berger R, Dastugue N, Busson M, Van Den Akker J, Perot C, Ballerini P, Hagemeijer A, Michaux L, Charrin C, Pages MP, Mugneret F, Andrieux J, Talmant P, Helias C, Mauvieux L, Lafage-Pochitaloff M, Mozziconacci MJ, Cornillet-Lefebvre P, Radford I, Asnafi V, Bilhou-Nabera C, Nguyen Khac F, Leonard C, Speleman F, Poppe B, Bastard C, Taviaux S, Quilichini B, Herens C, Gregoire MJ, Cave H, Bernard OA; Groupe Francais de Cytogenetique Hematologique (GFCH). Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1851-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970786&dopt=Abstract
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Tamoxifen inhibits arylamine N-acetyltransferase activity and DNA-2-aminofluorene adduct in human leukemia HL-60 cells. Author(s): Lu KH, Lin KL, Hsia TC, Hung CF, Chou MC, Hsiao YM, Chung JG. Source: Res Commun Mol Pathol Pharmacol. 2001; 109(5-6): 319-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12889515&dopt=Abstract
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T-cell large granular lymphocyte leukemia of donor origin after allogeneic bone marrow transplantation. Author(s): Au WY, Lam CC, Lie AK, Pang A, Kwong YL. Source: American Journal of Clinical Pathology. 2003 October; 120(4): 626-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14560574&dopt=Abstract
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T-cell receptor/CD28 engagement when combined with prostaglandin E2 treatment leads to potent activation of human T-cell leukemia virus type 1. Author(s): Dumais N, Pare ME, Mercier S, Bounou S, Marriot SJ, Barbeau B, Tremblay MJ. Source: Journal of Virology. 2003 October; 77(20): 11170-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512564&dopt=Abstract
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Telomere length in peripheral blood granulocytes reflects response to treatment with imatinib in patients with chronic myeloid leukemia. Author(s): Brummendorf TH, Ersoz I, Hartmann U, Bartolovic K, Balabanov S, Wahl A, Paschka P, Kreil S, Lahaye T, Berger U, Gschaidmeier H, Bokemeyer C, Hehlmann R, Dietz K, Lansdorp PM, Kanz L, Hochhaus A. Source: Blood. 2003 January 1; 101(1): 375-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12485943&dopt=Abstract
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Tetraploid acute promyelocytic leukemia with double t(15;17) and PML/RARA rearrangements detected by fluorescence in situ hybridization analysis. Author(s): Oh SH, Park TS, Kim HH, Chang CL, Lee EY, Son HC, Chung JS, Cho GJ. Source: Cancer Genetics and Cytogenetics. 2003 August; 145(1): 49-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885462&dopt=Abstract
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The angioregulatory phenotype of native human acute myelogenous leukemia cells: influence of karyotype, Flt3 abnormalities and differentiation status. Author(s): Glenjen N, Hovland R, Wergeland L, Wendelbo O, Ernst P, Bruserud O. Source: European Journal of Haematology. 2003 September; 71(3): 163-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930316&dopt=Abstract
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The ATRX syndrome protein forms a chromatin-remodeling complex with Daxx and localizes in promyelocytic leukemia nuclear bodies. Author(s): Xue Y, Gibbons R, Yan Z, Yang D, McDowell TL, Sechi S, Qin J, Zhou S, Higgs D, Wang W. Source: Proceedings of the National Academy of Sciences of the United States of America. 2003 September 16; 100(19): 10635-40. Epub 2003 Sep 02. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953102&dopt=Abstract
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The biology and therapy of adult acute lymphoblastic leukemia. Author(s): Faderl S, Jeha S, Kantarjian HM. Source: Cancer. 2003 October 1; 98(7): 1337-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508819&dopt=Abstract
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The circulating dendritic cell compartment in patients with chronic lymphocytic leukemia is severely defective and unable to stimulate an effective T-cell response. Author(s): Orsini E, Guarini A, Chiaretti S, Mauro FR, Foa R. Source: Cancer Research. 2003 August 1; 63(15): 4497-506. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907623&dopt=Abstract
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The clinical significance of soluble CD86 levels in patients with acute myeloid leukemia and myelodysplastic syndrome. Author(s): Hock BD, McKenzie JL, Patton WN, Haring LF, Yang Y, Shen Y, Estey EH, Albitar M. Source: Cancer. 2003 October 15; 98(8): 1681-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14534885&dopt=Abstract
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The emergence of Ph-, trisomy -8+ cells in patients with chronic myeloid leukemia treated with imatinib mesylate. Author(s): Feldman E, Najfeld V, Schuster M, Roboz G, Chadburn A, Silver RT. Source: Experimental Hematology. 2003 August; 31(8): 702-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901975&dopt=Abstract
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The fusion protein AML1-ETO in acute myeloid leukemia with translocation t(8;21) induces c-jun protein expression via the proximal AP-1 site of the c-jun promoter in an indirect, JNK-dependent manner. Author(s): Elsasser A, Franzen M, Kohlmann A, Weisser M, Schnittger S, Schoch C, Reddy VA, Burel S, Zhang DE, Ueffing M, Tenen DG, Hiddemann W, Behre G. Source: Oncogene. 2003 August 28; 22(36): 5646-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12944913&dopt=Abstract
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The graft-versus-leukemia effect in leukemia cutis. Author(s): Wong R, Couriel D, Prieto VG. Source: Transplantation. 2003 August 15; 76(3): 619-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12923456&dopt=Abstract
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The molecular mechanism of arsenic trioxide-induced apoptosis and oncosis in leukemia/lymphoma cell lines. Author(s): Zhu J, Okumura H, Ohtake S, Nakamura S, Nakao S. Source: Acta Haematologica. 2003; 110(1): 1-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975549&dopt=Abstract
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The Moloney murine leukemia virus repressor binding site represses expression in murine and human hematopoietic stem cells. Author(s): Haas DL, Lutzko C, Logan AC, Cho GJ, Skelton D, Jin Yu X, Pepper KA, Kohn DB. Source: Journal of Virology. 2003 September; 77(17): 9439-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915559&dopt=Abstract
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Therapy-related leukemia in mitozantrone treated patients. Author(s): Goodkin DE. Source: Multiple Sclerosis (Houndmills, Basingstoke, England). 2003 August; 9(4): 426. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926850&dopt=Abstract
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Thrombotic complications during induction chemotherapy of acute childhood lymphoblastic leukemia. Author(s): Kankirawatana S, Veerakul G, Sanpakit K, Tanphaichitr VS, Akkabutr P, Suwantol L, Mahasandana C. Source: J Med Assoc Thai. 2002 August; 85 Suppl 2: S549-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12403231&dopt=Abstract
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Ticarcillin-clavulanic acid plus amikacin versus ceftazidime plus amikacin in the empirical treatment of fever in acute leukemia: a prospective randomized trial. Author(s): Fanci R, Paci C, Leoni F, Casini C, Longo G. Source: Journal of Chemotherapy (Florence, Italy). 2003 June; 15(3): 253-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12868552&dopt=Abstract
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Translocation (8;20), a variant of t(8;21), in T-acute lymphoblastic leukemia: a first report. Author(s): Amare PS, Pais A, Nair C, Banavali S, Advani SH. Source: Cancer Genetics and Cytogenetics. 2003 August; 145(1): 88-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885471&dopt=Abstract
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Transmission of chronic myeloid leukemia through peripheral-blood stem-cell transplantation. Author(s): Baron F, Dresse MF, Beguin Y. Source: The New England Journal of Medicine. 2003 August 28; 349(9): 913-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12944584&dopt=Abstract
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Transplantation of marrow cells from children with standard risk-acute lymphoblastic leukemia at the end of therapy into NOD/SCID mice for detecting residual leukemic cells with in vivo growth potential. Author(s): Ramirez M, Diaz MA, Madero L, Bueren JA. Source: Leukemia Research. 2003 December; 27(12): 1153-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921954&dopt=Abstract
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Transplantation of peripheral blood stem cells as compared with bone marrow from HLA-identical siblings in adult patients with acute myeloid leukemia and acute lymphoblastic leukemia. Author(s): Ringden O, Labopin M, Bacigalupo A, Arcese W, Schaefer UW, Willemze R, Koc H, Bunjes D, Gluckman E, Rocha V, Schattenberg A, Frassoni F. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 15; 20(24): 4655-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488410&dopt=Abstract
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Treatment of acute promyelocytic leukemia and other hematologic malignancies with arsenic trioxide: review of clinical and basic studies. Author(s): Liu P, Han ZC. Source: International Journal of Hematology. 2003 July; 78(1): 32-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894848&dopt=Abstract
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Treatment of chronic lymphocytic leukemia with alemtuzumab: a review for nurses. Author(s): Lynn A, Williams ML, Sickler J, Burgess S. Source: Oncology Nursing Forum. 2003 July-August; 30(4): 689-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861328&dopt=Abstract
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Trends in survival rates after allogeneic hematopoietic stem-cell transplantation for acute and chronic leukemia by ethnicity in the United States and Canada. Author(s): Serna DS, Lee SJ, Zhang MJ, Baker S, Eapen M, Horowitz MM, Klein JP, Rizzo JD, Loberiza FR Jr. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 October 15; 21(20): 3754-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14551294&dopt=Abstract
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Trisomy 6 acquired in lymphoid blast transformation of chronic myelocytic leukemia with t(9;22). Author(s): Yilmaz Y, Klein R, Qumsiyeh MB. Source: Cancer Genetics and Cytogenetics. 2003 August; 145(1): 86-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885470&dopt=Abstract
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Tryptase-positive mast cells predict clinical outcome of patients with early B-cell chronic lymphocytic leukemia. Author(s): Molica S, Vacca A, Crivellato E, Cuneo A, Ribatti D. Source: European Journal of Haematology. 2003 August; 71(2): 137-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890156&dopt=Abstract
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Two distinct gene expression signatures in pediatric acute lymphoblastic leukemia with MLL rearrangements. Author(s): Tsutsumi S, Taketani T, Nishimura K, Ge X, Taki T, Sugita K, Ishii E, Hanada R, Ohki M, Aburatani H, Hayashi Y. Source: Cancer Research. 2003 August 15; 63(16): 4882-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941810&dopt=Abstract
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Ubiquinone does not rescue acute myeloid leukemia cells from growth inhibition by statins. Author(s): Burke LP, Lewis LD, Perez RP. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 January; 17(1): 267-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529692&dopt=Abstract
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UCN-01 (7-hydroxystauorsporine) blocks PMA-induced maturation and reciprocally promotes apoptosis in human myelomonocytic leukemia cells (U937). Author(s): Rahmani M, Grant S. Source: Cell Cycle (Georgetown, Tex.). 2002 July-August; 1(4): 273-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12429947&dopt=Abstract
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UCN-01 (7-hydroxystaurosporine) inhibits DNA repair and increases cytotoxicity in normal lymphocytes and chronic lymphocytic leukemia lymphocytes. Author(s): Yamauchi T, Keating MJ, Plunkett W. Source: Molecular Cancer Therapeutics. 2002 February; 1(4): 287-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12467224&dopt=Abstract
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Uncommon syndromes and treatment manifestations of malignancy: Case 4. Periorbital edema and imatinib mesylate therapy for chronic myelogenous leukemia. Author(s): Ramar K, Potti A, Mehdi SA. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 January 1; 21(1): 172-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12506189&dopt=Abstract
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Unmutated immunoglobulin variable heavy-chain gene status remains an adverse prognostic factor after autologous stem cell transplantation for chronic lymphocytic leukemia. Author(s): Ritgen M, Lange A, Stilgenbauer S, Dohner H, Bretscher C, Bosse H, Stuhr A, Kneba M, Dreger P. Source: Blood. 2003 March 1; 101(5): 2049-53. Epub 2002 October 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12411304&dopt=Abstract
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Unrelated donor bone marrow transplantation for acute mixed lineage (myeloid and B-lymphoid lineage) leukemia in an adult with Down syndrome. Author(s): Takagi K, Yoshida A, Kinoshita K, Iwashima D, Imamaura S, Iwasaki H, Tsutani H, Ueda T. Source: Annals of Hematology. 2003 April; 82(4): 236-40. Epub 2003 March 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707727&dopt=Abstract
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Unrelated donor stem cell transplantation compared with chemotherapy for children with acute lymphoblastic leukemia in a second remission: a matched-pair analysis. Author(s): Borgmann A, von Stackelberg A, Hartmann R, Ebell W, Klingebiel T, Peters C, Henze G; Berlin-Frankfurt-Munster Relapse Study Group. Source: Blood. 2003 May 15; 101(10): 3835-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12732501&dopt=Abstract
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Unusual karyotype aberrations involving 2p12, 3q27, 18q21, 8q24, and 14q32 in a patient with non-Hodgkin lymphoma/acute lymphoblastic leukemia. Author(s): Okhowat R, Dorner S, Hinterberger W, Fonatsch C. Source: Cancer Genetics and Cytogenetics. 2003 April 1; 142(1): 60-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12660035&dopt=Abstract
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Unusual manifestation of specific cutaneous involvement by B-cell chronic lymphocytic leukemia: spontaneous regression with scar formation. Author(s): Kazakov DV, Belousova IE, Michaelis S, Palmedo G, Samtsov AV, Kempf W. Source: Dermatology (Basel, Switzerland). 2003; 207(1): 111-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835570&dopt=Abstract
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Unusual skin lesions in chronic myelomonocytic leukemia. Author(s): McCollum A, Bigelow CL, Elkins SL, Hardy CL, Files JC. Source: Southern Medical Journal. 2003 July; 96(7): 681-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12940320&dopt=Abstract
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Unusually indolent T-cell prolymphocytic leukemia associated with a complex karyotype: is this T-cell chronic lymphocytic leukemia? Author(s): Soma L, Cornfield DB, Prager D, Nowell P, Bagg A. Source: American Journal of Hematology. 2002 November; 71(3): 224-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12410582&dopt=Abstract
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Update in childhood acute myeloid leukemia: recent developments in the molecular basis of disease and novel therapies. Author(s): Clark JJ, Smith FO, Arceci RJ. Source: Current Opinion in Hematology. 2003 January; 10(1): 31-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12483109&dopt=Abstract
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Uranium and other natural radionuclides in drinking water and risk of leukemia: a case-cohort study in Finland. Author(s): Auvinen A, Kurttio P, Pekkanen J, Pukkala E, Ilus T, Salonen L. Source: Cancer Causes & Control : Ccc. 2002 November; 13(9): 825-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12462547&dopt=Abstract
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Urolithiasis in pediatric patients with acute lymphoblastic leukemia. Author(s): Howard SC, Kaplan SD, Razzouk BI, Rivera GK, Sandlund JT, Ribeiro RC, Rubnitz JE, Gajjar AJ, Ke W, Hancock ML, Skoch JP, Roy S, Hudson M, Pui CH. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 March; 17(3): 541-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12646942&dopt=Abstract
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Urologic manifestations of hematologic disease sickle cell, leukemia, and thromboembolic disease. Author(s): Molitierno JA Jr, Carson CC 3rd. Source: The Urologic Clinics of North America. 2003 February; 30(1): 49-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580557&dopt=Abstract
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Use of arsenic trioxide (As2O3) in the treatment of patients with acute promyelocytic leukemia: the M. D. Anderson experience. Author(s): Lazo G, Kantarjian H, Estey E, Thomas D, O'Brien S, Cortes J. Source: Cancer. 2003 May 1; 97(9): 2218-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712474&dopt=Abstract
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Use of radiolabeled antibodies in the treatment of childhood acute leukemia. Author(s): Nemecek ER, Matthews DC. Source: Pediatric Transplantation. 2003; 7 Suppl 3: 89-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12603700&dopt=Abstract
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Utility of a prognostic scoring system for allogeneic stem cell transplantation in patients with chronic myeloid leukemia. Author(s): Qazilbash MH, Devetten MP, Abraham J, Lynch JP, Beall CL, Weisenborn R, Bunner P, Ericson SG. Source: Acta Haematologica. 2003; 109(3): 119-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714820&dopt=Abstract
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Vaccination of chronic myeloid leukemia patients with autologous in vitro cultured leukemic dendritic cells. Author(s): Ossenkoppele GJ, Stam AG, Westers TM, de Gruijl TD, Janssen JJ, van de Loosdrecht AA, Scheper RJ. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1424-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835739&dopt=Abstract
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Validation and clinical implication of a quantitative real-time PCR determination of MDR1 gene expression: comparison with semi-quantitative PCR in 101 patients with acute myeloid leukemia. Author(s): Olesen LH, Norgaard JM, Pallisgaard N, Bukh A, Hokland P. Source: European Journal of Haematology. 2003 May; 70(5): 296-303. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694165&dopt=Abstract
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Value of combined morphologic, cytochemical, and immunophenotypic features in predicting recurrent cytogenetic abnormalities in acute myeloid leukemia. Author(s): Arber DA, Carter NH, Ikle D, Slovak ML. Source: Human Pathology. 2003 May; 34(5): 479-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12792922&dopt=Abstract
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Variations in MLL amplification in a patient with acute myeloid leukemia. Author(s): Brezinova J, Zemanova Z, Cermak J, Kurkova S, Sindelarova L, Schwarz J, Michalova K. Source: Leukemia & Lymphoma. 2002 October; 43(10): 2031-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12481904&dopt=Abstract
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Vasculitis associated with all trans retinoic acid (ATRA) in a case with acute promyelocytic leukemia. Author(s): Paydas S, Yavuz S, Disel U, Sahin B, Canbolat T, Tuncer I. Source: Leukemia & Lymphoma. 2003 March; 44(3): 547-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688331&dopt=Abstract
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Voriconazole treatment of presumptive disseminated Aspergillus infection in a child with acute leukemia. Author(s): Shouldice E, Fernandez C, McCully B, Schmidt M, Fraser R, Cook C. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 September; 25(9): 732-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12972810&dopt=Abstract
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Wilms tumor gene peptide-based immunotherapy for patients with overt leukemia from myelodysplastic syndrome (MDS) or MDS with myelofibrosis. Author(s): Oka Y, Tsuboi A, Murakami M, Hirai M, Tominaga N, Nakajima H, Elisseeva OA, Masuda T, Nakano A, Kawakami M, Oji Y, Ikegame K, Hosen N, Udaka K, Yasukawa M, Ogawa H, Kawase I, Sugiyama H. Source: International Journal of Hematology. 2003 July; 78(1): 56-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894852&dopt=Abstract
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Work-related acute leukemia and mucor mycosis in a boat-builder. Author(s): Magnavita N, Placentino RA, Chiusolo P, Fiorini A, Laurenti L, Sica S. Source: Haematologica. 2002 December; 87(12): Ecr42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553331&dopt=Abstract
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WT1 in acute leukemia, chronic myelogenous leukemia and myelodysplastic syndrome: therapeutic potential of WT1 targeted therapies. Author(s): Rosenfeld C, Cheever MA, Gaiger A. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1301-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835718&dopt=Abstract
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WT1 mRNA in cerebrospinal fluid associated with relapse in pediatric lymphoblastic leukemia. Author(s): Ramirez O, Linares A, Trujillo ML, Caminos JE. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 June; 25(6): 453-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794523&dopt=Abstract
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ZAP-70 expression as a surrogate for immunoglobulin-variable-region mutations in chronic lymphocytic leukemia. Author(s): Crespo M, Bosch F, Villamor N, Bellosillo B, Colomer D, Rozman M, Marce S, Lopez-Guillermo A, Campo E, Montserrat E. Source: The New England Journal of Medicine. 2003 May 1; 348(18): 1764-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724482&dopt=Abstract
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ZAP-70 in chronic lymphocytic leukemia. Author(s): Murashige N, Kami M, Takaue Y. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 506-7; Author Reply 506-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890853&dopt=Abstract
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Zinc modulates c-Myc/Mad1 balance in human leukemia cells. Author(s): Sirinian MI, Pisegna S, Paroli M, Militi S, Testa U, Peschle C. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 January; 17(1): 272-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529695&dopt=Abstract
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CHAPTER 2. NUTRITION AND LEUKEMIA Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and leukemia.
Finding Nutrition Studies on Leukemia The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “leukemia” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7
Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following is a typical result when searching for recently indexed consumer information on leukemia: ·
7-hydroxystaurosporine (UCN-01) and ionizing radiation combine to inhibit the growth of Bcl-2-overexpressing U937 leukemia cells through a non-apoptotic mechanism. Author(s): Department of Medicine, Virginia Commonwealth University, Medical College of Virginia, Richmond, VA 23298, USA. Source: Cartee, L Sankala, H Davis, C Smith, R Maggio, S Lin, P S Dent, P Grant, S Int-JOncol. 2002 August; 21(2): 351-9 1019-6439
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A mathematical model of in vivo methotrexate accumulation in acute lymphoblastic leukemia. Author(s): St. Jude Children's Research Hospital, 332 North Lauderdale St., Memphis, TN 38105-2794, USA. Source: Panetta, J C Yanishevski, Y Pui, C H Sandlund, J T Rubnitz, J Rivera, G K Ribeiro, R Evans, W E Relling, M V Cancer-Chemother-Pharmacol. 2002 November; 50(5): 419-28 0344-5704
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A phase I and pharmacodynamic study of sequential topotecan and etoposide in patients with relapsed or refractory acute myelogenous and lymphoblastic leukemia. Author(s): Department of Medicine, University Hospitals of Cleveland, Cleveland, OH 44106, USA.
[email protected] Source: Cooper, B W Donaher, E Lazarus, H M Green, S B Gosky, D M Rosenthal, N S Berger, S J Li, X Ingalls, S T Hoppel, C L Gerson, S L Leuk-Res. 2003 January; 27(1): 35-44 0145-2126
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AML1 amplification in a child with acute lymphoblastic leukemia. Author(s): Departamento de Biologi;a Animal, Biologi;a Vegetal y Ecologi;a, Unidad de Antropologi;a, Facultad de Ciencias, Universidad Autonoma de Barcelona, Barcelona, Spain.
[email protected] Source: Alvarez, Y Coll, M D Bastida, P Ortega, J J Caballin, M R Cancer-GenetCytogenet. 2003 January 1; 140(1): 58-61 0165-4608
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Anti-leukemia effect of resveratrol. Author(s): Office of Research Compliance and Assurance, Department of Veterans Affairs, Washington, DC 20422, USA.
[email protected] Source: Tsan, M F White, J E Maheshwari, J G Chikkappa, G Leuk-Lymphoma. 2002 May; 43(5): 983-7 1042-8194
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Apoptosis of HL-60 leukemia cells induced by the bisindole alkaloids sungucine and isosungucine from Strychnos icaja. Author(s): INSERM U-524 et Centre Oscar Lambret, Lille, France. Source: Lansiaux, A Bailly, C Houssier, C Colson, P De Pauw Gillet, M C Frederich, M Tits, M Angenot, L Planta-Med. 2002 July; 68(7): 591-5 0032-0943
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Approval summary for imatinib mesylate capsules in the treatment of chronic myelogenous leukemia. Author(s): Division Oncology Drug Products, Center for Drug Evaluation and Research, Food and Drug Administration, Rockville, Maryland 20857, USA.
[email protected] Source: Cohen, M H Williams, G Johnson, J R Duan, J Gobburu, J Rahman, A Benson, K Leighton, J Kim, S K Wood, R Rothmann, M Chen, G U, K M Staten, A M Pazdur, R Clin-Cancer-Res. 2002 May; 8(5): 935-42 1078-0432
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Arginine butyrate increases the cytotoxicity of DAB(389)IL-2 in leukemia and lymphoma cells by upregulation of IL-2Rbeta gene. Author(s): Hematology-Oncology Department, New England Medical Center, Tufts University, Boston, MA, USA. Source: Shao, R H Tian, X Gorgun, G Urbano, A G Foss, F M Leuk-Res. 2002 December; 26(12): 1077-83 0145-2126
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Arsenic trioxide as effective therapy for relapsed acute promyelocytic leukemia. Author(s):
[email protected] Source: Mayorga, J Richardson Hardin, C Dicke, K A Clin-J-Oncol-Nurs. 2002 NovDecember; 6(6): 341-6 1092-1095
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Atypical t(15;17)(q13;q12) in a patient with all-trans retinoic acid refractory secondary acute promyelocytic leukemia: a case report and review of the literature. Author(s): Department of Medicine, West Virginia University, Morgantown, WV 26506, USA. Source: Kurian, S Hogan, T F Bleigh, O C Dowdy, Y G Merghoub, T Pandolfi, P P Wenger, S L Cancer-Genet-Cytogenet. 2002 October 15; 138(2): 143-8 0165-4608
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Automated analysis of differentiation-induced leukemic cells during all-trans retinoic Acid therapy of acute promyelocytic leukemia. Author(s): Department of Laboratory Medicine and Central Clinical Laboratory, Kyoto University Hospital, Kyoto, Japan.
[email protected] Source: Tohyama, K Shiga, S Fujimoto, H Hamaguchi, Y Ichiyama, S Arch-Pathol-LabMed. 2003 January; 127(1): e4-10 1543-2165
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Beta-hydroxyisovalerylshikonin induces apoptosis in human leukemia cells by inhibiting the activity of a polo-like kinase 1 (PLK1). Author(s): Laboratory of Biological Chemistry, School of Pharmaceutical Sciences, Showa University, Tokyo 142-8555, Japan. Source: Masuda, Y Nishida, A Hori, K Hirabayashi, T Kajimoto, S Nakajo, S Kondo, T Asaka, M Nakaya, K Oncogene. 2003 February 20; 22(7): 1012-23 0950-9232
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Biomic study of human myeloid leukemia cells differentiation to macrophages using DNA array, proteomic, and bioinformatic analytical methods. Author(s): Institute of Biological Chemistry, Academia Sinica, Taipei, Taiwan. Source: Juan, H F Lin, J Y Chang, W H Wu, C Y Pan, T L Tseng, M J Khoo, K H Chen, S T Electrophoresis. 2002 August; 23(15): 2490-504 0173-0835
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Bone mineral assessment with tibial ultrasonometry and dual-energy X-ray absorptiometry in long-term survivors of acute lymphoblastic leukemia in childhood. Author(s): Department of Pediatric Radiology, Sophia Children's Hospital, Rotterdam, The Netherlands.
[email protected] Source: Lequin, M H van der Shuis, I M Van Rijn, R R Hop, W C van ven Huevel Eibrink, M M MuinckKeizer Schrama, S M van Kuijk, C J-Clin-Densitom. 2002 Summer; 5(2): 167-73 1094-6950
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Characterization of a monoclonal antibody specific for a novel primate cell surface marker with distinct biochemical properties on human erythroleukemia and myeloid cell lines. Author(s): The John P. Robarts Research Institute, and Department of Microbiology and Immunology, The University of Western Ontario, London, Ontario, N6G 2V4 Canada. Source: Chang, C S McFadden, G Hybrid-Hybridomics. 2002 August; 21(4): 271-80 15368599
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Combretastatin-A4 prodrug induces mitotic catastrophe in chronic lymphocytic leukemia cell line independent of caspase activation and poly(ADP-ribose) polymerase cleavage. Author(s): Division of Hematology and Oncology, Department of Internal Medicine, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan 48201, USA. Source: Nabha, S M Mohammad, R M Dandashi, M H Coupaye Gerard, B Aboukameel, A Pettit, G R Al Katib, A M Clin-Cancer-Res. 2002 August; 8(8): 2735-41 1078-0432
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Composite mycosis fungoides and B-cell chronic lymphocytic leukemia. Author(s): Department of Pathology, The University of Alabama at Birmingham, AL 35233-7331, USA. Source: Volk, A L Vannucci, S A Cook, W Thompson, K A Listinsky, C M Ann-DiagnPathol. 2002 June; 6(3): 172-82 1092-9134
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Cotylenin A--a plant growth regulator as a differentiation-inducing agent against myeloid leukemia. Author(s): Saitama Cancer Center Research Institute, Ina, Japan.
[email protected] Source: Honma, Y Leuk-Lymphoma. 2002 June; 43(6): 1169-78 1042-8194
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Cryptic translocation of PML/RARA on 17q. A rare event in acute promyelocytic leukemia. Author(s): Hematology Unit, Santa Maria delle Croci Hospital, Viale Randi 5, 48100, Ravenna, Italy. Source: Zaccaria, A Valenti, A Toschi, M Salvucci, M Cipriani, R Ottaviani, E Martinelli, G Cancer-Genet-Cytogenet. 2002 October 15; 138(2): 169-73 0165-4608
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Dental abnormalities in children after chemotherapy treatment for acute lymphoid leukemia. Author(s): Department of Pathology, School of Medicine of Botucatu, Sao Paulo State University, SP, Sao Paulo, Brazil.
[email protected] Source: Minicucci, E M Lopes, L F Crocci, A J Leuk-Res. 2003 January; 27(1): 45-50 01452126
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Diol- and triol-types of phytol induce apoptosis in lymphoid leukemia Molt 4B cells. Author(s): Faculty of Medicine, Mie University, Tsu-city, Mie 514-0001, Japan. Source: Hibasami, H Kyohkon, M Owaki, S Katsuzaki, H Imai, K Ohnishi, K Ina, K Komiya, T Int-J-Mol-Med. 2002 November; 10(5): 555-9 1107-3756
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DNA methylation of multiple promoter-associated CpG islands in adult acute lymphocytic leukemia. Author(s): Departments of Leukemia, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
[email protected] Source: Garcia Manero, G Daniel, J Smith, T L Kornblau, S M Lee, M S Kantarjian, H M Issa, J P Clin-Cancer-Res. 2002 July; 8(7): 2217-24 1078-0432
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Effects of flavonoids on cisplatin-induced apoptosis of HL-60 and L1210 leukemia cells. Author(s): Cancer Research Institute, Vlarska 7, 833 91, Bratislava, Slovak Republic. Source: Cipak, L Rauko, P Miadokova, E Cipakova, I Novotny, L Leuk-Res. 2003 January; 27(1): 65-72 0145-2126
Nutrition 191
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Enhancement of sensitivity by bestatin of acute promyelocytic leukemia NB4 cells to all-trans retinoic acid. Author(s): Department of Applied Chemistry, Faculty of Science and Technology, Keio University, Yokohama, Japan. Source: Hirano, T Kizaki, M Kato, K Abe, F Masuda, N Umezawa, K Leuk-Res. 2002 December; 26(12): 1097-103 0145-2126
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In vitro comparative antileukemic activity of various glucocorticoids in childhood acute leukemia. Author(s): Department of Pediatric Hematology and Oncology; Medical University Bydgoszcz, Bydgoszcz, 85-094 Poland.
[email protected] Source: Styczynski, J Wysocki, M Balwierz, W Rokicka Milewska, R Matysiak, M Balcerska, A Kowalczyk, A Wachowiak, J Sonta Jakimczyk, D Chybicka, A Neoplasma. 2002; 49(3): 178-83 0028-2685
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Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412. Author(s): Dana-Farber Cancer Institute, Boston, Massachusetts, USA. Source: Weisberg, E Boulton, C Kelly, L M Manley, P Fabbro, D Meyer, T Gilliland, D G Griffin, J D Cancer-Cell. 2002 June; 1(5): 433-43 1535-6108
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Intermedeol isolated from the leaves of Ligularia fischeri var. spiciformis induces the differentiation of human acute promyeocytic leukemia HL-60 Cells. Author(s): Department of Food and Nutrition, Kyung Hee University, Seoul, Korea. Source: Jeong, S H Koo, S J Choi, J H Park, J H Ha, J Park, H J Lee, K T Planta-Med. 2002 October; 68(10): 881-5 0032-0943
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Intermediate doses of melphalan and dexamethasone are better than vincristine, adriamycin, and dexamethasone (VAD) and polychemotherapy for the treatment of primary plasma cell leukemia. Author(s): Department of Hematology, Hospital de Especialidades Centro Medico Nacional La Raza, Instituto Mexicano del Seguro Social, Apartado Postal 14-878, Codigo postal 07001, Mexico D.F., Mexico.
[email protected] Source: Vela Ojeda, J Garcia Ruiz Esparza, M A Rosas Cabral, A Padilla Gonzalez, Y Garcia Chavez, J Tripp Villanueva, F Sanchez Cortes, E Ayala Sanchez, M Garcia Leon, L D Montiel Cervantes, L Rubio Borja, M E Ann-Hematol. 2002 July; 81(7): 362-7 0939-5555
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Loss of heterozygosity of p16 correlates with minimal residual disease at the end of the induction therapy in non-high risk childhood B-cell precursor acute lymphoblastic leukemia. Author(s): Department of Genetics, Hospital de Paraplejicos, Toledo, Spain. Source: Tutor, O Diaz, M A Ramirez, M Algara, P Madero, L Martinez, P Leuk-Res. 2002 September; 26(9): 817-20 0145-2126
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MEK/ERK pathway protects ionizing radiation-induced loss of mitochondrial membrane potential and cell death in lymphocytic leukemia cells. Author(s): Department of Radiology, Sapporo Medical University School of Medicine, S1, W-16, Chuo-ku, Sapporo, 060-8543, Japan. Source: Shonai, T Adachi, M Sakata, K Takekawa, M Endo, T Imai, K Hareyama, M CellDeath-Differ. 2002 September; 9(9): 963-71 1350-9047
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Menadione biphasically controls JNK-linked cell death in leukemia Jurkat T cells. Author(s): Department of Medical Technology, Nagoya University School of Health Sciences, Nagoya 461-8673, Japan. Source: Ma, X Du, J Nakashima, I Nagase, F Antioxid-Redox-Signal. 2002 June; 4(3): 3718 1523-0864
192 Leukemia
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Methotrexate induced seizures associated with acute reversible magnetic resonance imaging (MRI) changes in a patient with acute lymphoblastic leukemia. Author(s): Division of Hematology and Internal Medicine, Rochester, MN 55905, USA. Source: Rao, R D Swanson, J W Dejesus, R S Hunt, C H Tefferi, A Leuk-Lymphoma. 2002 June; 43(6): 1333-6 1042-8194
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Methotrexate intracellular disposition in acute lymphoblastic leukemia: a mathematical model of gamma-glutamyl hydrolase activity. Author(s): Departments of Pharmaceutical Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794, USA. Source: Panetta, J C Wall, A Pui, C H Relling, M V Evans, W E Clin-Cancer-Res. 2002 July; 8(7): 2423-9 1078-0432
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Methotrexate-related neurotoxicity in the treatment of childhood acute lymphoblastic leukemia. Author(s): Department of Pediatric Oncology-Hematology, Schneider Children's Medical Center of Israel, Petah Tiqva, Israel.
[email protected] Source: Shuper, A Stark, B Kornreich, L Cohen, I J Avrahami, G Yaniv, I Isr-Med-AssocJ. 2002 November; 4(11): 1050-3 1565-1088
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Modulation of the phototoxic effect of hypericin in human leukemia CEM cell line by N-ethylmaleimide, amiloride and omeprazole. Author(s): Department of Pharmacology, Medical Faculty, P.J. Safarik University, Tr. SNP 1, 040 66 Kosice, Slovak
[email protected] Source: Mirossay, A Mirossay, L Sarissky, M Papp, P Mojzis, J Physiol-Res. 2002; 51(6): 641-4 0862-8408
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Nutritional support for chronic myelogenous and other leukemias: a review of the scientific literature. Source: Steriti, R Altern-Med-Revolume 2002 October; 7(5): 404-9 1089-5159
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Overexpression of gibbon ape leukemia virus (GALV) receptor (GLVR1) on human CD34(+) cells increases gene transfer mediated by GALV pseudotyped vectors. Author(s): Department of Molecular Medicine and Gene Therapy, University of Lund, Lund, Sweden. Source: Relander, T Brun, A C Olsson, K Pedersen, L Richter, J Mol-Ther. 2002 September; 6(3): 400-6 1525-0016
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Perfusion MRI and SPECT of brain after treatment for childhood acute lymphoblastic leukemia. Author(s): Department of Diagnostic Radiology, University of Oulu, Kajaanintie 50, 90220 Oulu, Finland.
[email protected] Source: Paakko, E Lehtinen, S Harila Saari, A Ahonen, A Jauhiainen, J Torniainen, P Pyhtinen, J Lanning, M Med-Pediatr-Oncol. 2003 February; 40(2): 88-92 0098-1532
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Peripheral keratitis associated with chronic myelomonocytic leukemia. Author(s): Department of Ophthalmology, University of Tennessee Health Science Center, Memphis 38163, USA.
[email protected] Source: Malecha, M A Holland, E J Cornea. 2002 October; 21(7): 723-4 0277-3740
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Phase I and pharmacokinetic study of DX-8951f (exatecan mesylate), a hexacyclic camptothecin, on a daily-times-five schedule in patients with advanced leukemia. Author(s): Department of Leukemia, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
[email protected] Source: Giles, F J Cortes, J E Thomas, D A Garcia Manero, G Faderl, S Jeha, S De Jager, R L Kantarjian, H M Clin-Cancer-Res. 2002 July; 8(7): 2134-41 1078-0432
Nutrition 193
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Proliferating or differentiating stimuli act on different lipid-dependent signaling pathways in nuclei of human leukemia cells. Author(s): Dipartimento di Morfologia ed Embriologia, Sezione di Anatomia Umana Normale, Universita di Ferrara, 44100 Ferrara, Italy. Source: Neri, L M Bortul, R Borgatti, P Tabellini, G Baldini, G Capitani, S Martelli, A M Mol-Biol-Cell. 2002 Mar; 13(3): 947-64 1059-1524
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Prolonged administration of all-trans retinoic acid in combination with intensive chemotherapy and G-CSF for adult acute myelogenous leukemia: single-centre pilot study in different risk groups. Author(s): Division of Haematology, Cytogenetics Unit, Ospedali Riuniti, Bergamo, Italy.
[email protected] Source: Bassan, R Chiodini, B Lerede, T Giussani, U Oldani, E Buelli, M Rossi, A Viero, P Rambaldi, A Barbui, T Hematol-J. 2002; 3(4): 193-200 1466-4860
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Prolonged single-agent versus combination chemotherapy in indolent follicular lymphomas: a study of the cancer and leukemia group B. Author(s): University of Minnesota Medical School, Division of Hematology, Oncology and Transplantation, Minneapolis, MN 55455, USA.
[email protected] Source: Peterson, B A Petroni, G R Frizzera, G Barcos, M Bloomfield, C D Nissen, N I Hurd, D D Henderson, E S Sartiano, G P Johnson, J L Holland, J F Gottlieb, A J J-ClinOncol. 2003 January 1; 21(1): 5-15 0732-183X
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Quercetin glucuronides inhibited 2-aminofluorene acetylation in human acute myeloid HL-60 leukemia cells. Author(s): Department of Parasitology, China Medical College, Taichung, Taiwan, Republic of China. Source: Kuo, H M Ho, H J Chao, P D Chung, J G Phytomedicine. 2002 October; 9(7): 62531 0944-7113
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Randomized phase II study of cisplatin with gemcitabine or paclitaxel or vinorelbine as induction chemotherapy followed by concomitant chemoradiotherapy for stage IIIB non-small-cell lung cancer: cancer and leukemia group B study 9431. Author(s): University of Chicago Medical Center and Cancer and Leukemia Group B, Chicago, IL, USA.
[email protected] Source: Vokes, E E Herndon, J E 2nd Crawford, J Leopold, K A Perry, M C Miller, A A Green, M R J-Clin-Oncol. 2002 October 15; 20(20): 4191-8 0732-183X
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RARA fluorescence in situ hybridization overcomes the drawback of PML/RARA fluorescence in situ hybridization in follow-up of acute promyelocytic leukemia. Author(s): Department of Clinical Pathology, Seoul National University College of Medicine, Seoul, South Korea.
[email protected] Source: Lee, D S Lee, Y S Kim, Y R Han, K S Park, K U She, C J Kim, E C Park, S Y Cho, H I Cancer-Genet-Cytogenet. 2002 December; 139(2): 104-8 0165-4608
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Requirement of caspase and p38MAPK activation in zinc-induced apoptosis in human leukemia HL-60 cells. Author(s): Department of Pharmaceutics and Biopharmaceutics, Showa Pharmaceutical University, Machida, Tokyo, Japan. Source: Kondoh, M Tasaki, E Araragi, S Takiguchi, M Higashimoto, M Watanabe, Y Sato, M Eur-J-Biochem. 2002 December; 269(24): 6204-11 0014-2956
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Selective induction of apoptosis by ar-turmerone isolated from turmeric (Curcuma longa L) in two human leukemia cell lines, but not in human stomach cancer cell line. Author(s): Faculty of Bioresources, Mie University, Tsu-city, Mie 514-0001, Japan.
194 Leukemia
Source: Aratanechemuge, Y Komiya, T Moteki, H Katsuzaki, H Imai, K Hibasami, H IntJ-Mol-Med. 2002 May; 9(5): 481-4 1107-3756 ·
Similar regulation of cell surface human T-cell leukemia virus type 1 (HTLV-1) surface binding proteins in cells highly and poorly transduced by HTLV-1pseudotyped virions. Author(s): Basic Research Program, SAIC-Frederick, National Cancer Institute at Frederick, Frederick, MD 21702-1201, USA. Source: Jones, K S Nath, M Petrow Sadowski, C Baines, A C Dambach, M Huang, Y Ruscetti, F W J-Virol. 2002 December; 76(24): 12723-34 0022-538X
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Synergistic induction of 1,25-dihydroxyvitamin D(3)- and all-trans-retinoic acidinduced differentiation of HL-60 leukemia cells by yomogin, a sesquiterpene lactone from Artemisia princeps. Author(s): Immunology Laboratory, College of Pharmacy, Chonnam National University, Kwangju, Republic of Korea. Source: Kim, S H Kim, T S Planta-Med. 2002 October; 68(10): 886-90 0032-0943
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The cyclin-dependent kinase inhibitor flavopiridol disrupts sodium butyrate-induced p21WAF1/CIP1 expression and maturation while reciprocally potentiating apoptosis in human leukemia cells. Source:
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The role of Aktand RAFTK in beta1 integrin mediated survival of precursor B-acute lymphoblastic leukemia cells. Author(s): Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115 USA. Source: Sarkar, S Svoboda, M de Beaumont, R Freedman, A S Leuk-Lymphoma. 2002 August; 43(8): 1663-71 1042-8194
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Treatment of refractory acute leukemia with timed sequential chemotherapy using topotecan followed by etoposide + mitoxantrone (T-EM) and correlation with topoisomerase II levels. Author(s): University of Florida College of Medicine, Division of Hematology/Oncology, Gainesville, USA.
[email protected] Source: Mainwaring, M G Rimsza, L M Chen, S F Gomez, S P Weeks, F W Reddy, V Lynch, J May, W S Kahn, S Moreb, J Leather, H Braylan, R Rowe, T C Fieniewicz, K J Wingard, J R Leuk-Lymphoma. 2002 May; 43(5): 989-99 1042-8194
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Two cases of therapy-related acute promyelocytic leukemia (t-APL) after mantle cell lymphoma and gestational trophoblastic disease. Author(s): University Department of Medicine, Professorial Block, Queen Mary Hospital, Pokfulam Road, Hong Kong.
[email protected] Source: Au, W Y Ma, S K Chung, L P Chim, C S Kwong, Y L Ann-Hematol. 2002 November; 81(11): 659-61 0939-5555
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UCN-01 (7-hydroxystauorsporine) blocks PMA-induced maturation and reciprocally promotes apoptosis in human myelomonocytic leukemia cells (U937). Author(s): Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA. Source: Rahmani, M Grant, S Cell-Cycle. 2002 Jul-August; 1(4): 273-81 1538-4101
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UCN-01 (7-hydroxystaurosporine) inhibits DNA repair and increases cytotoxicity in normal lymphocytes and chronic lymphocytic leukemia lymphocytes. Source:
Nutrition 195
The following information is typical of that found when using the “Full IBIDS Database” to search for “leukemia” (or a synonym): ·
7-hydroxystaurosporine (UCN-01) and ionizing radiation combine to inhibit the growth of Bcl-2-overexpressing U937 leukemia cells through a non-apoptotic mechanism. Author(s): Department of Medicine, Virginia Commonwealth University, Medical College of Virginia, Richmond, VA 23298, USA. Source: Cartee, L Sankala, H Davis, C Smith, R Maggio, S Lin, P S Dent, P Grant, S Int-JOncol. 2002 August; 21(2): 351-9 1019-6439
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A mathematical model of in vivo methotrexate accumulation in acute lymphoblastic leukemia. Author(s): St. Jude Children's Research Hospital, 332 North Lauderdale St., Memphis, TN 38105-2794, USA. Source: Panetta, J C Yanishevski, Y Pui, C H Sandlund, J T Rubnitz, J Rivera, G K Ribeiro, R Evans, W E Relling, M V Cancer-Chemother-Pharmacol. 2002 November; 50(5): 419-28 0344-5704
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A phase I and pharmacodynamic study of sequential topotecan and etoposide in patients with relapsed or refractory acute myelogenous and lymphoblastic leukemia. Author(s): Department of Medicine, University Hospitals of Cleveland, Cleveland, OH 44106, USA.
[email protected] Source: Cooper, B W Donaher, E Lazarus, H M Green, S B Gosky, D M Rosenthal, N S Berger, S J Li, X Ingalls, S T Hoppel, C L Gerson, S L Leuk-Res. 2003 January; 27(1): 35-44 0145-2126
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AML1 amplification in a child with acute lymphoblastic leukemia. Author(s): Departamento de Biologi;a Animal, Biologi;a Vegetal y Ecologi;a, Unidad de Antropologi;a, Facultad de Ciencias, Universidad Autonoma de Barcelona, Barcelona, Spain.
[email protected] Source: Alvarez, Y Coll, M D Bastida, P Ortega, J J Caballin, M R Cancer-GenetCytogenet. 2003 January 1; 140(1): 58-61 0165-4608
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Anti-leukemia effect of resveratrol. Author(s): Office of Research Compliance and Assurance, Department of Veterans Affairs, Washington, DC 20422, USA.
[email protected] Source: Tsan, M F White, J E Maheshwari, J G Chikkappa, G Leuk-Lymphoma. 2002 May; 43(5): 983-7 1042-8194
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Apoptosis of HL-60 leukemia cells induced by the bisindole alkaloids sungucine and isosungucine from Strychnos icaja. Author(s): INSERM U-524 et Centre Oscar Lambret, Lille, France. Source: Lansiaux, A Bailly, C Houssier, C Colson, P De Pauw Gillet, M C Frederich, M Tits, M Angenot, L Planta-Med. 2002 July; 68(7): 591-5 0032-0943
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Approval summary for imatinib mesylate capsules in the treatment of chronic myelogenous leukemia. Author(s): Division Oncology Drug Products, Center for Drug Evaluation and Research, Food and Drug Administration, Rockville, Maryland 20857, USA.
[email protected] Source: Cohen, M H Williams, G Johnson, J R Duan, J Gobburu, J Rahman, A Benson, K Leighton, J Kim, S K Wood, R Rothmann, M Chen, G U, K M Staten, A M Pazdur, R Clin-Cancer-Res. 2002 May; 8(5): 935-42 1078-0432
196 Leukemia
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Arginine butyrate increases the cytotoxicity of DAB(389)IL-2 in leukemia and lymphoma cells by upregulation of IL-2Rbeta gene. Author(s): Hematology-Oncology Department, New England Medical Center, Tufts University, Boston, MA, USA. Source: Shao, R H Tian, X Gorgun, G Urbano, A G Foss, F M Leuk-Res. 2002 December; 26(12): 1077-83 0145-2126
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Arsenic trioxide as effective therapy for relapsed acute promyelocytic leukemia. Author(s):
[email protected] Source: Mayorga, J Richardson Hardin, C Dicke, K A Clin-J-Oncol-Nurs. 2002 NovDecember; 6(6): 341-6 1092-1095
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Atypical t(15;17)(q13;q12) in a patient with all-trans retinoic acid refractory secondary acute promyelocytic leukemia: a case report and review of the literature. Author(s): Department of Medicine, West Virginia University, Morgantown, WV 26506, USA. Source: Kurian, S Hogan, T F Bleigh, O C Dowdy, Y G Merghoub, T Pandolfi, P P Wenger, S L Cancer-Genet-Cytogenet. 2002 October 15; 138(2): 143-8 0165-4608
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Automated analysis of differentiation-induced leukemic cells during all-trans retinoic Acid therapy of acute promyelocytic leukemia. Author(s): Department of Laboratory Medicine and Central Clinical Laboratory, Kyoto University Hospital, Kyoto, Japan.
[email protected] Source: Tohyama, K Shiga, S Fujimoto, H Hamaguchi, Y Ichiyama, S Arch-Pathol-LabMed. 2003 January; 127(1): e4-10 1543-2165
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Beta-hydroxyisovalerylshikonin induces apoptosis in human leukemia cells by inhibiting the activity of a polo-like kinase 1 (PLK1). Author(s): Laboratory of Biological Chemistry, School of Pharmaceutical Sciences, Showa University, Tokyo 142-8555, Japan. Source: Masuda, Y Nishida, A Hori, K Hirabayashi, T Kajimoto, S Nakajo, S Kondo, T Asaka, M Nakaya, K Oncogene. 2003 February 20; 22(7): 1012-23 0950-9232
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Biomic study of human myeloid leukemia cells differentiation to macrophages using DNA array, proteomic, and bioinformatic analytical methods. Author(s): Institute of Biological Chemistry, Academia Sinica, Taipei, Taiwan. Source: Juan, H F Lin, J Y Chang, W H Wu, C Y Pan, T L Tseng, M J Khoo, K H Chen, S T Electrophoresis. 2002 August; 23(15): 2490-504 0173-0835
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Bone mineral assessment with tibial ultrasonometry and dual-energy X-ray absorptiometry in long-term survivors of acute lymphoblastic leukemia in childhood. Author(s): Department of Pediatric Radiology, Sophia Children's Hospital, Rotterdam, The Netherlands.
[email protected] Source: Lequin, M H van der Shuis, I M Van Rijn, R R Hop, W C van ven Huevel Eibrink, M M MuinckKeizer Schrama, S M van Kuijk, C J-Clin-Densitom. 2002 Summer; 5(2): 167-73 1094-6950
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Characterization of a monoclonal antibody specific for a novel primate cell surface marker with distinct biochemical properties on human erythroleukemia and myeloid cell lines. Author(s): The John P. Robarts Research Institute, and Department of Microbiology and Immunology, The University of Western Ontario, London, Ontario, N6G 2V4 Canada. Source: Chang, C S McFadden, G Hybrid-Hybridomics. 2002 August; 21(4): 271-80 15368599
Nutrition 197
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Combretastatin-A4 prodrug induces mitotic catastrophe in chronic lymphocytic leukemia cell line independent of caspase activation and poly(ADP-ribose) polymerase cleavage. Author(s): Division of Hematology and Oncology, Department of Internal Medicine, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan 48201, USA. Source: Nabha, S M Mohammad, R M Dandashi, M H Coupaye Gerard, B Aboukameel, A Pettit, G R Al Katib, A M Clin-Cancer-Res. 2002 August; 8(8): 2735-41 1078-0432
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Composite mycosis fungoides and B-cell chronic lymphocytic leukemia. Author(s): Department of Pathology, The University of Alabama at Birmingham, AL 35233-7331, USA. Source: Volk, A L Vannucci, S A Cook, W Thompson, K A Listinsky, C M Ann-DiagnPathol. 2002 June; 6(3): 172-82 1092-9134
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Cotylenin A--a plant growth regulator as a differentiation-inducing agent against myeloid leukemia. Author(s): Saitama Cancer Center Research Institute, Ina, Japan.
[email protected] Source: Honma, Y Leuk-Lymphoma. 2002 June; 43(6): 1169-78 1042-8194
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Cryptic translocation of PML/RARA on 17q. A rare event in acute promyelocytic leukemia. Author(s): Hematology Unit, Santa Maria delle Croci Hospital, Viale Randi 5, 48100, Ravenna, Italy. Source: Zaccaria, A Valenti, A Toschi, M Salvucci, M Cipriani, R Ottaviani, E Martinelli, G Cancer-Genet-Cytogenet. 2002 October 15; 138(2): 169-73 0165-4608
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Dental abnormalities in children after chemotherapy treatment for acute lymphoid leukemia. Author(s): Department of Pathology, School of Medicine of Botucatu, Sao Paulo State University, SP, Sao Paulo, Brazil.
[email protected] Source: Minicucci, E M Lopes, L F Crocci, A J Leuk-Res. 2003 January; 27(1): 45-50 01452126
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Diol- and triol-types of phytol induce apoptosis in lymphoid leukemia Molt 4B cells. Author(s): Faculty of Medicine, Mie University, Tsu-city, Mie 514-0001, Japan. Source: Hibasami, H Kyohkon, M Owaki, S Katsuzaki, H Imai, K Ohnishi, K Ina, K Komiya, T Int-J-Mol-Med. 2002 November; 10(5): 555-9 1107-3756
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DNA methylation of multiple promoter-associated CpG islands in adult acute lymphocytic leukemia. Author(s): Departments of Leukemia, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
[email protected] Source: Garcia Manero, G Daniel, J Smith, T L Kornblau, S M Lee, M S Kantarjian, H M Issa, J P Clin-Cancer-Res. 2002 July; 8(7): 2217-24 1078-0432
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Effects of flavonoids on cisplatin-induced apoptosis of HL-60 and L1210 leukemia cells. Author(s): Cancer Research Institute, Vlarska 7, 833 91, Bratislava, Slovak Republic. Source: Cipak, L Rauko, P Miadokova, E Cipakova, I Novotny, L Leuk-Res. 2003 January; 27(1): 65-72 0145-2126
198 Leukemia
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Enhancement of sensitivity by bestatin of acute promyelocytic leukemia NB4 cells to all-trans retinoic acid. Author(s): Department of Applied Chemistry, Faculty of Science and Technology, Keio University, Yokohama, Japan. Source: Hirano, T Kizaki, M Kato, K Abe, F Masuda, N Umezawa, K Leuk-Res. 2002 December; 26(12): 1097-103 0145-2126
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In vitro comparative antileukemic activity of various glucocorticoids in childhood acute leukemia. Author(s): Department of Pediatric Hematology and Oncology; Medical University Bydgoszcz, Bydgoszcz, 85-094 Poland.
[email protected] Source: Styczynski, J Wysocki, M Balwierz, W Rokicka Milewska, R Matysiak, M Balcerska, A Kowalczyk, A Wachowiak, J Sonta Jakimczyk, D Chybicka, A Neoplasma. 2002; 49(3): 178-83 0028-2685
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Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412. Author(s): Dana-Farber Cancer Institute, Boston, Massachusetts, USA. Source: Weisberg, E Boulton, C Kelly, L M Manley, P Fabbro, D Meyer, T Gilliland, D G Griffin, J D Cancer-Cell. 2002 June; 1(5): 433-43 1535-6108
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Intermedeol isolated from the leaves of Ligularia fischeri var. spiciformis induces the differentiation of human acute promyeocytic leukemia HL-60 Cells. Author(s): Department of Food and Nutrition, Kyung Hee University, Seoul, Korea. Source: Jeong, S H Koo, S J Choi, J H Park, J H Ha, J Park, H J Lee, K T Planta-Med. 2002 October; 68(10): 881-5 0032-0943
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Intermediate doses of melphalan and dexamethasone are better than vincristine, adriamycin, and dexamethasone (VAD) and polychemotherapy for the treatment of primary plasma cell leukemia. Author(s): Department of Hematology, Hospital de Especialidades Centro Medico Nacional La Raza, Instituto Mexicano del Seguro Social, Apartado Postal 14-878, Codigo postal 07001, Mexico D.F., Mexico.
[email protected] Source: Vela Ojeda, J Garcia Ruiz Esparza, M A Rosas Cabral, A Padilla Gonzalez, Y Garcia Chavez, J Tripp Villanueva, F Sanchez Cortes, E Ayala Sanchez, M Garcia Leon, L D Montiel Cervantes, L Rubio Borja, M E Ann-Hematol. 2002 July; 81(7): 362-7 0939-5555
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Loss of heterozygosity of p16 correlates with minimal residual disease at the end of the induction therapy in non-high risk childhood B-cell precursor acute lymphoblastic leukemia. Author(s): Department of Genetics, Hospital de Paraplejicos, Toledo, Spain. Source: Tutor, O Diaz, M A Ramirez, M Algara, P Madero, L Martinez, P Leuk-Res. 2002 September; 26(9): 817-20 0145-2126
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MEK/ERK pathway protects ionizing radiation-induced loss of mitochondrial membrane potential and cell death in lymphocytic leukemia cells. Author(s): Department of Radiology, Sapporo Medical University School of Medicine, S1, W-16, Chuo-ku, Sapporo, 060-8543, Japan. Source: Shonai, T Adachi, M Sakata, K Takekawa, M Endo, T Imai, K Hareyama, M CellDeath-Differ. 2002 September; 9(9): 963-71 1350-9047
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Menadione biphasically controls JNK-linked cell death in leukemia Jurkat T cells. Author(s): Department of Medical Technology, Nagoya University School of Health Sciences, Nagoya 461-8673, Japan. Source: Ma, X Du, J Nakashima, I Nagase, F Antioxid-Redox-Signal. 2002 June; 4(3): 3718 1523-0864
Nutrition 199
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Methotrexate induced seizures associated with acute reversible magnetic resonance imaging (MRI) changes in a patient with acute lymphoblastic leukemia. Author(s): Division of Hematology and Internal Medicine, Rochester, MN 55905, USA. Source: Rao, R D Swanson, J W Dejesus, R S Hunt, C H Tefferi, A Leuk-Lymphoma. 2002 June; 43(6): 1333-6 1042-8194
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Methotrexate intracellular disposition in acute lymphoblastic leukemia: a mathematical model of gamma-glutamyl hydrolase activity. Author(s): Departments of Pharmaceutical Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794, USA. Source: Panetta, J C Wall, A Pui, C H Relling, M V Evans, W E Clin-Cancer-Res. 2002 July; 8(7): 2423-9 1078-0432
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Methotrexate-related neurotoxicity in the treatment of childhood acute lymphoblastic leukemia. Author(s): Department of Pediatric Oncology-Hematology, Schneider Children's Medical Center of Israel, Petah Tiqva, Israel.
[email protected] Source: Shuper, A Stark, B Kornreich, L Cohen, I J Avrahami, G Yaniv, I Isr-Med-AssocJ. 2002 November; 4(11): 1050-3 1565-1088
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Modulation of the phototoxic effect of hypericin in human leukemia CEM cell line by N-ethylmaleimide, amiloride and omeprazole. Author(s): Department of Pharmacology, Medical Faculty, P.J. Safarik University, Tr. SNP 1, 040 66 Kosice, Slovak
[email protected] Source: Mirossay, A Mirossay, L Sarissky, M Papp, P Mojzis, J Physiol-Res. 2002; 51(6): 641-4 0862-8408
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Nutritional support for chronic myelogenous and other leukemias: a review of the scientific literature. Source: Steriti, R Altern-Med-Revolume 2002 October; 7(5): 404-9 1089-5159
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Overexpression of gibbon ape leukemia virus (GALV) receptor (GLVR1) on human CD34(+) cells increases gene transfer mediated by GALV pseudotyped vectors. Author(s): Department of Molecular Medicine and Gene Therapy, University of Lund, Lund, Sweden. Source: Relander, T Brun, A C Olsson, K Pedersen, L Richter, J Mol-Ther. 2002 September; 6(3): 400-6 1525-0016
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Perfusion MRI and SPECT of brain after treatment for childhood acute lymphoblastic leukemia. Author(s): Department of Diagnostic Radiology, University of Oulu, Kajaanintie 50, 90220 Oulu, Finland.
[email protected] Source: Paakko, E Lehtinen, S Harila Saari, A Ahonen, A Jauhiainen, J Torniainen, P Pyhtinen, J Lanning, M Med-Pediatr-Oncol. 2003 February; 40(2): 88-92 0098-1532
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Peripheral keratitis associated with chronic myelomonocytic leukemia. Author(s): Department of Ophthalmology, University of Tennessee Health Science Center, Memphis 38163, USA.
[email protected] Source: Malecha, M A Holland, E J Cornea. 2002 October; 21(7): 723-4 0277-3740
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Phase I and pharmacokinetic study of DX-8951f (exatecan mesylate), a hexacyclic camptothecin, on a daily-times-five schedule in patients with advanced leukemia. Author(s): Department of Leukemia, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
[email protected] Source: Giles, F J Cortes, J E Thomas, D A Garcia Manero, G Faderl, S Jeha, S De Jager, R L Kantarjian, H M Clin-Cancer-Res. 2002 July; 8(7): 2134-41 1078-0432
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Proliferating or differentiating stimuli act on different lipid-dependent signaling pathways in nuclei of human leukemia cells. Author(s): Dipartimento di Morfologia ed Embriologia, Sezione di Anatomia Umana Normale, Universita di Ferrara, 44100 Ferrara, Italy. Source: Neri, L M Bortul, R Borgatti, P Tabellini, G Baldini, G Capitani, S Martelli, A M Mol-Biol-Cell. 2002 Mar; 13(3): 947-64 1059-1524
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Prolonged administration of all-trans retinoic acid in combination with intensive chemotherapy and G-CSF for adult acute myelogenous leukemia: single-centre pilot study in different risk groups. Author(s): Division of Haematology, Cytogenetics Unit, Ospedali Riuniti, Bergamo, Italy.
[email protected] Source: Bassan, R Chiodini, B Lerede, T Giussani, U Oldani, E Buelli, M Rossi, A Viero, P Rambaldi, A Barbui, T Hematol-J. 2002; 3(4): 193-200 1466-4860
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Prolonged single-agent versus combination chemotherapy in indolent follicular lymphomas: a study of the cancer and leukemia group B. Author(s): University of Minnesota Medical School, Division of Hematology, Oncology and Transplantation, Minneapolis, MN 55455, USA.
[email protected] Source: Peterson, B A Petroni, G R Frizzera, G Barcos, M Bloomfield, C D Nissen, N I Hurd, D D Henderson, E S Sartiano, G P Johnson, J L Holland, J F Gottlieb, A J J-ClinOncol. 2003 January 1; 21(1): 5-15 0732-183X
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Quercetin glucuronides inhibited 2-aminofluorene acetylation in human acute myeloid HL-60 leukemia cells. Author(s): Department of Parasitology, China Medical College, Taichung, Taiwan, Republic of China. Source: Kuo, H M Ho, H J Chao, P D Chung, J G Phytomedicine. 2002 October; 9(7): 62531 0944-7113
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Randomized phase II study of cisplatin with gemcitabine or paclitaxel or vinorelbine as induction chemotherapy followed by concomitant chemoradiotherapy for stage IIIB non-small-cell lung cancer: cancer and leukemia group B study 9431. Author(s): University of Chicago Medical Center and Cancer and Leukemia Group B, Chicago, IL, USA.
[email protected] Source: Vokes, E E Herndon, J E 2nd Crawford, J Leopold, K A Perry, M C Miller, A A Green, M R J-Clin-Oncol. 2002 October 15; 20(20): 4191-8 0732-183X
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RARA fluorescence in situ hybridization overcomes the drawback of PML/RARA fluorescence in situ hybridization in follow-up of acute promyelocytic leukemia. Author(s): Department of Clinical Pathology, Seoul National University College of Medicine, Seoul, South Korea.
[email protected] Source: Lee, D S Lee, Y S Kim, Y R Han, K S Park, K U She, C J Kim, E C Park, S Y Cho, H I Cancer-Genet-Cytogenet. 2002 December; 139(2): 104-8 0165-4608
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Requirement of caspase and p38MAPK activation in zinc-induced apoptosis in human leukemia HL-60 cells. Author(s): Department of Pharmaceutics and Biopharmaceutics, Showa Pharmaceutical University, Machida, Tokyo, Japan. Source: Kondoh, M Tasaki, E Araragi, S Takiguchi, M Higashimoto, M Watanabe, Y Sato, M Eur-J-Biochem. 2002 December; 269(24): 6204-11 0014-2956
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Selective induction of apoptosis by ar-turmerone isolated from turmeric (Curcuma longa L) in two human leukemia cell lines, but not in human stomach cancer cell line. Author(s): Faculty of Bioresources, Mie University, Tsu-city, Mie 514-0001, Japan.
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Source: Aratanechemuge, Y Komiya, T Moteki, H Katsuzaki, H Imai, K Hibasami, H IntJ-Mol-Med. 2002 May; 9(5): 481-4 1107-3756 ·
Similar regulation of cell surface human T-cell leukemia virus type 1 (HTLV-1) surface binding proteins in cells highly and poorly transduced by HTLV-1pseudotyped virions. Author(s): Basic Research Program, SAIC-Frederick, National Cancer Institute at Frederick, Frederick, MD 21702-1201, USA. Source: Jones, K S Nath, M Petrow Sadowski, C Baines, A C Dambach, M Huang, Y Ruscetti, F W J-Virol. 2002 December; 76(24): 12723-34 0022-538X
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Synergistic induction of 1,25-dihydroxyvitamin D(3)- and all-trans-retinoic acidinduced differentiation of HL-60 leukemia cells by yomogin, a sesquiterpene lactone from Artemisia princeps. Author(s): Immunology Laboratory, College of Pharmacy, Chonnam National University, Kwangju, Republic of Korea. Source: Kim, S H Kim, T S Planta-Med. 2002 October; 68(10): 886-90 0032-0943
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The cyclin-dependent kinase inhibitor flavopiridol disrupts sodium butyrate-induced p21WAF1/CIP1 expression and maturation while reciprocally potentiating apoptosis in human leukemia cells. Source:
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The role of Aktand RAFTK in beta1 integrin mediated survival of precursor B-acute lymphoblastic leukemia cells. Author(s): Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115 USA. Source: Sarkar, S Svoboda, M de Beaumont, R Freedman, A S Leuk-Lymphoma. 2002 August; 43(8): 1663-71 1042-8194
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Treatment of refractory acute leukemia with timed sequential chemotherapy using topotecan followed by etoposide + mitoxantrone (T-EM) and correlation with topoisomerase II levels. Author(s): University of Florida College of Medicine, Division of Hematology/Oncology, Gainesville, USA.
[email protected] Source: Mainwaring, M G Rimsza, L M Chen, S F Gomez, S P Weeks, F W Reddy, V Lynch, J May, W S Kahn, S Moreb, J Leather, H Braylan, R Rowe, T C Fieniewicz, K J Wingard, J R Leuk-Lymphoma. 2002 May; 43(5): 989-99 1042-8194
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Two cases of therapy-related acute promyelocytic leukemia (t-APL) after mantle cell lymphoma and gestational trophoblastic disease. Author(s): University Department of Medicine, Professorial Block, Queen Mary Hospital, Pokfulam Road, Hong Kong.
[email protected] Source: Au, W Y Ma, S K Chung, L P Chim, C S Kwong, Y L Ann-Hematol. 2002 November; 81(11): 659-61 0939-5555
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UCN-01 (7-hydroxystauorsporine) blocks PMA-induced maturation and reciprocally promotes apoptosis in human myelomonocytic leukemia cells (U937). Author(s): Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA. Source: Rahmani, M Grant, S Cell-Cycle. 2002 Jul-August; 1(4): 273-81 1538-4101
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Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: ·
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: ·
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDÒHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
The following is a specific Web list relating to leukemia; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation:
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Vitamins Folic Acid Source: Healthnotes, Inc.; www.healthnotes.com Vitamin a Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10066,00.html Vitamin D Alternative names: Calciferol, Calcitrol, Cholecalciferol, Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Vitamin K Source: Healthnotes, Inc.; www.healthnotes.com Vitamin K Alternative names: Menadione, Menaphthone, Menaquinone, Phylloquinone Source: Integrative Medicine Communications; www.drkoop.com
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Minerals Cisplatin Source: Healthnotes, Inc.; www.healthnotes.com Retinol Source: Integrative Medicine Communications; www.drkoop.com Tretinoin Source: Healthnotes, Inc.; www.healthnotes.com Vitamin a (retinol) Source: Integrative Medicine Communications; www.drkoop.com
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Food and Diet Bruising Source: Healthnotes, Inc.; www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND LEUKEMIA Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to leukemia. At the conclusion of this chapter, we will provide additional sources.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to leukemia and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “leukemia” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to leukemia: ·
A case of acantholytic dermatosis and leukemia cutis: cause or effect? Author(s): Sakalosky PE, Fenske N, Morgan MB. Source: The American Journal of Dermatopathology. 2002 June; 24(3): 257-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12140444&dopt=Abstract
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A case of primary plasma cell leukemia with hairy-cell morphology and lambda-type Bence-Jones protein. Immunohistochemical and molecular analysis. Author(s): Tanioka F, Tamashima S, Shimizu S, Kobayashi H, Kobayashi Y, Sugimura H. Source: Japanese Journal of Clinical Oncology. 2003 May; 33(5): 232-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865467&dopt=Abstract
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A case of treatment-related myelodysplastic syndrome and acute myelogenous leukemia following high-dose chemotherapy with autologous stem cell transplantation for non-Hodgkin's lymphoma.
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Author(s): Jang GD, Kim SW, Suh CW, Kim EK, Bahng HS, Jeong YH, Park IG, Kim WK, Kim SH, Suh EJ, Park CJ, Ji HS, Lee JS. Source: Journal of Korean Medical Science. 2002 August; 17(4): 555-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12172056&dopt=Abstract ·
A constitutional translocation t(1;4)(p21;p15) in a case of chronic lymphocytic leukemia. Author(s): Eclache V, Benzacken B, Kettaneh A, Fain O. Source: Annales De Genetique. 2002 October-December; 45(4): 169-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668161&dopt=Abstract
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A homoharringtonine-based regimen for childhood acute myelogenous leukemia. Author(s): Tang J, Xue H, Pan C, Chen J, Gu L, Zhao H. Source: Medical and Pediatric Oncology. 2003 July; 41(1): 70-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764750&dopt=Abstract
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A hybrid form of myeloid/NK-cell acute leukemia and myeloid/NK-cell precursor acute leukemia. Author(s): Sun T, Pashaei S, Jaffrey I, Ryder J. Source: Human Pathology. 2003 May; 34(5): 504-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12792926&dopt=Abstract
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A new multidrug reinduction protocol with topotecan, vinorelbine, thiotepa, dexamethasone, and gemcitabine for relapsed or refractory acute leukemia. Author(s): Kolb EA, Steinherz PG. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 1967-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513046&dopt=Abstract
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A new selective AKT pharmacological inhibitor reduces resistance to chemotherapeutic drugs, TRAIL, all-trans-retinoic acid, and ionizing radiation of human leukemia cells. Author(s): Martelli AM, Tazzari PL, Tabellini G, Bortul R, Billi AM, Manzoli L, Ruggeri A, Conte R, Cocco L. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1794-805. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970779&dopt=Abstract
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A novel c-kit positive biphenotypic acute leukemia cell line, TMBL-1, carrying a p53 point mutation. Author(s): Suzuki S, Uozumi K, Hanada S, Lin XY, Ohno N, Takatsuka Y, Takeuchi S, Owatari S, Takeshita T, Arima T.
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Source: Leukemia & Lymphoma. 2003 May; 44(5): 849-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802925&dopt=Abstract ·
A phase I and pharmacodynamic study of sequential topotecan and etoposide in patients with relapsed or refractory acute myelogenous and lymphoblastic leukemia. Author(s): Cooper BW, Donaher E, Lazarus HM, Green SB, Gosky DM, Rosenthal NS, Berger SJ, Li X, Ingalls ST, Hoppel CL, Gerson SL. Source: Leukemia Research. 2003 January; 27(1): 35-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12479850&dopt=Abstract
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Activity of drugs from traditional Chinese medicine toward sensitive and MDR1- or MRP1-overexpressing multidrug-resistant human CCRF-CEM leukemia cells. Author(s): Efferth T, Davey M, Olbrich A, Rucker G, Gebhart E, Davey R. Source: Blood Cells, Molecules & Diseases. 2002 March-April; 28(2): 160-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12064912&dopt=Abstract
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Acute lymphoblastic leukemia in the context of a disorder resembling X-linked lymphoproliferative (XLP) syndrome. Author(s): Risitano AM, Camera A, Chiurazzi F, Rossi M, D'Arco AM, Rotoli B. Source: Haematologica. 2002 August; 87(8): Elt36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12161381&dopt=Abstract
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Acute myocardial infarction as the presenting symptom of acute myeloblastic leukemia with extreme hyperleukocytosis. Author(s): Cohen Y, Amir G, Da'as N, Gillis S, Rund D, Polliack A. Source: American Journal of Hematology. 2002 September; 71(1): 47-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12221675&dopt=Abstract
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Aleukemic monocytic leukemia cutis. Author(s): Barzilai A, Lyakhovitsky A, Goldberg I, Meytes D, Trau H. Source: Cutis; Cutaneous Medicine for the Practitioner. 2002 April; 69(4): 301-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12080951&dopt=Abstract
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AML1 amplification in a child with acute lymphoblastic leukemia. Author(s): Alvarez Y, Coll MD, Bastida P, Ortega JJ, Caballin MR. Source: Cancer Genetics and Cytogenetics. 2003 January 1; 140(1): 58-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12550760&dopt=Abstract
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Analysis of t(9;11) chromosomal breakpoint sequences in childhood acute leukemia: almost identical MLL breakpoints in therapy-related AML after treatment without etoposides. Author(s): Langer T, Metzler M, Reinhardt D, Viehmann S, Borkhardt A, Reichel M,
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Stanulla M, Schrappe M, Creutzig U, Ritter J, Leis T, Jacobs U, Harbott J, Beck JD, Rascher W, Repp R. Source: Genes, Chromosomes & Cancer. 2003 April; 36(4): 393-401. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12619163&dopt=Abstract ·
Anti-leukemia activities of Lup-28-al-20(29)-en-3-one, a lupane triterpene. Author(s): Hata K, Hori K, Ogasawara H, Takahashi S. Source: Toxicology Letters. 2003 June 5; 143(1): 1-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12697374&dopt=Abstract
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Anti-leukemia effect of resveratrol. Author(s): Tsan MF, White JE, Maheshwari JG, Chikkappa G. Source: Leukemia & Lymphoma. 2002 May; 43(5): 983-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12148909&dopt=Abstract
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Anti-proliferative and differentiation-inducing activities of the green tea catechin epigallocatechin-3-gallate (EGCG) on the human eosinophilic leukemia EoL-1 cell line. Author(s): Lung HL, Ip WK, Wong CK, Mak NK, Chen ZY, Leung KN. Source: Life Sciences. 2002 December 6; 72(3): 257-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12427485&dopt=Abstract
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Apoptosis in leukemia cells is accompanied by alterations in the levels and localization of nucleolin. Author(s): Mi Y, Thomas SD, Xu X, Casson LK, Miller DM, Bates PJ. Source: The Journal of Biological Chemistry. 2003 March 7; 278(10): 8572-9. Epub 2002 December 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12506112&dopt=Abstract
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Apoptosis induction of Persicae Semen extract in human promyelocytic leukemia (HL-60) cells. Author(s): Kwon HY, Hong SP, Hahn DH, Kim JH. Source: Arch Pharm Res. 2003 February; 26(2): 157-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643594&dopt=Abstract
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Apoptosis of HL-60 leukemia cells induced by the bisindole alkaloids sungucine and isosungucine from Strychnos icaja. Author(s): Lansiaux A, Bailly C, Houssier C, Colson P, De Pauw-Gillet MC, Frederich M, Tits M, Angenot L. Source: Planta Medica. 2002 July; 68(7): 591-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12142990&dopt=Abstract
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Association of a novel single nucleotide polymorphism, G(-248)A, in the 5'-UTR of BAX gene in chronic lymphocytic leukemia with disease progression and treatment resistance. Author(s): Saxena A, Moshynska O, Sankaran K, Viswanathan S, Sheridan DP. Source: Cancer Letters. 2002 December 10; 187(1-2): 199-205. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359369&dopt=Abstract
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ATPase inhibitors suppress actinomycin D-induced apoptosis in leukemia cells. Author(s): Shiono Y, Fujita Y, Oka S, Yamazaki Y. Source: Anticancer Res. 2002 September-October; 22(5): 2907-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530016&dopt=Abstract
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Avoidance of bioflavonoid supplements during pregnancy: a pathway to infant leukemia? Author(s): Paolini M, Sapone A, Valgimigli L. Source: Mutation Research. 2003 June 19; 527(1-2): 99-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787918&dopt=Abstract
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BAALC expression predicts clinical outcome of de novo acute myeloid leukemia patients with normal cytogenetics: a Cancer and Leukemia Group B Study. Author(s): Baldus CD, Tanner SM, Ruppert AS, Whitman SP, Archer KJ, Marcucci G, Caligiuri MA, Carroll AJ, Vardiman JW, Powell BL, Allen SL, Moore JO, Larson RA, Kolitz JE, de la Chapelle A, Bloomfield CD. Source: Blood. 2003 September 1; 102(5): 1613-8. Epub 2003 May 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750167&dopt=Abstract
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Benign intracranial hypertension in association with acute lymphoblastic leukemia. Author(s): Sastry J, Karandikar SS, English MW. Source: Pediatric Hematology and Oncology. 2003 March; 20(2): 157-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12554527&dopt=Abstract
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Beta-hydroxyisovalerylshikonin induces apoptosis in human leukemia cells by inhibiting the activity of a polo-like kinase 1 (PLK1). Author(s): Masuda Y, Nishida A, Hori K, Hirabayashi T, Kajimoto S, Nakajo S, Kondo T, Asaka M, Nakaya K. Source: Oncogene. 2003 February 20; 22(7): 1012-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592388&dopt=Abstract
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Blast crisis of chronic myeloid leukemia: diagnosis prompted by T(8;9). Author(s): Borker A, Yu L, Ode D.
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Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 November; 24(8): 670-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439042&dopt=Abstract ·
Capsaicin inhibits growth of adult T-cell leukemia cells. Author(s): Zhang J, Nagasaki M, Tanaka Y, Morikawa S. Source: Leukemia Research. 2003 March; 27(3): 275-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12537981&dopt=Abstract
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Carnosic acid potentiates the antioxidant and prodifferentiation effects of 1alpha,25dihydroxyvitamin D3 in leukemia cells but does not promote elevation of basal levels of intracellular calcium. Author(s): Danilenko M, Wang Q, Wang X, Levy J, Sharoni Y, Studzinski GP. Source: Cancer Research. 2003 March 15; 63(6): 1325-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649194&dopt=Abstract
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CD7+ and CD56+ myeloid/natural killer cell precursor acute leukemia treated with idarubicin and cytosine arabinoside. Author(s): Handa H, Motohashi S, Isozumi K, Komatsumoto S, Nara M. Source: Acta Haematologica. 2002; 108(1): 47-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12145468&dopt=Abstract
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Cellular drug resistance in childhood acute myeloid leukemia is related to chromosomal abnormalities. Author(s): Zwaan CM, Kaspers GJ, Pieters R, Hahlen K, Huismans DR, Zimmermann M, Harbott J, Slater RM, Creutzig U, Veerman AJ. Source: Blood. 2002 November 1; 100(9): 3352-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12384437&dopt=Abstract
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Central nervous system prophylaxis with high-dose methotrexate does not give rise to significant electroencephalographic changes in children with acute lymphoblastic leukemia. Author(s): Korinthenberg R, Schneider A, Niemeyer C. Source: Journal of Child Neurology. 2002 June; 17(6): 409-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12174959&dopt=Abstract
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Cholestane glycosides from the bulbs of Ornithogalum thyrsoides and their cytotoxic activity against HL-60 leukemia cells. Author(s): Kuroda M, Mimaki Y, Yokosuka A, Hasegawa F, Sashida Y. Source: Journal of Natural Products. 2002 October; 65(10): 1417-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12398536&dopt=Abstract
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Cinnamaldehyde induces apoptosis by ROS-mediated mitochondrial permeability transition in human promyelocytic leukemia HL-60 cells. Author(s): Ka H, Park HJ, Jung HJ, Choi JW, Cho KS, Ha J, Lee KT. Source: Cancer Letters. 2003 July 10; 196(2): 143-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860272&dopt=Abstract
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Combretastatin-A4 prodrug induces mitotic catastrophe in chronic lymphocytic leukemia cell line independent of caspase activation and poly(ADP-ribose) polymerase cleavage. Author(s): Nabha SM, Mohammad RM, Dandashi MH, Coupaye-Gerard B, Aboukameel A, Pettit GR, Al-Katib AM. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2002 August; 8(8): 2735-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12171907&dopt=Abstract
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Commentary: topoisomerases as targets in acute leukemia: I, II, I plus II or none? Author(s): Malek SN, Gore SD. Source: Leukemia Research. 2003 January; 27(1): 1-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12479845&dopt=Abstract
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Comparative antiproliferative and apoptotic effects of resveratrol, epsilon-viniferin and vine-shots derived polyphenols (vineatrols) on chronic B lymphocytic leukemia cells and normal human lymphocytes. Author(s): Billard C, Izard JC, Roman V, Kern C, Mathiot C, Mentz F, Kolb JP. Source: Leukemia & Lymphoma. 2002 October; 43(10): 1991-2002. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12481898&dopt=Abstract
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Comparative cytotoxicity of dimethylamide-crotonin in the promyelocytic leukemia cell line (HL60) and human peripheral blood mononuclear cells. Author(s): Anazetti MC, Melo PS, Duran N, Haun M. Source: Toxicology. 2003 June 30; 188(2-3): 261-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767696&dopt=Abstract
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Complete remission in advanced blastic NK-cell lymphoma/leukemia in elderly patients using the hyper-CVAD regimen. Author(s): Shapiro M, Wasik MA, Junkins-Hopkins JM, Rook AH, Vittorio CC, Itakura H, Frankel MC, Georgala S, Schuster SJ. Source: American Journal of Hematology. 2003 September; 74(1): 46-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949889&dopt=Abstract
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Composite mycosis fungoides and B-cell chronic lymphocytic leukemia. Author(s): Volk AL, Vannucci SA, Cook W, Thompson KA, Listinsky CM.
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Source: Annals of Diagnostic Pathology. 2002 June; 6(3): 172-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12089729&dopt=Abstract ·
Concurrent mediastinal B cell lymphoma and chronic myeloid leukemia with an unusually favorable response to chemotherapy. Author(s): Au WY, Ma SK, Wan TS, Wang EP, Lau TC, Kwong YL. Source: Leukemia & Lymphoma. 2003 March; 44(3): 535-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688328&dopt=Abstract
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Contribution of the induction of heme oxygenase-1 to etoposide-induced apoptosis in acute myeloblastic leukemia. Author(s): Siitonen T, Siitonen P, Kinnula V, Mantymaa P, Savolainen ER, Koistinen P. Source: Haematologica. 2003 January; 88(1): 112-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12551835&dopt=Abstract
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Costunolide induces differentiation of human leukemia HL-60 cells. Author(s): Choi JH, Seo BR, Seo SH, Lee KT, Park JH, Park HJ, Choi JW, Itoh Y, Miyamoto K. Source: Arch Pharm Res. 2002 August; 25(4): 480-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12214860&dopt=Abstract
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Costunolide triggers apoptosis in human leukemia U937 cells by depleting intracellular thiols. Author(s): Choi JH, Ha J, Park JH, Lee JY, Lee YS, Park HJ, Choi JW, Masuda Y, Nakaya K, Lee KT. Source: Japanese Journal of Cancer Research : Gann. 2002 December; 93(12): 1327-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495472&dopt=Abstract
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Cotylenin A--a plant growth regulator as a differentiation-inducing agent against myeloid leukemia. Author(s): Honma Y. Source: Leukemia & Lymphoma. 2002 June; 43(6): 1169-78. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12152984&dopt=Abstract
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Cytotoxic effect of the diterpene lactone dehydrocrotonin from Croton cajucara on human promyelocytic leukemia cells. Author(s): Freire AC, da Silva Melo P, Aoyama H, Haun M, Duran N, Ferreira CV. Source: Planta Medica. 2003 January; 69(1): 67-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12567283&dopt=Abstract
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Cytotoxicity of paclitaxel or cisplatin on carcinoma cell lines is not inhibited by leukemia inhibitory factor (LIF). Author(s): O'Flaherty E, Cook W, Boyd J, Grant SL, Kurek J, Begley CG.
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Source: Growth Factors (Chur, Switzerland). 2002 September; 20(3): 141-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519017&dopt=Abstract ·
Degradation of vincristine by myeloperoxidase and hypochlorous acid in children with acute lymphoblastic leukemia. Author(s): Ozgen U, Turkoz Y, Stout M, Ozugurlu F, Pelik F, Bulut Y, Aslan M, Ravindranath Y, Savasan S. Source: Leukemia Research. 2003 December; 27(12): 1109-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921949&dopt=Abstract
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Dental abnormalities in children after chemotherapy treatment for acute lymphoid leukemia. Author(s): Minicucci EM, Lopes LF, Crocci AJ. Source: Leukemia Research. 2003 January; 27(1): 45-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12479851&dopt=Abstract
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Deoxycoformycin-containing combination chemotherapy for adult T-cell leukemialymphoma: Japan Clinical Oncology Group Study (JCOG9109). Author(s): Tsukasaki K, Tobinai K, Shimoyama M, Kozuru M, Uike N, Yamada Y, Tomonaga M, Araki K, Kasai M, Takatsuki K, Tara M, Mikuni C, Hotta T; Lymphoma Study Group of the Japan Clinical Oncology Group. Source: International Journal of Hematology. 2003 February; 77(2): 164-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12627852&dopt=Abstract
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Detection of extramedullary infiltrates in acute myelogenous leukemia with wholebody positron emission tomography and 2-deoxy-2-[18F]-fluoro-D-glucose. Author(s): Kuenzle K, Taverna C, Steinert HC. Source: Molecular Imaging and Biology : Mib : the Official Publication of the Academy of Molecular Imaging. 2002 March; 4(2): 179-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14537141&dopt=Abstract
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Development of secondary anaplastic oligoastrocytoma after matched unrelated bone marrow transplantation in a child with acute myeloid leukemia. Author(s): Panigrahi S, Das M, Stagler D, Konstantini S, Gmori M, Slavin S, Nagler A. Source: Acta Haematologica. 2003; 109(4): 196-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853693&dopt=Abstract
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Dexamethasone-associated toxicity during induction chemotherapy for childhood acute lymphoblastic leukemia is augmented by concurrent use of daunomycin. Author(s): Belgaumi AF, Al-Bakrah M, Al-Mahr M, Al-Jefri A, Al-Musa A, Saleh M, Salim MF, Osman M, Osman L, El-Solh H.
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Source: Cancer. 2003 June 1; 97(11): 2898-903. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767105&dopt=Abstract ·
Differential effect of Bcl-xl over-expression on cell death of the monocytic leukemia cell line U937. Author(s): Abdelhaleem M. Source: Anticancer Res. 2002 November-December; 22(6C): 3911-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553012&dopt=Abstract
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Differentiation-inducing effects of verticinone, an isosteroidal alkaloid isolated from the bulbus of Fritillaria ussuriensis, on human promyelocytic leukemia HL-60 cells. Author(s): Pae HO, Oh H, Choi BM, Oh GS, Paik SG, Jeong S, Hwang KM, Yun YG, Chung HT. Source: Biological & Pharmaceutical Bulletin. 2002 November; 25(11): 1409-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419949&dopt=Abstract
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Dissimilar invasive and metastatic behavior of vincristine and doxorubicin-resistant cell lines derived from a murine T cell lymphoid leukemia. Author(s): Lopes EC, Ernst G, Aulicino P, Vanzulli S, Garcia M, Alvarez E, Hajos SE. Source: Clinical & Experimental Metastasis. 2002; 19(4): 283-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12090468&dopt=Abstract
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Distribution of actin in etoposide-induced human leukemia cell line K-562 using fluorescence and immunoelectron microscopy technique. Author(s): Grzanka A, Grzanka D. Source: Pol J Pathol. 2002; 53(2): 43-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12140866&dopt=Abstract
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DNA methylation of multiple promoter-associated CpG islands in adult acute lymphocytic leukemia. Author(s): Garcia-Manero G, Daniel J, Smith TL, Kornblau SM, Lee MS, Kantarjian HM, Issa JP. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2002 July; 8(7): 2217-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12114423&dopt=Abstract
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Effects of garlic components diallyl sulfide and diallyl disulfide on arylamine Nacetyltransferase activity and 2-aminofluorene-DNA adducts in human promyelocytic leukemia cells. Author(s): Lin JG, Chen GW, Su CC, Hung CF, Yang CC, Lee JH, Chung JG. Source: The American Journal of Chinese Medicine. 2002; 30(2-3): 315-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12230020&dopt=Abstract
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Effects of inhibitors of the chemokine receptor CXCR4 on acute lymphoblastic leukemia cells in vitro. Author(s): Juarez J, Bradstock KF, Gottlieb DJ, Bendall LJ. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1294-300. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835717&dopt=Abstract
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Effects of polyphenolic anthrone derivatives, resistomycin and hypercin, on apoptosis in human megakaryoblastic leukemia CMK-7 cell line. Author(s): Shiono Y, Shiono N, Seo S, Oka S, Yamazaki Y. Source: Z Naturforsch [c]. 2002 September-October; 57(9-10): 923-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12440735&dopt=Abstract
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Enhanced MTT-reducing activity under growth inhibition by resveratrol in CEMC7H2 lymphocytic leukemia cells. Author(s): Bernhard D, Schwaiger W, Crazzolara R, Tinhofer I, Kofler R, Csordas A. Source: Cancer Letters. 2003 June 10; 195(2): 193-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767528&dopt=Abstract
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Ex vivo purging with NK-92 prior to autografting for chronic myelogenous leukemia. Author(s): Maki G, Tam YK, Berkahn L, Klingemann HG. Source: Bone Marrow Transplantation. 2003 June; 31(12): 1119-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796791&dopt=Abstract
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Factors influencing outcome and incidence of long-term complications in children who underwent autologous stem cell transplantation for acute myeloid leukemia in first complete remission. Author(s): Locatelli F, Labopin M, Ortega J, Meloni G, Dini G, Messina C, Yaniv I, Fagioli F, Castel V, Shaw PJ, Ferrant A, Pession A, Socie G, Frassoni F; European Blood and Marrow Transplantation Acute Leukemia Working Party. Source: Blood. 2003 February 15; 101(4): 1611-9. Epub 2002 October 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393725&dopt=Abstract
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Faith, identity, and leukemia: when blood products are not an option. Author(s): Knuti KA, Amrein PC, Chabner BA, Lynch TJ Jr, Penson RT. Source: The Oncologist. 2002; 7(4): 371-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12185299&dopt=Abstract
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Flexible low-intensity combination chemotherapy for elderly patients with acute myeloid leukemia. Author(s): Manoharan A, Trickett A, Kwan YL, Brighton T.
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Source: International Journal of Hematology. 2002 June; 75(5): 519-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12095154&dopt=Abstract ·
Fludarabine combination therapy for the treatment of chronic lymphocytic leukemia. Author(s): Schmitt B, Wendtner CM, Bergmann M, Busch R, Franke A, Pasold R, Schlag R, Hopfinger G, Hiddemann W, Emmerich B, Hallek M. Source: Clin Lymphoma. 2002 June; 3(1): 26-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12141952&dopt=Abstract
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Fractionated cyclophosphamide, vincristine, liposomal daunorubicin, and dexamethasone plus rituximab and granulocyte-macrophage-colony stimulating factor (GM-CSF) alternating with methotrexate and cytarabine plus rituximab and GM-CSF in patients with Richter syndrome or fludarabine-refractory chronic lymphocytic leukemia. Author(s): Tsimberidou AM, Kantarjian HM, Cortes J, Thomas DA, Faderl S, GarciaManero G, Verstovsek S, Ferrajoli A, Wierda W, Alvarado Y, O'Brien SM, Albitar M, Keating MJ, Giles FJ. Source: Cancer. 2003 April 1; 97(7): 1711-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12655528&dopt=Abstract
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Gene expression in human neural stem cells: effects of leukemia inhibitory factor. Author(s): Wright LS, Li J, Caldwell MA, Wallace K, Johnson JA, Svendsen CN. Source: Journal of Neurochemistry. 2003 July; 86(1): 179-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12807438&dopt=Abstract
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Genistein, a protein tyrosine kinase inhibitor, suppresses the fusogenicity of Moloney murine leukemia virus envelope protein in XC cells. Author(s): Kubo Y, Ishimoto A, Amanuma H. Source: Archives of Virology. 2003 October; 148(10): 1899-914. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14551814&dopt=Abstract
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Genomic imbalances in drug-resistant T-cell acute lymphoblastic CEM leukemia cell lines. Author(s): Efferth T, Verdorfer I, Miyachi H, Sauerbrey A, Drexler HG, Chitambar CR, Haber M, Gebhart E. Source: Blood Cells, Molecules & Diseases. 2002 July-August; 29(1): 1-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12482398&dopt=Abstract
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Hereditary hemorrhagic telangiectasia, idiopathic thrombocytopenic purpura, and chronic lymphocytic leukemia treated with rituximab. Author(s): Choueiri T, Lichtin AE.
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Source: The American Journal of Medicine. 2002 December 1; 113(8): 700-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12505128&dopt=Abstract ·
High-dose cyclophosphamide and etoposide for patients with refractory acute myeloid leukemia: a case series. Author(s): Talbot J, Rizzieri DA, DeCastro CM, Moore JO, Buckley P, Laney R, Stevenson D, Brumbaugh H, Gockerman JP. Source: American Journal of Hematology. 2003 August; 73(4): 295-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879438&dopt=Abstract
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Human granulocyte colony-stimulating factor in children with high-risk acute lymphoblastic leukemia: a Children's Cancer Group Study. Author(s): Heath JA, Steinherz PG, Altman A, Sather H, Jhanwar S, Halpern S, Pieters R, Shah N, Steinherz L, Tannous R, Terry W, Trigg ME; Children's Cancer Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 April 15; 21(8): 1612-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12697887&dopt=Abstract
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Hydrolytically activated etoposide prodrugs inhibit MDR-1 function and eradicate established MDR-1 multidrug-resistant T-cell leukemia. Author(s): Schroeder U, Bernt KM, Lange B, Wenkel J, Jikai J, Shabat D, Amir R, Huebener N, Niethammer AG, Hagemeier C, Wiebusch L, Gaedicke G, Wrasidlo W, Reisfeld RA, Lode HN. Source: Blood. 2003 July 1; 102(1): 246-53. Epub 2003 March 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623853&dopt=Abstract
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Imatinib in combination with cytarabine for the treatment of Philadelphia-positive chronic myelogenous leukemia chronic-phase patients: rationale and design of phase I/II trials. Author(s): Guilhot F, Gardembas M, Rousselot P, Tulliez M, Vigier M, Buzyn A, RigalHuguet F, Legros L, Michallet M, Berthou C, Najman A, Maloisel F, Mahon FX, Facon T, Berthaud P, Guilhot J; CML French Group. Source: Semin Hematol. 2003 April; 40(2 Suppl 2): 92-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12783382&dopt=Abstract
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Imatinib Mesylate (Gleevec) is a useful agent in the salvage treatment of adults with relapsed/refractory Philadelphia positive acute leukemias. Author(s): Gupta V, Kamel-Reid S, Minden MD, Lipton JH, Brandwein J, Messner HA. Source: Hematology (Amsterdam, Netherlands). 2003 June; 8(3): 139-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745646&dopt=Abstract
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Immunophenotypic characterization of normal peripheral blood B lymphocyte by flow cytometry: reference for diagnosis of chronic B cell leukemia/lymphoma. Author(s): Zheng ZJ, Xu RL.
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Source: Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2003 August; 11(4): 398-404. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12962571&dopt=Abstract ·
Immunophenotypic evidence of leukemia after induction therapy predicts relapse: results from a prospective Children's Cancer Group study of 252 patients with acute myeloid leukemia. Author(s): Sievers EL, Lange BJ, Alonzo TA, Gerbing RB, Bernstein ID, Smith FO, Arceci RJ, Woods WG, Loken MR. Source: Blood. 2003 May 1; 101(9): 3398-406. Epub 2002 December 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12506020&dopt=Abstract
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Impact of granulocyte colony-stimulating factor use during induction for acute myelogenous leukemia in children: a report from the Children's Cancer Group. Author(s): Alonzo TA, Kobrinsky NL, Aledo A, Lange BJ, Buxton AB, Woods WG. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 November; 24(8): 627-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439034&dopt=Abstract
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Impaired adrenal function after glucocorticoid therapy in children with acute lymphoblastic leukemia. Author(s): Petersen KB, Muller J, Rasmussen M, Schmiegelow K. Source: Medical and Pediatric Oncology. 2003 August; 41(2): 110-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12825213&dopt=Abstract
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Improved outcome in high-risk childhood acute lymphoblastic leukemia defined by prednisone-poor response treated with double Berlin-Frankfurt-Muenster protocol II. Author(s): Arico M, Valsecchi MG, Conter V, Rizzari C, Pession A, Messina C, Barisone E, Poggi V, De Rossi G, Locatelli F, Micalizzi MC, Basso G, Masera G. Source: Blood. 2002 July 15; 100(2): 420-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12091331&dopt=Abstract
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Improvement of molecular monitoring of residual disease in leukemias by bedside RNA stabilization. Author(s): Muller MC, Merx K, Weisser A, Kreil S, Lahaye T, Hehlmann R, Hochhaus A. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2002 December; 16(12): 2395-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454744&dopt=Abstract
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Improvement over time in outcome for children with acute lymphoblastic leukemia in second remission given hematopoietic stem cell transplantation from unrelated donors. Author(s): Locatelli F, Zecca M, Messina C, Rondelli R, Lanino E, Sacchi N, Uderzo C, Fagioli F, Conter V, Bonetti F, Favre C, Porta F, Giorgiani G, Pession A.
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Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2002 November; 16(11): 2228-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399966&dopt=Abstract ·
In vitro effects of STI 571-containing drug combinations on the growth of Philadelphia-positive chronic myelogenous leukemia cells. Author(s): Scappini B, Onida F, Kantarjian HM, Dong L, Verstovsek S, Keating MJ, Beran M. Source: Cancer. 2002 May 15; 94(10): 2653-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12173333&dopt=Abstract
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Increased expression of fibroblast growth factor receptor 3 in CD34+ BCR-ABL+ cells from patients with chronic myeloid leukemia. Author(s): Dvorak P, Dvorakova D, Doubek M, Faitova J, Pacholikova J, Hampl A, Mayer J. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October 9 [epub Ahead of Print] http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14562121&dopt=Abstract
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Induction of apoptosis by Paljin-Hangahmdan on human leukemia cells. Author(s): Yi JM, Kim MS, Lee EH, Wi DH, Lee JK, Cho KH, Hong SH, Kim HM. Source: Journal of Ethnopharmacology. 2003 September; 88(1): 79-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902055&dopt=Abstract
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Induction of apoptosis in the human mast cell leukemia cell line HMC-1 by various antineoplastic drugs. Author(s): Samorapoompichit P, Steiner M, Lucas T, Wachtler F, Schedled A, Sperr WR, Valent P. Source: Leukemia & Lymphoma. 2003 March; 44(3): 509-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688323&dopt=Abstract
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Induction of long-term remission of a relapsed childhood B-acute lymphoblastic leukemia with rituximab chimeric anti-CD20 monoclonal antibody and autologous stem cell transplantation. Author(s): Corbacioglu S, Eber S, Gungor T, Hummerjohann J, Niggli F. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 April; 25(4): 327-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679650&dopt=Abstract
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Induction of tumor necrosis factor by bryostatin 1 is involved in synergistic interactions with paclitaxel in human myeloid leukemia cells. Author(s): Wang S, Wang Z, Dent P, Grant S.
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Source: Blood. 2003 May 1; 101(9): 3648-57. Epub 2003 January 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522001&dopt=Abstract ·
Induction therapy by frequent administration of doxorubicin with four other drugs, followed by intensive consolidation and maintenance therapy for adult acute lymphoblastic leukemia: the JALSG-ALL93 study. Author(s): Takeuchi J, Kyo T, Naito K, Sao H, Takahashi M, Miyawaki S, Kuriyama K, Ohtake S, Yagasaki F, Murakami H, Asou N, Ino T, Okamoto T, Usui N, Nishimura M, Shinagawa K, Fukushima T, Taguchi H, Morii T, Mizuta S, Akiyama H, Nakamura Y, Ohshima T, Ohno R. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2002 July; 16(7): 1259-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12094249&dopt=Abstract
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Influence of ceramide metabolism on P-glycoprotein function in immature acute myeloid leukemia KG1a cells. Author(s): Plo I, Lehne G, Beckstrom KJ, Maestre N, Bettaieb A, Laurent G, Lautier D. Source: Molecular Pharmacology. 2002 August; 62(2): 304-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12130682&dopt=Abstract
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Intensified double induction therapy with high dose mitoxantrone, etoposide, mamsacrine and high dose ara-C for elderly acute myeloid leukemia patients aged 61-65 years. Author(s): Schaich M, Illmer T, Aulitzky W, Bodenstein H, Clemens M, Neubauer A, Repp R, Schakel U, Soucek S, Wandt H, Ehninger G; SHG AML96 Study Group. Source: Haematologica. 2002 August; 87(8): 808-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12161356&dopt=Abstract
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Interferon-alpha therapy following autologous peripheral blood stem cell transplantation for adult T cell leukemia/lymphoma. Author(s): Fujiwara H, Arima N, Akasaki Y, Ohtsubo H, Ozaki A, Kukita T, Matsushita K, Arimura K, Suruga Y, Wakamatsu S, Matsumoto T, Hidaka S, Eizuru Y, Tei C. Source: Acta Haematologica. 2002; 107(4): 213-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12053149&dopt=Abstract
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Interim comparison of a continuous infusion versus a short daily infusion of cytarabine given in combination with cladribine for pediatric acute myeloid leukemia. Author(s): Crews KR, Gandhi V, Srivastava DK, Razzouk BI, Tong X, Behm FG, Plunkett W, Raimondi SC, Pui CH, Rubnitz JE, Stewart CF, Ribeiro RC. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 October 15; 20(20): 4217-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377965&dopt=Abstract
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Intermedeol isolated from the leaves of Ligularia fischeri var. spiciformis induces the differentiation of human acute promyeocytic leukemia HL-60 Cells. Author(s): Jeong SH, Koo SJ, Choi JH, Park JH, Ha J, Park HJ, Lee KT. Source: Planta Medica. 2002 October; 68(10): 881-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391549&dopt=Abstract
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Intermediate doses of melphalan and dexamethasone are better than vincristine, adriamycin, and dexamethasone (VAD) and polychemotherapy for the treatment of primary plasma cell leukemia. Author(s): Vela-Ojeda J, Garcia-Ruiz Esparza MA, Rosas-Cabral A, Padilla-Gonzalez Y, Garcia-Chavez J, Tripp-Villanueva F, Sanchez-Cortes E, Ayala-Sanchez M, Garcia-Leon LD, Montiel-Cervantes L, Rubio-Borja ME. Source: Annals of Hematology. 2002 July; 81(7): 362-7. Epub 2002 June 25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12185504&dopt=Abstract
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Limited and optimal sampling strategies for etoposide and etoposide catechol in children with leukemia. Author(s): Panetta JC, Wilkinson M, Pui CH, Relling MV. Source: Journal of Pharmacokinetics and Pharmacodynamics. 2002 April; 29(2): 171-88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12361242&dopt=Abstract
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Long-term disease-free survival in a primary plasma cell leukemia treated by VAD, autologous PBSC transplantation, and IFN-alpha. Author(s): Buchler T, Ferra C, Domingo A, Gallardo D, Sarra J, Granena A. Source: American Journal of Hematology. 2002 September; 71(1): 62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12221683&dopt=Abstract
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Long-term outcomes of acute myeloid leukemia in adults in Pakistan. Author(s): Kakepoto GN, Burney IA, Zaki S, Adil SN, Khurshid M. Source: J Pak Med Assoc. 2002 October; 52(10): 482-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553679&dopt=Abstract
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Loss of heterozygosity of p16 correlates with minimal residual disease at the end of the induction therapy in non-high risk childhood B-cell precursor acute lymphoblastic leukemia. Author(s): Tutor O, Diaz MA, Ramirez M, Algara P, Madero L, Martinez P. Source: Leukemia Research. 2002 September; 26(9): 817-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12127556&dopt=Abstract
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Methotrexate induced seizures associated with acute reversible magnetic resonance imaging (MRI) changes in a patient with acute lymphoblastic leukemia. Author(s): Rao RD, Swanson JW, Dejesus RS, Hunt CH, Tefferi A.
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Source: Leukemia & Lymphoma. 2002 June; 43(6): 1333-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12153004&dopt=Abstract ·
Methotrexate polyglutamation may lack prognostic significance in children with Bcell precursor acute lymphoblastic leukemia treated with intensive oral methotrexate. Author(s): Mantadakis E, Smith AK, Hynan L, Winick NJ, Kamen BA. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 November; 24(8): 636-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439035&dopt=Abstract
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Minor histocompatibility antigens--targets of graft versus leukemia responses. Author(s): Riddell SR, Murata M, Bryant S, Warren EH. Source: International Journal of Hematology. 2002 August; 76 Suppl 2: 155-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12430918&dopt=Abstract
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Mitoxantrone and cytarabine induction, high-dose cytarabine, and etoposide intensification for pediatric patients with relapsed or refractory acute myeloid leukemia: Children's Cancer Group Study 2951. Author(s): Wells RJ, Adams MT, Alonzo TA, Arceci RJ, Buckley J, Buxton AB, Dusenbery K, Gamis A, Masterson M, Vik T, Warkentin P, Whitlock JA; Children's Cancer Group Study 2951. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 1; 21(15): 2940-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885813&dopt=Abstract
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Modulation of the phototoxic effect of hypericin in human leukemia CEM cell line by N-ethylmaleimide, amiloride and omeprazole. Author(s): Mirossay A, Mirossay L, Sarissky M, Papp P, Mojzis J. Source: Physiological Research / Academia Scientiarum Bohemoslovaca. 2002; 51(6): 641-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12511190&dopt=Abstract
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Molecular analysis of Tripterygium hypoglaucum (level) Hutch-induced mutations at the HPRT locus in human promyelocytic leukemia cells by multiplex polymerase chain reaction. Author(s): Liu SX, Cao J, An H. Source: Mutagenesis. 2003 January; 18(1): 77-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473739&dopt=Abstract
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Molecular cytogenetic characterization of drug-resistant leukemia cell lines by comparative genomic hybridization and fluorescence in situ hybridization. Author(s): Shimizu H, Fukuda T, Ghazizadeh M, Nagashima M, Kawanami O, Suzuki T.
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Source: Japanese Journal of Cancer Research : Gann. 2002 August; 93(8): 902-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716468&dopt=Abstract ·
Multidrug resistance modulators PSC 833 and CsA show differential capacity to induce apoptosis in lymphoid leukemia cell lines independently of their MDR phenotype. Author(s): Lopes EC, Garcia M, Benavides F, Shen J, Conti CJ, Alvarez E, Hajos SE. Source: Leukemia Research. 2003 May; 27(5): 413-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12620293&dopt=Abstract
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Multifactorial activities of nonsteroidal antiestrogens against leukemia. Author(s): Hayon T, Atlas L, Levy E, Dvilansky A, Shpilberg O, Nathan I. Source: Cancer Detection and Prevention. 2003; 27(5): 389-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14585326&dopt=Abstract
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Myelodysplastic syndrome and acute myeloid leukemia after autotransplantation for lymphoma: a multicenter case-control study. Author(s): Metayer C, Curtis RE, Vose J, Sobocinski KA, Horowitz MM, Bhatia S, Fay JW, Freytes CO, Goldstein SC, Herzig RH, Keating A, Miller CB, Nevill TJ, Pecora AL, Rizzo JD, Williams SF, Li CY, Travis LB, Weisdorf DJ. Source: Blood. 2003 March 1; 101(5): 2015-23. Epub 2002 October 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393427&dopt=Abstract
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Natural history of more than 20 years of node-positive primary breast carcinoma treated with cyclophosphamide, methotrexate, and fluorouracil-based adjuvant chemotherapy: a study by the Cancer and Leukemia Group B. Author(s): Weiss RB, Woolf SH, Demakos E, Holland JF, Berry DA, Falkson G, Cirrincione CT, Robbins A, Bothun S, Henderson IC, Norton L; Cancer and Leukemia Group B. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 May 1; 21(9): 1825-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12721260&dopt=Abstract
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Novel plant triterpenoid drug amooranin overcomes multidrug resistance in human leukemia and colon carcinoma cell lines. Author(s): Ramachandran C, Rabi T, Fonseca HB, Melnick SJ, Escalon EA. Source: International Journal of Cancer. Journal International Du Cancer. 2003 July 20; 105(6): 784-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767063&dopt=Abstract
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Nutritional support for chronic myelogenous and other leukemias: a review of the scientific literature. Author(s): Steriti R.
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Source: Alternative Medicine Review : a Journal of Clinical Therapeutic. 2002 October; 7(5): 404-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12410624&dopt=Abstract ·
Obstructive sleep apnea secondary to chronic lymphocytic leukemia. Author(s): Chehal A, Haidar JH, Jabbour R, Yammout B, Bazarbachi A. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 November; 13(11): 1833. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419760&dopt=Abstract
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Occurrence of a pulmonary carcinoid following allogeneic stem cell transplantation for chronic myelogenous leukemia: a case report. Author(s): Fiebiger W, Kurtaran A, Novotny C, Kainberger F, Dekan G, Raderer M. Source: Annals of Hematology. 2003 June; 82(6): 374-6. Epub 2003 April 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12719884&dopt=Abstract
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Oral induction and consolidation chemotherapy with idarubicin and etoposide in elderly patients with acute myeloid leukemia. Author(s): Oriol A, Ribera JM, Brunet S, Esteve J, Bueno J, Llorente A. Source: Haematologica. 2003 February; 88(2): 229-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604418&dopt=Abstract
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Outcome after induction chemotherapy for older patients with acute myeloid leukemia is not improved with mitoxantrone and etoposide compared to cytarabine and daunorubicin: a Southwest Oncology Group study. Author(s): Anderson JE, Kopecky KJ, Willman CL, Head D, O'Donnell MR, Luthardt FW, Norwood TH, Chen IM, Balcerzak SP, Johnson DB, Appelbaum FR. Source: Blood. 2002 December 1; 100(12): 3869-76. Epub 2002 August 01. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393614&dopt=Abstract
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Overexpression of the atypical protein kinase C zeta reduces topoisomerase II catalytic activity, cleavable complexes formation, and drug-induced cytotoxicity in monocytic U937 leukemia cells. Author(s): Plo I, Hernandez H, Kohlhagen G, Lautier D, Pommier Y, Laurent G. Source: The Journal of Biological Chemistry. 2002 August 30; 277(35): 31407-15. Epub 2002 June 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12105221&dopt=Abstract
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Partially successful treatment of a patient with chronic lymphocytic leukemia and Hodgkin's disease: case report and literature review. Author(s): Adiga GU, Abebe L, Wiernik PH.
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Source: American Journal of Hematology. 2003 April; 72(4): 267-73. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666139&dopt=Abstract ·
Patient stratification based on prednisolone-vincristine-asparaginase resistance profiles in children with acute lymphoblastic leukemia. Author(s): Den Boer ML, Harms DO, Pieters R, Kazemier KM, Gobel U, Korholz D, Graubner U, Haas RJ, Jorch N, Spaar HJ, Kaspers GJ, Kamps WA, Van der Does-Van den Berg A, Van Wering ER, Veerman AJ, Janka-Schaub GE. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 September 1; 21(17): 3262-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947061&dopt=Abstract
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PC-SPES decreases proliferation and induces differentiation and apoptosis of human acute myeloid leukemia cells. Author(s): Ikezoe T, Chen S, Saito T, Asou H, Kyo T, Tanosaki S, Heber D, Taguchi H, Koeffler HP. Source: International Journal of Oncology. 2003 October; 23(4): 1203-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12964005&dopt=Abstract
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Pentacyclic triterpenes from Chrysobalanaceae species: cytotoxicity on multidrug resistant and sensitive leukemia cell lines. Author(s): Fernandes J, Castilho RO, da Costa MR, Wagner-Souza K, Coelho Kaplan MA, Gattass CR. Source: Cancer Letters. 2003 February 20; 190(2): 165-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12565171&dopt=Abstract
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Perfusion MRI and SPECT of brain after treatment for childhood acute lymphoblastic leukemia. Author(s): Paakko E, Lehtinen S, Harila-Saari A, Ahonen A, Jauhiainen J, Torniainen P, Pyhtinen J, Lanning M. Source: Medical and Pediatric Oncology. 2003 February; 40(2): 88-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461791&dopt=Abstract
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Peripheral blood stem cell collection in children with acute leukemia: effectiveness of the 'DIAVE' mobilizing regimen. Author(s): Balduzzi A, Perseghin P, Dassi M, Bonanomi S, Rovelli A, Gaipa G, Biondi A, Uderzo C. Source: Bone Marrow Transplantation. 2002 October; 30(7): 413-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12368951&dopt=Abstract
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Pharmacokinetics and pharmacodynamics of oral etoposide in children with relapsed or refractory acute lymphoblastic leukemia. Author(s): Edick MJ, Gajjar A, Mahmoud HH, van de Poll ME, Harrison PL, Panetta JC, Rivera GK, Ribeiro RC, Sandlund JT, Boyett JM, Pui CH, Relling MV.
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Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 April 1; 21(7): 1340-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663724&dopt=Abstract ·
Pharmacokinetics of vincristine monotherapy in childhood acute lymphoblastic leukemia. Author(s): Groninger E, Meeuwsen-de Boar T, Koopmans P, Uges D, Sluiter W, Veerman A, Kamps W, de Graaf S. Source: Pediatric Research. 2002 July; 52(1): 113-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12084857&dopt=Abstract
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Phase 3 study of the multidrug resistance modulator PSC-833 in previously untreated patients 60 years of age and older with acute myeloid leukemia: Cancer and Leukemia Group B Study 9720. Author(s): Baer MR, George SL, Dodge RK, O'Loughlin KL, Minderman H, Caligiuri MA, Anastasi J, Powell BL, Kolitz JE, Schiffer CA, Bloomfield CD, Larson RA. Source: Blood. 2002 August 15; 100(4): 1224-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12149202&dopt=Abstract
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Phase I and pharmacokinetic study of DX-8951f (exatecan mesylate), a hexacyclic camptothecin, on a daily-times-five schedule in patients with advanced leukemia. Author(s): Giles FJ, Cortes JE, Thomas DA, Garcia-Manero G, Faderl S, Jeha S, De Jager RL, Kantarjian HM. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2002 July; 8(7): 2134-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12114413&dopt=Abstract
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Phase I evaluation of prolonged-infusion gemcitabine with irinotecan for relapsed or refractory leukemia or lymphoma. Author(s): Bass AJ, Gockerman JP, Hammett E, DeCastro CM, Adams DJ, Rosner GL, Payne N, Davis P, Foster T, Moore JO, Rizzieri DA. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 July 1; 20(13): 2995-3000. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12089230&dopt=Abstract
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Phase III trial of a humanized anti-CD33 antibody (HuM195) in patients with relapsed or refractory acute myeloid leukemia. Author(s): Gibson AD. Source: Clin Lymphoma. 2002 June; 3(1): 18-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12141950&dopt=Abstract
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Possible dominant-negative mutation of the SHIP gene in acute myeloid leukemia. Author(s): Luo JM, Yoshida H, Komura S, Ohishi N, Pan L, Shigeno K, Hanamura I, Miura K, Iida S, Ueda R, Naoe T, Akao Y, Ohno R, Ohnishi K.
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Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 January; 17(1): 1-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529653&dopt=Abstract ·
Postremission therapy with low-dose interleukin 2 with or without intermediate pulse dose interleukin 2 therapy is well tolerated in elderly patients with acute myeloid leukemia: Cancer and Leukemia Group B study 9420. Author(s): Farag SS, George SL, Lee EJ, Baer M, Dodge RK, Becknell B, Fehniger TA, Silverman LR, Crawford J, Bloomfield CD, Larson RA, Schiffer CA, Caligiuri MA. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2002 September; 8(9): 2812-9. Erratum In: Clin Cancer Res. 2002 November; 8(11): 3639. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12231521&dopt=Abstract
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Potentiation of 1,25-dihydroxyvitamin D(3)-induced differentiation of human promyelocytic leukemia cells into monocytes by costunolide, a germacranolide sesquiterpene lactone. Author(s): Kim SH, Kang SN, Kim HJ, Kim TS. Source: Biochemical Pharmacology. 2002 October 15; 64(8): 1233-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12234604&dopt=Abstract
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Prolonged administration of all-trans retinoic acid in combination with intensive chemotherapy and G-CSF for adult acute myelogenous leukemia: single-centre pilot study in different risk groups. Author(s): Bassan R, Chiodini B, Lerede T, Giussani U, Oldani E, Buelli M, Rossi A, Viero P, Rambaldi A, Barbui T. Source: The Hematology Journal : the Official Journal of the European Haematology Association / Eha. 2002; 3(4): 193-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12189565&dopt=Abstract
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Prolonged single-agent versus combination chemotherapy in indolent follicular lymphomas: a study of the cancer and leukemia group B. Author(s): Peterson BA, Petroni GR, Frizzera G, Barcos M, Bloomfield CD, Nissen NI, Hurd DD, Henderson ES, Sartiano GP, Johnson JL, Holland JF, Gottlieb AJ. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 January 1; 21(1): 5-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12506163&dopt=Abstract
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Quercetin glucuronides inhibited 2-aminofluorene acetylation in human acute myeloid HL-60 leukemia cells. Author(s): Kuo HM, Ho HJ, Chao PD, Chung JG. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2002 October; 9(7): 625-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12487326&dopt=Abstract
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Randomized phase II study of cisplatin with gemcitabine or paclitaxel or vinorelbine as induction chemotherapy followed by concomitant chemoradiotherapy for stage IIIB non-small-cell lung cancer: cancer and leukemia group B study 9431. Author(s): Vokes EE, Herndon JE 2nd, Crawford J, Leopold KA, Perry MC, Miller AA, Green MR. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 October 15; 20(20): 4191-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377962&dopt=Abstract
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Randomized trial of dose-dense versus conventionally scheduled and sequential versus concurrent combination chemotherapy as postoperative adjuvant treatment of node-positive primary breast cancer: first report of Intergroup Trial C9741/Cancer and Leukemia Group B Trial 9741. Author(s): Citron ML, Berry DA, Cirrincione C, Hudis C, Winer EP, Gradishar WJ, Davidson NE, Martino S, Livingston R, Ingle JN, Perez EA, Carpenter J, Hurd D, Holland JF, Smith BL, Sartor CI, Leung EH, Abrams J, Schilsky RL, Muss HB, Norton L. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 April 15; 21(8): 1431-9. Epub 2003 February 13. Erratum In: J Clin Oncol. 2003 June 1; 21(11): 2226. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668651&dopt=Abstract
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Results of triple therapy with interferon-alpha, cytarabine, and homoharringtonine, and the impact of adding imatinib to the treatment sequence in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in early chronic phase. Author(s): O'Brien S, Giles F, Talpaz M, Cortes J, Rios MB, Shan J, Thomas D, Andreeff M, Kornblau S, Faderl S, Garcia-Manero G, White K, Mallard S, Freireich E, Kantarjian HM. Source: Cancer. 2003 September 1; 98(5): 888-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12942553&dopt=Abstract
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Resveratrol blocks interleukin-1beta-induced activation of the nuclear transcription factor NF-kappaB, inhibits proliferation, causes S-phase arrest, and induces apoptosis of acute myeloid leukemia cells. Author(s): Estrov Z, Shishodia S, Faderl S, Harris D, Van Q, Kantarjian HM, Talpaz M, Aggarwal BB. Source: Blood. 2003 August 1; 102(3): 987-95. Epub 2003 April 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12689943&dopt=Abstract
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Resveratrol, a natural product derived from grapes, is a new inducer of differentiation in human myeloid leukemias. Author(s): Asou H, Koshizuka K, Kyo T, Takata N, Kamada N, Koeffier HP. Source: International Journal of Hematology. 2002 June; 75(5): 528-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12095155&dopt=Abstract
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Reversible vincristine-related flaccid paralysis in a child with acute lymphoblastic leukemia. Author(s): Fioredda F, Micalizzi C, Lanciotti M, Dufour C, Lamba LD, Fiocchi I. Source: Medical and Pediatric Oncology. 2002 August; 39(2): 141-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12116067&dopt=Abstract
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Risk of secondary leukemia after a solid tumor in childhood according to the dose of epipodophyllotoxins and anthracyclines: a case-control study by the Societe Francaise d'Oncologie Pediatrique. Author(s): Le Deley MC, Leblanc T, Shamsaldin A, Raquin MA, Lacour B, Sommelet D, Chompret A, Cayuela JM, Bayle C, Bernheim A, de Vathaire F, Vassal G, Hill C; Societe Francaise d'Oncologie Pediatrique. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 March 15; 21(6): 1074-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637473&dopt=Abstract
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RNA interference is a functional pathway with therapeutic potential in human myeloid leukemia cell lines. Author(s): Cioca DP, Aoki Y, Kiyosawa K. Source: Cancer Gene Therapy. 2003 February; 10(2): 125-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12536201&dopt=Abstract
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Sesquiterpenes (costunolide and zaluzanin D) isolated from laurel (Laurus nobilis L.) induce cell death and morphological change indicative of apoptotic chromatin condensation in leukemia HL-60 cells. Author(s): Hibasami H, Yamada Y, Moteki H, Katsuzaki H, Imai K, Yoshioka K, Komiya T. Source: International Journal of Molecular Medicine. 2003 August; 12(2): 147-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851709&dopt=Abstract
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Severe hyperglycemia as a complication of big ICE chemotherapy in a patient with acute myeloblastic leukemia. Author(s): Beyan C, Kaptan K, Cetin T, Nevruz O. Source: Haematologia. 2002; 32(4): 505-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803126&dopt=Abstract
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Severe hyperphosphatemia resulting from high-dose liposomal amphotericin in a child with leukemia. Author(s): Jain A, Butani L. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 April; 25(4): 324-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679649&dopt=Abstract
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Sophoranone, extracted from a traditional Chinese medicine Shan Dou Gen, induces apoptosis in human leukemia U937 cells via formation of reactive oxygen species and opening of mitochondrial permeability transition pores. Author(s): Kajimoto S, Takanashi N, Kajimoto T, Xu M, Cao J, Masuda Y, Aiuchi T, Nakajo S, Ida Y, Nakaya K. Source: International Journal of Cancer. Journal International Du Cancer. 2002 June 20; 99(6): 879-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12115492&dopt=Abstract
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Specific induction of apoptosis by 1,8-cineole in two human leukemia cell lines, but not a in human stomach cancer cell line. Author(s): Moteki H, Hibasami H, Yamada Y, Katsuzaki H, Imai K, Komiya T. Source: Oncol Rep. 2002 July-August; 9(4): 757-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12066204&dopt=Abstract
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Structure-function relationship exists for ginsenosides in reducing cell proliferation and inducing apoptosis in the human leukemia (THP-1) cell line. Author(s): Popovich DG, Kitts DD. Source: Archives of Biochemistry and Biophysics. 2002 October 1; 406(1): 1-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12234484&dopt=Abstract
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Successful treatment of B cell chronic lymphocytic leukemia-associated severe paraneoplastic pemphigus with cyclosporin A. Author(s): Gergely L, Varoczy L, Vadasz G, Remenyik E, Illes A. Source: Acta Haematologica. 2003; 109(4): 202-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853695&dopt=Abstract
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Suppression of phorbol ester-induced NF-kappaB activation by capsaicin in cultured human promyelocytic leukemia cells. Author(s): Han SS, Keum YS, Chun KS, Surh YJ. Source: Arch Pharm Res. 2002 August; 25(4): 475-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12214859&dopt=Abstract
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Symptomatic hypoglycemia in children receiving oral purine analogues for treatment of childhood acute lymphoblastic leukemia. Author(s): Ziino O, Russo D, Orlando MA, Benigno V, Locatelli F, Arico M. Source: Medical and Pediatric Oncology. 2002 July; 39(1): 32-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12116076&dopt=Abstract
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Synergistic induction of 1,25-dihydroxyvitamin D(3)- and all-trans-retinoic acidinduced differentiation of HL-60 leukemia cells by yomogin, a sesquiterpene lactone from Artemisia princeps. Author(s): Kim SH, Kim TS.
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Source: Planta Medica. 2002 October; 68(10): 886-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391550&dopt=Abstract ·
The combined effects of antibacterial peptide cecropin A and anti-cancer agents on leukemia cells. Author(s): Hui L, Leung K, Chen HM. Source: Anticancer Res. 2002 September-October; 22(5): 2811-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530001&dopt=Abstract
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The comprehensive evaluation on four indices of drug resistance in acute myeloid leukemia. Author(s): Chen Y, He M, Xiang Z, Wu Y, Yue B, Yu D, Li H. Source: J Tongji Med Univ. 1999; 19(3): 194-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840892&dopt=Abstract
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The dose related effect of steroids on blast reduction rate and event free survival in children with acute lymphoblastic leukemia. Author(s): Yetgin S, Cetin M. Source: Leukemia & Lymphoma. 2003 March; 44(3): 489-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688320&dopt=Abstract
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The influence of etoposide on the distribution of tubulin in human leukemia cell line HL-60. Author(s): Grzanka A, Grzanka D. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2003 January; 9(1): Br66-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552240&dopt=Abstract
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The presence of an HLA-identical sibling donor has no impact on outcome of patients with high-risk MDS or secondary AML (sAML) treated with intensive chemotherapy followed by transplantation: results of a prospective study of the EORTC, EBMT, SAKK and GIMEMA Leukemia Groups (EORTC study 06921). Author(s): Oosterveld M, Suciu S, Verhoef G, Labar B, Belhabri A, Aul C, Selleslag D, Ferrant A, Wijermans P, Mandelli F, Amadori S, Jehn U, Muus P, Zittoun R, Hess U, Anak O, Beeldens F, Willemze R, de Witte T. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 May; 17(5): 859-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750698&dopt=Abstract
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The role of posttransplantation maintenance chemotherapy in improving the outcome of autotransplantation in adult acute lymphoblastic leukemia. Author(s): Powles R, Sirohi B, Treleaven J, Kulkarni S, Tait D, Singhal S, Mehta J.
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Source: Blood. 2002 September 1; 100(5): 1641-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12176883&dopt=Abstract ·
The third-generation bisphosphonate zoledronate synergistically augments the antiPh+ leukemia activity of imatinib mesylate. Author(s): Kuroda J, Kimura S, Segawa H, Kobayashi Y, Yoshikawa T, Urasaki Y, Ueda T, Enjo F, Tokuda H, Ottmann OG, Maekawa T. Source: Blood. 2003 September 15; 102(6): 2229-35. Epub 2003 May 22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763930&dopt=Abstract
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The topoisomerase I-binding RING protein, topors, is associated with promyelocytic leukemia nuclear bodies. Author(s): Rasheed ZA, Saleem A, Ravee Y, Pandolfi PP, Rubin EH. Source: Experimental Cell Research. 2002 July 15; 277(2): 152-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12083797&dopt=Abstract
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The treatment of acute myeloid leukemia with mitoxantrone, etoposide and low-dose cytarabine in elderly patients - a report of Polish Acute Leukemia Group (PALG) phase II study. Author(s): Wrzesien-Kus A, Robak T, Jamroziak K, Wierzbowska A, Dmoszynska A, Adamczyk-Cioch M, Kuliczkowski K, Mazur G, Holowiecki J, Konopka L, Maj S, Marianska B, Zawilska K; Polish Acute Leukemia Group (PALG) phase II study. Source: Neoplasma. 2002; 49(6): 405-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584589&dopt=Abstract
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Therapy-related myelodysplastic syndrome or acute myelogenous leukemia in patients with acute promyelocytic leukemia (APL). Author(s): Garcia-Manero G, Kantarjian HM, Kornblau S, Estey E. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2002 September; 16(9): 1888. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12200720&dopt=Abstract
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Thromboembolic events in children with acute lymphoblastic leukemia (BFM protocols): prednisone versus dexamethasone administration. Author(s): Nowak-Gottl U, Ahlke E, Fleischhack G, Schwabe D, Schobess R, Schumann C, Junker R. Source: Blood. 2003 April 1; 101(7): 2529-33. Epub 2002 November 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12517808&dopt=Abstract
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Timed sequential therapy of acute myelogenous leukemia in adults: a phase II study of retinoids in combination with the sequential administration of cytosine arabinoside, idarubicin and etoposide. Author(s): Bolanos-Meade J, Karp JE, Guo C, Sarkodee-Adoo CB, Rapoport AP, Tidwell ML, Buddharaju LN, Chen TT.
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Source: Leukemia Research. 2003 April; 27(4): 313-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531222&dopt=Abstract ·
Timed-sequential chemotherapy with concomitant granulocyte colony-stimulating factor for newly diagnosed de novo acute myelogenous leukemia. Author(s): He XY, Pohlman B, Lichtin A, Rybicki L, Kalaycio M. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 June; 17(6): 1078-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764371&dopt=Abstract
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Translocation (11;11)(p13- p15;q23) in a child with therapy-related acute myeloid leukemia following chemotherapy with DNA-topoisomerase II inhibitors for Langerhans cell histiocytosis. Author(s): Silva ML, Land MG, Maradei S, Otero L, Veith M, Brito G, Klumb C, Fernandez T, Pombo-de-Oliveira MS. Source: Cancer Genetics and Cytogenetics. 2002 May; 135(1): 101-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12072208&dopt=Abstract
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Treatment of adult T-cell leukemia-lymphoma by CHOP followed by therapy with antinucleosides, alpha interferon and oral etoposide. Author(s): Besson C, Panelatti G, Delaunay C, Gonin C, Brebion A, Hermine O, Plumelle Y. Source: Leukemia & Lymphoma. 2002 December; 43(12): 2275-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12613513&dopt=Abstract
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Treatment of refractory acute leukemia with timed sequential chemotherapy using topotecan followed by etoposide + mitoxantrone (T-EM) and correlation with topoisomerase II levels. Author(s): Mainwaring MG, Rimsza LM, Chen SF, Gomez SP, Weeks FW, Reddy V, Lynch J, May WS, Kahn S, Moreb J, Leather H, Braylan R, Rowe TC, Fieniewicz KJ, Wingard JR. Source: Leukemia & Lymphoma. 2002 May; 43(5): 989-99. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12148910&dopt=Abstract
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Treatment outcome of adult acute lymphocytic leukemia with VPD(L) regimen: analysis of prognostic factors. Author(s): Park SR, Kim JH, Kim do Y, Lee S, Lee SY, Choi IS, Yoon SS, Park S, Kim BG, Kim NK. Source: Korean J Intern Med. 2003 March; 18(1): 21-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760264&dopt=Abstract
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Two cases of therapy-related acute promyelocytic leukemia (t-APL) after mantle cell lymphoma and gestational trophoblastic disease. Author(s): Au WY, Ma SK, Chung LP, Chim CS, Kwong YL.
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Source: Annals of Hematology. 2002 November; 81(11): 659-61. Epub 2002 November 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454706&dopt=Abstract ·
Urate-oxidase in the prevention and treatment of metabolic complications in patients with B-cell lymphoma and leukemia, treated in the Societe Francaise d'Oncologie Pediatrique LMB89 protocol. Author(s): Patte C, Sakiroglu C, Ansoborlo S, Baruchel A, Plouvier E, Pacquement H, Babin-Boilletot A; Societe Francaise d'Oncologie Pediatrique. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 May; 13(5): 789-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12075750&dopt=Abstract
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Variant translocations of 11q23 in infant acute lymphoblastic leukemia (ALL): do outcomes differ from t(4;11)? Author(s): Jakab Z, Balogh E, Karaszi E, Kappelmayer J, Kiss C, Olah E. Source: Medical and Pediatric Oncology. 2002 July; 39(1): 63-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12116086&dopt=Abstract
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Veno-occlusive disease in a male patient with Marfan syndrome and common acute lymphoblastic leukemia during induction therapy. Author(s): Kraemer DM, Waschke J, Kunzmann V, Wilhelm M. Source: Annals of Hematology. 2003 July; 82(7): 444-7. Epub 2003 May 22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761649&dopt=Abstract
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Vincristine-induced neuropathy as the initial presentation of charcot-marie-tooth disease in acute lymphoblastic leukemia: a Pediatric Oncology Group study. Author(s): Chauvenet AR, Shashi V, Selsky C, Morgan E, Kurtzberg J, Bell B; Pediatric Oncology Group Study. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 April; 25(4): 316-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679647&dopt=Abstract
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Viridans streptococcal sepsis: clinical features and complications in childhood acute myeloid leukemia. Author(s): Okamoto Y, Ribeiro RC, Srivastava DK, Shenep JL, Pui CH, Razzouk BI. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 September; 25(9): 696-703. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12972804&dopt=Abstract
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Vitamin D2 analog 19-nor-1,25-dihydroxyvitamin D2: antitumor activity against leukemia, myeloma, and colon cancer cells. Author(s): Kumagai T, O'Kelly J, Said JW, Koeffler HP.
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Source: Journal of the National Cancer Institute. 2003 June 18; 95(12): 896-905. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12813173&dopt=Abstract ·
Voriconazole in the management of invasive aspergillosis in two patients with acute myeloid leukemia undergoing stem cell transplantation. Author(s): Mattei D, Mordini N, Lo Nigro C, Ghirardo D, Ferrua MT, Osenda M, Gallamini A, Bacigalupo A, Viscoli C. Source: Bone Marrow Transplantation. 2002 December; 30(12): 967-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12476292&dopt=Abstract
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Weekly, high-dose paclitaxel in advanced lung carcinoma: a phase II study with pharmacokinetics by the Cancer and Leukemia Group B. Author(s): Akerley W, Herndon JE, Egorin MJ, Lyss AP, Kindler HL, Savarese DM, Sherman CA, Rosen DM, Hollis D, Ratain MJ, Green MR. Source: Cancer. 2003 May 15; 97(10): 2480-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733147&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: ·
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.comÒ: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDÒHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to leukemia; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation:
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General Overview Angioedema Source: Integrative Medicine Communications; www.drkoop.com Bone Marrow Disorders Source: Integrative Medicine Communications; www.drkoop.com Brain Cancer Source: Integrative Medicine Communications; www.drkoop.com Cancer Prevention and Diet Source: Healthnotes, Inc.; www.healthnotes.com Candida/yeast Hypersensitivity Syndrome Source: Prima Communications, Inc.www.personalhealthzone.com Capillary Fragility Source: Healthnotes, Inc.; www.healthnotes.com Chronic Myelogenous Leukemia Source: Integrative Medicine Communications; www.drkoop.com Gout Source: Integrative Medicine Communications; www.drkoop.com Hives Source: Healthnotes, Inc.; www.healthnotes.com Leukemia Source: Integrative Medicine Communications; www.drkoop.com Lung Cancer Source: Healthnotes, Inc.; www.healthnotes.com Lymphoma Source: Integrative Medicine Communications; www.drkoop.com Myelofibrosis Source: Integrative Medicine Communications; www.drkoop.com Myeloproliferative Disorders Source: Integrative Medicine Communications; www.drkoop.com Polycythemia Vera Source: Integrative Medicine Communications; www.drkoop.com Sinus Congestion Source: Healthnotes, Inc.; www.healthnotes.com Thrombocytosis Source: Integrative Medicine Communications; www.drkoop.com
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Uveitis Source: Integrative Medicine Communications; www.drkoop.com ·
Alternative Therapy Myotherapy Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,931,00.html
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Herbs and Supplements Acanthopanax Senticosus Source: Integrative Medicine Communications; www.drkoop.com Achillea Alternative names: Yarrow; Achillea millefolium L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Aesculus Alternative names: Horse Chestnut; Aesculus hippocastanum L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Aloe Source: Prima Communications, Inc.www.personalhealthzone.com Aloe Vera Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10001,00.html Arctium Alternative names: Burdock, Gobo; Arctium lappa L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Arnica Alternative names: Arnica montana L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Betula Alternative names: Birch; Betula sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Boswellia Alternative names: Frankincense; Boswellia serrata Roxb. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Calciferol Source: Integrative Medicine Communications; www.drkoop.com
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Calcitrol Source: Integrative Medicine Communications; www.drkoop.com Cat's Claw Source: Prima Communications, Inc.www.personalhealthzone.com Chemotherapy Source: Healthnotes, Inc.; www.healthnotes.com Cholecalciferol Source: Integrative Medicine Communications; www.drkoop.com Coenzyme Q10 Source: Integrative Medicine Communications; www.drkoop.com Coq10 Source: Integrative Medicine Communications; www.drkoop.com Curcuma Alternative names: Turmeric; Curcuma longa L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Cyclophosphamide Source: Healthnotes, Inc.; www.healthnotes.com Docetaxel Source: Healthnotes, Inc.; www.healthnotes.com Eleuthero Alternative names: Siberian Ginseng, Eleuthero; Acanthopanax/Eleutherococcus senticosus Rupr. & Maxim. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Eleuthero Source: Integrative Medicine Communications; www.drkoop.com Eleutherococcus Senticosus Source: Integrative Medicine Communications; www.drkoop.com Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Eugenia Clove Alternative names: Cloves; Eugenia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Fluorouracil Source: Healthnotes, Inc.; www.healthnotes.com Glycyrrhiza1 Alternative names: Licorice; Glycyrrhiza glabra L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Humulus Alternative names: Hops; Humulus lupulus L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Hydrastis Alternative names: Goldenseal; Hydrastis canadensis L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Melatonin Source: Integrative Medicine Communications; www.drkoop.com Melatonin Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,804,00.html Menadione Source: Integrative Medicine Communications; www.drkoop.com Menaphthone Source: Integrative Medicine Communications; www.drkoop.com Menaquinone Source: Integrative Medicine Communications; www.drkoop.com Methotrexate Source: Healthnotes, Inc.; www.healthnotes.com Paclitaxel Source: Healthnotes, Inc.; www.healthnotes.com Panax Alternative names: Ginseng; Panax ginseng Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Passiflora Alternative names: Passion Flower; Passiflora alata L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Pau D' Arco Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Phylloquinone Source: Integrative Medicine Communications; www.drkoop.com Phytolacca Alternative names: Poke root, Endod; Phytolacca dodecandra L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Siberian Ginseng Alternative names: Eleutherococcus senticosus, Acanthopanax senticosus, Eleuthero Source: Integrative Medicine Communications; www.drkoop.com Syzygium Clove Alternative names: Clove, Jamun; Syzygium sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Tanacetum Alternative names: Feverfew; Tanacetum parthenium (L.) Schultz-Bip. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Uncaria Catclaw Alternative names: Cat's Claw, Uno de Gato; Uncaria tomentosa (Willd.) D.C. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Viburnum Alternative names: Cramp Bark, Highbush Cranberry; Viburnum sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON LEUKEMIA Overview In this chapter, we will give you a bibliography on recent dissertations relating to leukemia. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “leukemia” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on leukemia, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Leukemia ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to leukemia. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: ·
A Study of Retroviral Neutralization by Monoclonal Antibodies Specific for the Murine Leukemia Virus Envelope Subunit Su by Burkhart, Michael Dominic; Phd from New York University, 2002, 163 pages http://wwwlib.umi.com/dissertations/fullcit/3062791
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A Study of the Pseudotypes of Vesicular Stomatitis Virus and Murine Leukemia Viruses by Sengupta, Sutapa; Phd from Mcmaster University (canada), 1976 http://wwwlib.umi.com/dissertations/fullcit/NK38024
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Adrenal Cortical Function in Murine Leukemia by Khalid, Rauf A; Advdeg from Mcgill University (canada), 1969 http://wwwlib.umi.com/dissertations/fullcit/NK03962
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An Immunological Study of Soluble Human Leukemia Associated Antigens by Yong, David C. T; Phd from The University of Manitoba (canada), 1973 http://wwwlib.umi.com/dissertations/fullcit/NK18113
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An Investigation of Functional Polymorphisms in the Folate Metabolic Pathway and Their Implications in Leukemia Risk by Skibola, Christine Frances; Phd from University of California, Berkeley, 2002, 142 pages http://wwwlib.umi.com/dissertations/fullcit/3063628
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An Ultrastructural and Immunocytochemical Investigation of the Assembly of Rauchscher Murine Leukemia Virus Temperature Sensitive Mutants by Yeger, Herman; Phd from University of Toronto (canada), 1978 http://wwwlib.umi.com/dissertations/fullcit/NK38876
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Antisense and Drug-resistance Gene Therapy in a Mouse Model of Chronic Myeloid Leukemia by Sweeney, Colin Lee; Phd from University of Minnesota, 2003, 216 pages http://wwwlib.umi.com/dissertations/fullcit/3087792
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Assessing the Relationship among Locus of Control, Perceived Competence and School Performance Variables for Pediatric Leukemia Patients by Loewy, Ben Zion; Phd from University of California, Berkeley, 2001, 68 pages http://wwwlib.umi.com/dissertations/fullcit/3044570
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Bovine Leukemia Virus Alters Growth Properties and Casein Synthesis in Mammary Epithelial Cells by Motton, Deborah Dianne; Phd from University of California, Berkeley, 2002, 101 pages http://wwwlib.umi.com/dissertations/fullcit/3082336
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Bovine Leukemia Virus: in Utero Transmission and Pathogenesis by Perdrizet, John Andrew; Phd from Cornell University, 2002, 268 pages http://wwwlib.umi.com/dissertations/fullcit/3037292
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Characterization of a Novel Myeloid Differentiation Antigen Associated with Acute Myelogenous Leukemia by Askew, David Stephen; Phd from The University of British Columbia (canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL35031
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Characterization of Ig Loci and V(d)j Recombination Activity in a Population of Abelson Murine Leukemia Virus-transformed Pre-b Cells Derived from Embryonic Stem Cells in Vitro by Webber, Travis David; Msc from University of Toronto (canada), 2002, 97 pages http://wwwlib.umi.com/dissertations/fullcit/MQ68757
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Characterization of the Receptors for Ige of Rat Basophilic Leukemia Cells by Helm, Ricki M; Phd from The University of Manitoba (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK47203
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Characterization of the Transformation and Signal Transduction Properties of Tel/jak2 Fusion Proteins Associated with Human Leukemias by Frantsve, Julie Carolyn; Phd from Harvard University, 2002, 264 pages http://wwwlib.umi.com/dissertations/fullcit/3038468
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Chemotherapy in Childhood Acute Lymphoblastic Leukemia. in Vitro Cellular Drug Resistance and Pharmacokinetics by Frost, Britt-marie Elisabeth; Phd from Uppsala Universitet (sweden), 2002, 85 pages http://wwwlib.umi.com/dissertations/fullcit/f738865
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Children Who Have Survived Leukemia: the Neuropsychological Deficits Associated with Their Arithmetic Performance by Penland, Elizabeth Ann, Phd from Texas A&m University - Commerce, 1996, 127 pages http://wwwlib.umi.com/dissertations/fullcit/9724622
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Cognitive and Emotional Late-effects from Treatment in Long-term Survivors of Childhood Acute Lymphocytic Leukemia (leukemia) by Hiltz, Nicolee Mengel, Phd from Temple University, 1989, 99 pages http://wwwlib.umi.com/dissertations/fullcit/9007355
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Cognitive Functioning in Long Term Survivors of Childhood Leukemia by Rubinstein, Cherryl Lee, Phd from University of California, Los Angeles, 1984, 109 pages http://wwwlib.umi.com/dissertations/fullcit/8420236
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Comparison of the Various Ige Receptors of Rat Basophilic Leukemia Cells by Roth, Patricia A; Phd from The University of Manitoba (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NL14890
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Correlation of the D-type Cyclins with Clinical Features and Survival in Chronic Lymphocytic Leukemia (cll) by Paul, James Traquair; Msc from The University of Manitoba (canada), 2002, 123 pages http://wwwlib.umi.com/dissertations/fullcit/MQ76842
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Cross-reactivity of Solubilized Fc Receptors of Rat Basophilic Leukemia Cells with Rat and Mouse Igg Subclasses and Other Immunoglobulins by Kepron, Michael R; Phd from The University of Manitoba (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/NL54796
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Culture, Characterization, and Cytotoxic Activity of Gammadelta T Cells from Patients with Ph(+) Chronic Myeloid Leukemia: a Potential Role in Cell Therapy by Malas Al-beirouti, Bassim Tahseen; Msc from University of Toronto (canada), 2002, 166 pages http://wwwlib.umi.com/dissertations/fullcit/MQ74109
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Detection and Possible Significance of a Common Leukemia-associated Antigen, Camal, in Human Myeloid Leukemia by Logan, Patricia Marie; Phd from The University of British Columbia (canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL44581
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Development of Swinepox Virus Vectors Delivering Feline Leukemia Virus Gag and Env Structural Proteins and Feline B7.1 and B7.2 Costimulatory Ligands by Winslow, Barbara Jean; Phd from Texas A&m University, 2003, 143 pages http://wwwlib.umi.com/dissertations/fullcit/3088197
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Differential Toxicity of Vincristine and Vinblasting against Human Promyelocytic Leukemia Hl-60/c1 Cells by Ferguson, Peter J; Phd from University of Alberta (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NK67508
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Dissecting Molecular Mechanisms of Leukemogenesis with a Mouse Chronic Myelogenous Leukemia Model by Gross, Alec William; Phd from Brandeis University, 2002, 274 pages http://wwwlib.umi.com/dissertations/fullcit/3045891
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Educational Implications of Surviving Acute Lymphoblastic Leukemia and Its Treatment Regimes: Perspectives and Reflections of Long-term Survivors by Sullivan, Nanci A., Edd from University of Pittsburgh, 1995, 240 pages http://wwwlib.umi.com/dissertations/fullcit/9529144
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Educational Late Effects in Long-term Survivors of Acute Lymphocytic Leukemia in Childhood (cancer, Learning Disabilities) by Peckham, Virginia Cronin, Phd from Temple University, 1986, 157 pages http://wwwlib.umi.com/dissertations/fullcit/8627496
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Effects of Folates and Products of Folate Metabolism on Proliferation of Human Leukemia Cell Line K562 in Culture by Watkins, David; Phd from Mcgill University (canada), 1983 http://wwwlib.umi.com/dissertations/fullcit/NK66644
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Efficient Adenovirus-mediated Transgene Expression in Human Acute Myeloid Leukemia Cells: the Roles of the Integrins Alphavbeta5, Alphavbeta3, and of the Coxsackievirus and Adenovirus Receptor by Aswald, Sandra; Msc from University of Toronto (canada), 2002, 188 pages http://wwwlib.umi.com/dissertations/fullcit/MQ74098
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Erythroleukemia Inducing Isolates of Friend Leukemia Virus by Macdonald, Marcy E; Phd from University of Toronto (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK47106
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Experimental Bovine Leukemia Virus Infection in Sheep Host Response and Control by Vaccination by Stirtzinger, Tatiana; Phd from University of Guelph (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NK67649
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From the Philadelphia Chromosome to the Cytoskeleton: the Role of Bcr-abl in Modulating Cell Adhesion and Initiating Leukemia by Wertheim, Jason Albert; Phd from University of Pennsylvania, 2002, 250 pages http://wwwlib.umi.com/dissertations/fullcit/3073071
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Functional and Structural Analysis of the Rnase H Domain of the Moloney Murine Leukemia Virus Reverse Transcriptase by Lim, David; Phd from Columbia University, 2002, 162 pages http://wwwlib.umi.com/dissertations/fullcit/3037733
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Functional Studies of Wilms' Tumor Gene 1 (wt1) in Hematopoiesis and Leukemia by Svedberg, Helena Anna; Phd from Lunds Universitet (sweden), 2002, 120 pages http://wwwlib.umi.com/dissertations/fullcit/f738769
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Genetic Analysis of Murine Leukemia Virus-induced Leukemia and Lymphoma Indicates a Role for Rho Family Guanosine Triphosphatase Signaling in Oncogenesis by Himmel, Karen Lynn; Phd from University of Minnesota, 2002, 119 pages http://wwwlib.umi.com/dissertations/fullcit/3058643
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Genetic Control of Host Cell Response to Murine Leukemia Viruses in Vitro by Ware, Linda Maureen; Phd from University of Toronto (canada), 1972 http://wwwlib.umi.com/dissertations/fullcit/NK13085
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Global and Gene-specific Dna Methylation Analysis in Human Leukemia by Rush, Laura Jo; Phd from The Ohio State University, 2003, 114 pages http://wwwlib.umi.com/dissertations/fullcit/3088885
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Identification and Structural Characterization of a High-affinity Nucleocapsid Protein Binding Site Within the Moloney Murine Leukemia Virus Psi-rna Packaging Signal: Implications for Genome Recognition by D'souza, Victoria Manuel; Phd from University of Maryland Baltimore County, 2002, 186 pages http://wwwlib.umi.com/dissertations/fullcit/3062582
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In Vitro Cytogenetic Studies in Chronic Myeloid Leukemia (cml) by Dubé Ian David; Phd from The University of British Columbia (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NK66815
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Insertional Mutagenesis by Provirus Integration in Moloney Murine Leukemia Virusinduced Rat Thymomas by Villeneuve, Luc; Phd from Mcgill University (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL52199
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Intracellular Cytokine Analysis in T-cells of Patients with Chronic Myeloid Leukemia by Aswald, Jorg Michael; Msc from University of Toronto (canada), 2002, 157 pages http://wwwlib.umi.com/dissertations/fullcit/MQ74097
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Lipid Rafts, Exosomes, and Human T-cell Leukemia Virus Type 1 Biology: a New Model of Viral Pathogenesis by Niyogi, Kakoli; Phd from The Johns Hopkins University, 2003, 149 pages http://wwwlib.umi.com/dissertations/fullcit/3080734
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Living Beyond the Sword of Damocles: the Quality of Life of Long-term Survivors of Leukemia and Lymphoma by Zebrack, Bradley Jay; Phd from University of Michigan, 1999, 255 pages http://wwwlib.umi.com/dissertations/fullcit/9959895
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Mechanism of Decrease of Protein Synthesis by Sodium Cyanate in Murine P388 Leukemia Cells by Lazarus, Philip; Phd from Mcgill University (canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL38342
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Membrane and Azurophilic Granule Proteins of Human Myeloid Leukemia Cell Lines by Peyman, John A; Phd from Mcgill University (canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL34346
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Methodological Issues in Epidemiologic Studies of Childhood Leukemia: Control Selection and Exposure Assessment by Reinier, Kyndaron Sybil; Phd from University of California, Berkeley, 2002, 215 pages http://wwwlib.umi.com/dissertations/fullcit/3063528
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Modelling Leukemia in the Mouse: Novel Strategies in Genome Engineering by Testa, Giuseppe; Phd from Open University (united Kingdom), 2002 http://wwwlib.umi.com/dissertations/fullcit/f351585
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Modifying Paclitaxel Induced Apoptosis by Controlling Signal Transduction Pathways in Human Leukemia Cells by Ahmed, Wesam B.; Phd from Virginia Commonwealth University, 2003, 155 pages http://wwwlib.umi.com/dissertations/fullcit/3080569
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Molecular Aspects of Differentiation in the Hl-60 Human Promyelocytic Leukemia Cell Line Signal Transduction, Gene Regulation and Cloning of the Major Protein Kinase C Substrate of Platelets (p47) by Tyers, Michael David; Phd from Mcmaster University (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/NL50260
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Molecular Cloning and Characterization of Hsag-1, a Middle Repetitive Genetic Element Capable of Determining a Cell Surface Antigen Correlated with Human Chronic Lymphocytic Leukemia by Chamberlain, John William; Phd from University of Toronto (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NK66699
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Molecular Mechanisms of Phorbol 12-myristate 13-acetate (pma)-induced Growth Inhibition of Human Promonocytic Leukemia Cells (thp-1) by Traore, Kassim; Phd from Howard University, 2002, 83 pages http://wwwlib.umi.com/dissertations/fullcit/3085424
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Mrna Localization to Rat Basophilic Leukemia (rbl)-2h3 Cell Lipid Bodies by Noonan, Vikki Louise; Dmsc from Harvard University, 2002 http://wwwlib.umi.com/dissertations/fullcit/f309201
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Mycoplasma Infection of Rat Basophilic Leukemia Cells and Establishment of Rat Mast Cell Lines by Chan, Bosco M. C; Phd from The University of Manitoba (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL47892
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Oncogene Cooperation in the Pathogenesis of Acute Myeloid Leukemia by Cuenco, Grace Montevirgen; Phd from Brandeis University, 2003, 213 pages http://wwwlib.umi.com/dissertations/fullcit/3081812
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Parents Confronting and Comprehending the Medical and Nightmare Worlds of Childhood Leukemia by Fisher, Darleen Louise, Phd from Syracuse University, 1986, 292 pages http://wwwlib.umi.com/dissertations/fullcit/8625827
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Parents' Initial Experience with Childhood Acute Lymphocytic Leukemia by O'brien, Patricia Edwina, Phd from The University of Michigan, 1988, 152 pages http://wwwlib.umi.com/dissertations/fullcit/8907120
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Perinatal Risk Factors for Childhood Leukemia by Naumburg, Estelle Noree; Phd from Uppsala Universitet (sweden), 2002, 45 pages http://wwwlib.umi.com/dissertations/fullcit/f721601
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Pharmacogenetics of Thiopurine- and Etoposide-induced Malignancies in Childhood Acute Lymphoblastic Leukemia by Edick, Mathew James; Phd from The University of Tennessee Center for the Health Sciences, 2003, 157 pages http://wwwlib.umi.com/dissertations/fullcit/3077410
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Properties of Blast Cells in Acute Myeloblastic Leukemia by Minden, Mark David; Phd from University of Toronto (canada), 1979 http://wwwlib.umi.com/dissertations/fullcit/NK42273
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Protein Motifs in the Cytoplasmic Tail of the Bovine Leukemia Virus Transmembrane Protein Govern Protein Expression on the Cell Surface by Novakovic, Sinisa; Phd from University of California, Davis, 2002, 157 pages http://wwwlib.umi.com/dissertations/fullcit/3074596
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Psychosexual Function in Survivors of Adult Acute Leukemia by Wolchok, Silkaly M., Phd from New York University, 1995, 212 pages http://wwwlib.umi.com/dissertations/fullcit/9603314
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Quantitative Virological and Immunological Studies on Murine Leukemia by Steeves, Richard Allison; Advdeg from University of Toronto (canada), 1966 http://wwwlib.umi.com/dissertations/fullcit/NK01041
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Regulation of Bcr-abl Signal Transduction in the Differentiation and Survival of Chronic Myelogenous Leukemia Cells by Dorsey, Jay Fitzgerald; Phd from University of South Florida, 2003, 124 pages http://wwwlib.umi.com/dissertations/fullcit/3079979
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Role of Ras Activation in the Pathogenesis of Myeloid Leukemia by Subrahmanyam, Ramesh; Phd from Brandeis University, 2003, 189 pages http://wwwlib.umi.com/dissertations/fullcit/3081831
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Sodium-driven Nucleoside Transport in Mouse Leukemia L1210 Cells by Dagnino, Lina; Phd from University of Alberta (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL45748
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Studies of Hemic Cells from Patients with Leukemia by Aye, M. T; , Phd from University of Toronto (canada), 1974 http://wwwlib.umi.com/dissertations/fullcit/NK27781
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Studies on Antisera to Rat Mast Cells and Rat Basophilic Leukemia Cells by Yiu, Suk Hing; Phd from The University of Manitoba (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK47255
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Studies on Erythroid Differentiation of Murine Hemopoietic Cells in Vitro and Cells Transformed by Friend Leukemia Virus by Stephenson, John R; Advdeg from University of Toronto (canada), 1971 http://wwwlib.umi.com/dissertations/fullcit/NK09929
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Studies on the Role of the Helper Virus in Abelson Murine Leukemia Virus Lymphomagenesis by Poirier, Yves; Phd from Mcgill University (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/NL52190
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The Analysis of Human Myelogenous Leukemia Cells in the Fluorescence-activated Cell Sorter by Malcolm, Andrew James; Phd from The University of British Columbia (canada), 1983 http://wwwlib.umi.com/dissertations/fullcit/NK66927
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The Biological Consequences of G2a Function in Lymphocyte Growth Control and Leukemia by Le, Lu Quang; Phd from University of California, Los Angeles, 2002, 110 pages http://wwwlib.umi.com/dissertations/fullcit/3045573
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The Diffusion of Leukemia Chemotherapy: a Study in the Nonmarket Economics of Medical Care. by Warner, Kenneth Edgar, Phd from Yale University, 1974, 318 pages http://wwwlib.umi.com/dissertations/fullcit/7515391
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The Effect on the Computational Ability of Children with Acute Lymphocytic Leukemia due to Prophylactic Treatment of the Central Nervous System by Bath, Barbara Blake, Phd from The American University, 1984, 112 pages http://wwwlib.umi.com/dissertations/fullcit/8417450
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The Incidence of Learning Disabilities in Children and Adolescents in Remission with Acute Lymphoblastic Leukemia by Seale, Janet Strawsnyder, Edd from University of Virginia, 1987, 141 pages http://wwwlib.umi.com/dissertations/fullcit/8902456
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The Role of Stat1 in Retinoic Acid-induced Myelomonocytic Differentiation of Human Leukemia Cells by Dimberg, Anna; Phd from Uppsala Universitet (sweden), 2002, 55 pages http://wwwlib.umi.com/dissertations/fullcit/f740897
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Understanding Raralpha Chimeric Proteins Associated with Acute Promyelocytic Leukemia: Evidence Supporting the Deregulation of Npm in Apl by Hummel, Jeffrey Lawrence; Phd from University of Toronto (canada), 2003, 235 pages http://wwwlib.umi.com/dissertations/fullcit/NQ78418
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Unique Molecular Differences between Acute Myelogenous Leukemia and Normal Hematopoietic Stem Cells by Guzman, Monica Liliana; Phd from University of Kentucky, 2002, 88 pages http://wwwlib.umi.com/dissertations/fullcit/3047782
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Vaccination and the Risk of Childhood Acute Lymphoblastic Leukemia by Spector, Logan Garrett; Phd from Emory University, 2002, 295 pages http://wwwlib.umi.com/dissertations/fullcit/3059025
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND LEUKEMIA Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning leukemia.
Recent Trials on Leukemia The following is a list of recent trials dedicated to leukemia.8 Further information on a trial is available at the Web site indicated. ·
Azacitidine Plus Phenylbutyrate in Treating Patients With Acute Myeloid Leukemia or Myelodysplastic Syndrome Condition(s): adult acute myeloid leukemia; atypical chronic myeloid leukemia; Chronic Myelomonocytic Leukemia; myelodysplastic and myeloproliferative disease; Myelodysplastic Syndromes Study Status: This study is currently recruiting patients. Sponsor(s): Sidney Kimmel Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Azacitidine plus phenylbutyrate may help leukemia cells develop into normal white blood cells. PURPOSE: Phase I trial to study the effectiveness of combining azacitidine and phenylbutyrate in treating patients who have acute myeloid leukemia or myelodysplastic syndrome. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004871
8
These are listed at www.ClinicalTrials.gov.
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Biological Therapy in Treating Patients With Advanced Acute Myeloid Leukemia or Acute Lymphoblastic Leukemia Who Are Undergoing Stem Cell Transplantation Condition(s): adult acute lymphoblastic leukemia; adult acute myeloid leukemia; childhood acute lymphoblastic leukemia; childhood acute myeloid leukemia and other myeloid malignancies; secondary acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Fred Hutchinson Cancer Research Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Biological therapies use different ways to stimulate the immune system and stop cancer cells from growing. Combining different types of biological therapies may kill more cancer cells in patients undergoing donor stem cell transplantation. PURPOSE: Phase I/II trial to study the effectiveness of biological therapy in treating patients with advanced acute myeloid leukemia or acute lymphoblastic leukemia. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00052520
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Busulfan and Cyclophosphamide Followed by Bone Marrow Transplantation in Treating Patients With Acute Myelogenous Leukemia or Myelodysplastic Syndrome Condition(s): adult acute monocytic leukemia; adult acute myeloid leukemia; atypical chronic myeloid leukemia; childhood acute myeloid leukemia and other myeloid malignancies; Chronic Myelomonocytic Leukemia; myelodysplastic and myeloproliferative disease Study Status: This study is currently recruiting patients. Sponsor(s): Robert H. Lurie Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining chemotherapy with donor bone marrow transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of busulfan and cyclophosphamide followed by bone marrow transplantation in treating patients who have acute myelogenous leukemia or myelodysplastic syndrome. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004896
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Chemotherapy Plus Bone Marrow Transplantation and Filgrastim in Treating Patients With Acute Myelogenous Leukemia or Myelodysplastic Syndrome Condition(s): Acute Myeloid Leukemia; adult acute monocytic leukemia; atypical chronic myeloid leukemia; childhood acute monocytic leukemia; myelodysplastic and myeloproliferative disease Study Status: This study is currently recruiting patients.
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Sponsor(s): Robert H. Lurie Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing and die. Bone marrow transplantation may be able to replace cells that were destroyed by chemotherapy. Colony-stimulating factors such as filgrastim may increase the number of immune cells found in bone marrow or peripheral blood and may help a person's immune system recover from the side effects of chemotherapy. PURPOSE: Phase II trial to study the effectiveness of chemotherapy plus bone marrow transplantation and filgrastim in treating patients who have acute myelogenous leukemia or myelodysplastic syndrome. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004899 ·
Chemotherapy With or Without Gemtuzumab Ozogamicin in Treating Older Patients With Acute Myeloid Leukemia Condition(s): adult acute monocytic leukemia; adult acute myeloid leukemia; secondary acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): EORTC Leukemia Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Monoclonal antibodies can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. It is not yet known if combining combination chemotherapy with monoclonal antibody therapy will kill more cancer cells. PURPOSE: Randomized phase III trial to determine the effectiveness of combination chemotherapy with or without gemtuzumab ozogamicin in treating patients who have acute myeloid leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00052299
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Combination Chemotherapy and Thalidomide in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia, Chronic Myelogenous Leukemia, or Advanced Myelodysplastic Syndromes Condition(s): adult acute myeloid leukemia; atypical chronic myeloid leukemia; childhood acute myeloid leukemia and other myeloid malignancies; Chronic Myelogenous Leukemia; myelodysplastic and myeloproliferative disease; secondary acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Ireland Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Thalidomide may stop the growth of cancer cells by stopping blood flow to the tumor. Combining chemotherapy
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with thalidomide may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combining fludarabine, carboplatin, and topotecan with thalidomide in treating patients who have relapsed or refractory acute myeloid leukemia, chronic myelogenous leukemia, or advanced myelodysplastic syndromes. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00053287 ·
Combination Chemotherapy Followed By Filgrastim or Sargramostim in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia or Acute Lymphoblastic Leukemia Condition(s): recurrent adult acute myeloid leukemia; recurrent childhood acute myeloid leukemia; recurrent adult acute lymphoblastic leukemia; recurrent childhood acute lymphoblastic leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Roswell Park Cancer Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Colony-stimulating factors such as filgrastim and sargramostim may increase the number of immune cells found in bone marrow or peripheral blood and may help a person's immune system recover from the side effects of chemotherapy. It is not yet known whether combination chemotherapy is more effective followed by filgrastim or sargramostim in treating leukemia. PURPOSE: Randomized phase II trial to compare the effectiveness of combination chemotherapy followed by filgrastim with that of combination chemotherapy followed by sargramostim in treating patients who have relapsed or refractory acute myeloid leukemia or acute lymphoblastic leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00053131
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Combination Chemotherapy Followed by Peripheral Stem Cell Transplantation and Interleukin-2 in Treating Patients With Acute Leukemia Condition(s): adult acute lymphoblastic leukemia; adult acute myeloid leukemia; childhood acute lymphoblastic leukemia; childhood acute myeloid leukemia; secondary acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Herbert Irving Comprehensive Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining chemotherapy with peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more cancer cells. Interleukin-2 may stimulate a person's white blood cells to kill leukemia cells. PURPOSE: Phase II trial to study the
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effectiveness of combination chemotherapy followed by peripheral stem cell transplantation and interleukin-2 in treating patients who have acute leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00008190 ·
Combination Chemotherapy Plus Steroid Therapy in Treating Children With Acute Lymphoblastic Leukemia or Lymphoblastic Non-Hodgkin's Lymphoma Condition(s): acute undifferentiated leukemia; childhood acute lymphoblastic leukemia; childhood lymphoblastic lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): EORTC Children's Leukemia Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug may kill more tumor cells. It is not yet known which regimen of combination chemotherapy plus steroid therapy is more effective for acute lymphoblastic leukemia or lymphoblastic non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of different regimens of combination chemotherapy plus steroid therapy in treating children who have acute lymphoblastic leukemia or lymphoblastic non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003728
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Combination Chemotherapy With or Without Filgrastim and/or Tretinoin in Treating Patients With Acute Myeloid Leukemia Condition(s): Acute Myeloid Leukemia; adult acute monocytic leukemia; atypical chronic myeloid leukemia; childhood acute monocytic leukemia; myelodysplastic and myeloproliferative disease Study Status: This study is currently recruiting patients. Sponsor(s): Medical Research Council Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Colony-stimulating factors such as filgrastim may increase the number of immune cells found in bone marrow or peripheral blood and may help a person's immune system recover from the side effects of chemotherapy. It is not yet known whether combination chemotherapy with filgrastim and/or tretinoin is more effective than combination chemotherapy alone for acute myeloid leukemia. PURPOSE: Randomized phase III trial to compare the effectiveness of combination chemotherapy with or without filgrastim and/or tretinoin in treating patients who have acute myeloid leukemia. Phase(s): Phase III Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005863 ·
Combination Chemotherapy With or Without Monoclonal Antibody Therapy Followed by Stem Cell Transplantation in Treating Patients With Acute Myeloid Leukemia Condition(s): adult acute monocytic leukemia; adult acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Eastern Cooperative Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Monoclonal antibodies can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. Combining chemotherapy and monoclonal antibody therapy with peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more tumor cells. It is not yet known whether combination chemotherapy is more effective with or without gemtuzumab ozogamicin followed by peripheral stem cell transplantation in treating acute myeloid leukemia. PURPOSE: Randomized phase III trial to determine the effectiveness of combination chemotherapy with or without gemtuzumab ozogamicin followed by peripheral stem cell transplantation in treating patients who have acute myeloid leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049517
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Combination Chemotherapy With or Without PSC 833, Peripheral Stem Cell Transplantation, and/or Interleukin-2 in Treating Patients With Acute Myeloid Leukemia Condition(s): adult acute monocytic leukemia; adult acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Cancer and Leukemia Group B; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PSC 833 may increase the effectiveness of chemotherapy by making cancer cells more sensitive to the drugs. Combining chemotherapy with peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more cancer cells. Interleukin-2 may stimulate a person's white blood cells to kill cancer cells. PURPOSE: Randomized phase III trial to determine the effectiveness of combination chemotherapy with or without PSC 833, peripheral stem cell transplantation, and interleukin-2 in treating patients who have acute myeloid leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006363
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Combination Chemotherapy, Interleukin-2, and Peripheral Stem Cell Transplantation in Treating Patients With Acute Myeloid Leukemia Condition(s): adult acute monocytic leukemia; adult acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): EORTC Leukemia Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Interleukin-2 may stimulate a person's white blood cells to kill cancer cells. Peripheral stem cell transplantation may allow doctors to give higher doses of chemotherapy drugs and kill more cancer cells. PURPOSE: Randomized phase III trial to study the effectiveness of combination chemotherapy, interleukin-2, and peripheral stem cell transplantation in treating patients who have acute myeloid leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004128
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Daunorubicin and Cytarabine With or Without Zosuquidar Trihydrochloride in Treating Older Patients With Newly Diagnosed Acute Myeloid Leukemia or Refractory Anemia Condition(s): adult acute monocytic leukemia; adult acute myeloid leukemia; Myelodysplastic Syndromes; secondary acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Eastern Cooperative Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Zosuquidar trihydrochloride may help daunorubicin and cytarabine kill more cancer cells by making cancer cells more sensitive to the drugs. It is not yet known whether daunorubicin and cytarabine are more effective with or without zosuquidar trihydrochloride in treating acute myeloid leukemia or anemia. PURPOSE: Randomized phase III trial to compare the effectiveness of daunorubicin combined with cytarabine with or without zosuquidar trihydrochloride in treating older patients who have newly diagnosed acute myeloid leukemia or anemia that has not responded to previous treatment. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00046930
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Decitabine in Treating Children With Relapsed or Refractory Acute Myeloid Leukemia or Acute Lymphoblastic Leukemia Condition(s): recurrent childhood acute lymphoblastic leukemia; recurrent childhood acute myeloid leukemia; childhood acute myeloblastic leukemia with maturation (M2); childhood acute promyelocytic leukemia (M3); secondary acute myeloid leukemia Study Status: This study is currently recruiting patients.
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Sponsor(s): Children's Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase I trial to study the effectiveness of decitabine in treating children who have relapsed or refractory acute myeloid leukemia or acute lymphoblastic leukemia. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00042796 ·
Decitabine in Treating Patients With Myelodysplastic Syndrome or Acute Myeloid Leukemia Condition(s): adult acute myeloid leukemia; atypical chronic myeloid leukemia; myelodysplastic and myeloproliferative disease; Myelodysplastic Syndromes; secondary acute myeloid leukemia; untreated adult acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Princess Margaret Hospital; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase I trial to study the effectiveness of decitabine in treating patients who have myelodysplastic syndrome or acute myeloid leukemia. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049582
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Dose-Determining Study of R115777 for Childhood Leukemia Condition(s): Acute Lymphocytic Leukemia; Chronic Myelogenous Leukemia; Acute Nonlymphocytic Leukemia; Acute Myelomonocytic Leukemia; Chronic Myelomonocytic Leukemia Study Status: This study is currently recruiting patients. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: This study will determine what dose of R115777 can safely be given to children with leukemia. R115777 interferes with the function of certain proteins that control cell growth. In many types of cancer, including leukemia, one of these proteins, called ras does not function properly, so that cell growth is unchecked. Besides determining a safe dose of R115777, this study will also look at the drug's side effects, its possible benefits in treating childhood leukemia, how the body uses and eliminates it, and what changes occur in leukemia cells and in the gene that produces the ras protein after giving R115777. Patients 21 years of age or younger with acute lymphoblastic leukemia (ALL), acute non-lymphoblastic leukemia) ANLL), juvenile myelomonocytic leukemia (JMML), or chronic myelogenous leukemia (CML) who do not respond to standard therapy may be eligible for this study. Candidates will be screened with a history and physical examination, eye examination, blood and urine tests, lumbar puncture (spinal tap) and bone marrow aspiration. Lumbar puncture is done to examine
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the cerebrospinal fluid (CSF), which bathes the brain and spinal cord. After a local anesthetic is administered, a needle is inserted in the space between the bones in the lower back where the CSF circulates below the spinal cord. A small amount of fluid is collected through the needle. For the bone marrow test, the hip area is anesthetized and a special needle is used to draw bone marrow from the hipbone. Patients enrolled in the study will take R115777 tablets every 12 hours for 21 days, followed by a 7-day rest period, completing one treatment cycle. To determine the highest dose of drug that can be given safely, the starting dose will be low and will be increased gradually in small groups of patients. Treatment cycles will continue unless unacceptable side effects occur or the leukemia does not respond to the drug. Patients will undergo the following tests and procedures to monitor for side effects and evaluate the response of the leukemia to treatment: - Physical examinations - every week, initially - Eye examinations - regularly Blood tests- periodically throughout treatment - Bone marrow examination - before the start of each treatment cycle for three cycles and then less often - Buccal swab (scraping the inside of the cheek with a tongue depressor to collect a cell sample) - before the first treatment dose and once during the first treatment cycle. Additional blood samples will be collected as follows: - To study the pharmacology of R115777, 12 small blood samples will be collected on days 1 and 2 after the first dose of R115777, and one sample will be taken between days 6 and 10 during the first treatment cycle only. If possible, the blood will be drawn through an indwelling catheter to avoid multiple needle sticks. - Samples will be collected before the first treatment dose, once during the first treatment cycle, and before cycles 3,6, 9 and 12, to measure the effect of R115777 on a substance called nerve growth factor to see if it can predict which patients may be at risk for developing side effects from R115777 Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00017888 ·
Fludarabine and Cyclophosphamide Followed by Peripheral Transplantation in Treating Patients With Leukemia or Lymphoma
Stem
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Condition(s): adult non-Hodgkin's lymphoma; Chronic Lymphocytic Leukemia; Prolymphocytic Leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Cancer and Leukemia Group B; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Peripheral stem cell transplantation may be able to replace immune cells that were destroyed by chemotherapy. PURPOSE: Phase II trial to study the effectiveness of fludarabine and cyclophosphamide followed by peripheral stem cell transplantation in treating patients who have leukemia or lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006252
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Fludarabine and Total-Body Irradiation Followed By Donor Peripheral Stem Cell Transplantation in Treating Patients With Acute Lymphoblastic Leukemia or Chronic Myelogenous Leukemia That Has Responded to Treatment With Imatinib Mesylate Condition(s): recurrent childhood acute lymphoblastic leukemia; recurrent adult acute lymphoblastic leukemia; blastic phase chronic myelogenous leukemia; Philadelphia chromosome positive chronic myelogenous leukemia; childhood chronic myelogenous leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Fred Hutchinson Cancer Research Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Imatinib mesylate may stop the growth of cancer cells by blocking the enzymes necessary for cancer cell growth. Peripheral stem cell transplantation may be able to replace immune cells that were destroyed by chemotherapy and radiation therapy used to kill cancer cells. Combining imatinib mesylate with fludarabine and total-body irradiation followed by donor peripheral stem cell transplantation may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of fludarabine and total-body irradiation followed by donor peripheral stem cell transplantation in treating patients who have acute lymphoblastic leukemia or chronic myelogenous leukemia that has responded to previous treatment with imatinib mesylate. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00036738
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FR901228 in Treating Patients With Myelodysplastic Syndrome, Acute Myeloid Leukemia, or Non-Hodgkin's Lymphoma Condition(s): adult acute myeloid leukemia; adult non-Hodgkin's lymphoma; atypical chronic myeloid leukemia; childhood acute myeloid leukemia and other myeloid malignancies; Chronic Myelomonocytic Leukemia; myelodysplastic and myeloproliferative disease Study Status: This study is currently recruiting patients. Sponsor(s): Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of FR901228 in treating patients who have myelodysplastic syndrome, acute myeloid leukemia, or non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00042822
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Genetic Study of Patients With Acute Myeloid Leukemia, Acute Lymphoblastic Leukemia, or Myelodysplastic Syndromes Condition(s): adult acute lymphoblastic leukemia; adult acute myeloid leukemia; atypical chronic myeloid leukemia; childhood acute lymphoblastic leukemia; childhood
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acute myeloid leukemia and other myeloid malignancies; myelodysplastic and myeloproliferative disease Study Status: This study is currently recruiting patients. Sponsor(s): Cancer and Leukemia Group B; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Cytogenetic tests may help predict how cancer will respond to treatment and allow doctors to plan more effective therapy. PURPOSE: Diagnostic trial to study genetic differences in patients who have untreated acute myeloid leukemia, acute lymphoblastic leukemia, or myelodysplastic syndromes. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00048958 ·
Intensive Compared With Nonintensive Chemotherapy in Treating Older Patients with Acute Myeloid Leukemia or Myelodysplastic Syndrome Condition(s): Acute Myeloid Leukemia; adult acute monocytic leukemia; atypical chronic myeloid leukemia; Chronic Myelomonocytic Leukemia; myelodysplastic and myeloproliferative disease Study Status: This study is currently recruiting patients. Sponsor(s): Leukemia Research Fund Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. It is not yet known if stronger doses of chemotherapy given over a longer period of time are as well tolerated or as effective as less intensive chemotherapy. PURPOSE: Randomized phase III trial to compare intensive with nonintensive regimens of chemotherapy in treating older patients who have acute myeloid leukemia or myelodysplastic syndrome. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005823
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Molecular Epidemiology of Childhood Leukemia in Northern and Central California Condition(s): Leukemia; Acute Myelocytic Leukemia; Acute Lymphoblastic Leukemia; Acute Myelogenous Leukemia Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS); National Cancer Institute (NCI) Purpose - Excerpt: This study is a case-control study investigating the causes of childhood leukemia in Northern California. The overall purpose of this epidemiologic study is to find specific genetic or environmental factors that may increase the risk of leukemia in children. The study is being conducted by Patricia Buffler, PhD at the School of Public Health, the University of California Berkeley, with collaboration by the California Department of Health Services and nine other Bay Area and Central Valley hospitals. The study began in 1995 and will continue to 2003. Study Type: Observational
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00015587 ·
Monoclonal Antibody, Cyclophosphamide, and Radiation Therapy Followed by Bone Marrow Transplant in Treating Patients With Advanced Acute Myeloid Leukemia or Myelodysplastic Syndrome Condition(s): adult acute myeloid leukemia; childhood acute myeloid leukemia; Chronic Myelomonocytic Leukemia; Myelodysplastic Syndromes; secondary acute myeloid leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Fred Hutchinson Cancer Research Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Monoclonal antibodies can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage cancer cells. Combining monoclonal antibody therapy with chemotherapy and radiation therapy may kill more cancer cells. Bone marrow transplantation may be able to replace immune cells that were destroyed by chemotherapy and radiation therapy. PURPOSE: Phase II trial to study the effectiveness of monoclonal antibody, cyclophosphamide, total-body irradiation, and bone marrow transplant in treating patients who have advanced acute myeloid leukemia or myelodysplastic syndrome. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003868
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Radiolabeled Monoclonal Antibody Therapy and Etoposide Followed by Peripheral Stem Cell Transplantation in Treating Patients With Advanced Myelodysplastic Syndrome or Refractory Leukemia Condition(s): adult acute lymphoblastic leukemia; adult acute myeloid leukemia; atypical chronic myeloid leukemia; childhood acute myeloid leukemia and other myeloid malignancies; Chronic Myelogenous Leukemia; myelodysplastic and myeloproliferative disease Study Status: This study is currently recruiting patients. Sponsor(s): Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Radiolabeled monoclonal antibodies can locate cancer cells and deliver radiation to them without harming normal cells. Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Peripheral stem cell transplantation may allow the doctor to give higher doses of radiation and chemotherapy drugs and kill more cancer cells. PURPOSE: Phase I trial to study the effectiveness of radiolabeled monoclonal antibody therapy plus etoposide followed by peripheral stem cell transplantation in treating patients who have advanced myelodysplastic syndrome or refractory leukemia. Phase(s): Phase I Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006040 ·
Rituximab, Chemotherapy, and Filgrastim in Treating Patients With Burkitt's Lymphoma or Burkitt's Leukemia Condition(s): L3 adult acute lymphoblastic leukemia; adult diffuse small noncleaved cell and Burkitt's lymphoma; untreated adult acute lymphoblastic leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Cancer and Leukemia Group B; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Monoclonal antibodies such as rituximab can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Colony-stimulating factors such as filgrastim may increase the numbers of immune cells found in bone marrow or peripheral blood and may help a person's immune system recover from the side effects of chemotherapy. Combining chemotherapy with rituximab and filgrastim may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combining rituximab with chemotherapy and filgrastim in treating patients who have Burkitt's lymphoma or Burkitt's leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00039130
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Sodium Salicylate in Treating Patients With Advanced Myelodysplastic Syndrome, Acute Myelogenous Leukemia, or Chronic Lymphocytic Leukemia Condition(s): adult acute myeloid leukemia; atypical chronic myeloid leukemia; Chronic Myelomonocytic Leukemia; myelodysplastic and myeloproliferative disease; Myelodysplastic Syndromes; refractory chronic lymphocytic leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase I trial to study the effectiveness of sodium salicylate in treating patients who have advanced myelodysplastic syndrome , acute myelogenous leukemia or chronic lymphocytic leukemia. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004245
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Vaccine Therapy Plus Immune Adjuvant in Treating Patients With Chronic Myeloid Leukemia, Acute Myeloid Leukemia, or Myelodysplastic Syndrome Condition(s): adult acute myeloid leukemia; atypical chronic myeloid leukemia; childhood acute myeloid leukemia and other myeloid malignancies; Chronic Myelogenous Leukemia; myelodysplastic and myeloproliferative disease Study Status: This study is currently recruiting patients. Sponsor(s): M.D. Anderson Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Vaccines made from peptides that are found on leukemia cells may make the body build an immune response and kill cancer cells. Combining vaccine therapy with the immune adjuvant Montanide ISA-51 may be a more effective treatment for chronic myeloid leukemia, acute myeloid leukemia, or myelodysplastic syndrome. PURPOSE: Phase I/II trial to study the effectiveness of vaccine therapy plus Montanide ISA-51 in treating patients who have chronic myeloid leukemia, acute myeloid leukemia, or myelodysplastic syndrome. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004918
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Arsenic Trioxide in Treating Patients With Recurrent or Refractory Acute Lymphoblastic Leukemia or Chronic Myelogenous Leukemia Condition(s): recurrent adult acute lymphoblastic leukemia; relapsing chronic myelogenous leukemia; blastic phase chronic myelogenous leukemia; Philadelphia chromosome positive chronic myelogenous leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): H. Lee Moffitt Cancer Center and Research Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have recurrent or refractory acute lymphoblastic leukemia or chronic myelogenous leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006092
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Combination Chemotherapy in Treating Children With Newly Diagnosed Acute Myeloid Leukemia or Myelodysplastic Syndrome Condition(s): Myeloid Leukemia; Myelodysplastic Syndromes; Refractory Anemia Study Status: This study is no longer recruiting patients. Sponsor(s): EORTC Children's Leukemia Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. It is not yet known which regimen of combination
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chemotherapy is more effective for acute myeloid leukemia or myelodysplastic syndrome. PURPOSE: Randomized phase III trial to compare the effectiveness of different combination chemotherapy regimens in treating children who have newly diagnosed acute myeloid leukemia or myelodysplastic syndrome. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002517 ·
Combination Chemotherapy in Treating Patients With Chronic Myelogenous Leukemia or Recurrent Acute Leukemia Condition(s): Leukemia, Myeloid, Aggressive-Phase; Neutropenia; recurrent adult acute lymphoblastic leukemia; relapsing chronic myelogenous leukemia; recurrent adult acute myeloid leukemia; blastic phase chronic myelogenous leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Mayo Clinic Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase I trial to study the effectiveness of combination chemotherapy with carboplatin and topotecan in treating patients with chronic myelogenous leukemia or recurrent acute leukemia. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002693
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Combination Chemotherapy in Treating Patients With Non-Hodgkin's Lymphoma or Acute Lymphocytic Leukemia Condition(s): L3 adult acute lymphoblastic leukemia; stage IV adult diffuse small noncleaved cell/Burkitt's lymphoma; Burkitt's Lymphoma; stage IV childhood small noncleaved cell lymphoma; B-cell childhood acute lymphoblastic leukemia; stage III adult diffuse small noncleaved cell/Burkitt's lymphoma; B-cell adult acute lymphoblastic leukemia; L3 childhood acute lymphoblastic leukemia; stage III childhood small noncleaved cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Pediatric Oncology Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy in treating patients who have non-Hodgkin's lymphoma or acute lymphocytic leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00005977 ·
Combination Chemotherapy Plus PSC 833 Followed by Interleukin-2 in Treating Older Patients With Acute Myeloid Leukemia Condition(s): untreated adult acute myeloid leukemia; adult acute differentiated monocytic leukemia (M5b); adult acute myeloblastic leukemia without maturation (M1); adult acute minimally differentiated myeloid leukemia (M0); adult acute poorly differentiated monocytic leukemia (M5a); adult acute erythroleukemia (M6); adult acute myelomonocytic leukemia (M4); adult acute myeloblastic leukemia with maturation (M2); adult acute megakaryocytic leukemia (M7) Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Cancer and Leukemia Group B Purpose - Excerpt: RATIONALE: Some cancers become resistant to chemotherapy drugs. Combining PSC 833 with more than one chemotherapy drug may reduce resistance to the drugs and allow the cancer cells to be killed. Combining interleukin-2 with combination chemotherapy plus PSC 833 may kill more cancer cells. PURPOSE: Randomized phase III trial to compare the effectiveness of combination chemotherapy with or without PSC 833 followed by interleukin-2 or no further therapy in treating older patients who have acute myeloid leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003190
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Combination Chemotherapy With or Without Bone Marrow Transplantation in Treating Children With Acute Myeloid Leukemia Condition(s): refractory anemia with excess blasts in transformation; refractory anemia with excess blasts; childhood acute promyelocytic leukemia (M3); secondary myelodysplastic syndromes; de novo myelodysplastic syndromes; secondary acute myeloid leukemia; untreated childhood acute myeloid leukemia and other myeloid malignancies Study Status: This study is no longer recruiting patients. Sponsor(s): Medical Research Council Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining chemotherapy with bone marrow transplantation may allow doctors to give higher doses of chemotherapy and kill more cancer cells. It is not yet known whether chemotherapy is more effective with or without bone marrow transplantation for acute myeloid leukemia. PURPOSE: Randomized phase III trial to compare the effectiveness of chemotherapy with or without bone marrow transplantation in treating children who have acute myeloid leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003436
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Combination Chemotherapy With or Without Bone Marrow Transplantation in Treating Patients With Acute Promyelocytic Leukemia Condition(s): untreated adult acute myeloid leukemia; adult acute promyelocytic leukemia (M3) Study Status: This study is no longer recruiting patients. Sponsor(s): EORTC Leukemia Cooperative Group; Gruppo Italiano di Malattie Ematologiche Maligne de l'Aduklto-Associazione Italiana de Ematologia e Oncologia Pediatric Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Bone marrow transplantation may be able to replace immune cells that were destroyed by chemotherapy to kill tumor cells. It is not yet known which regimen of combination chemotherapy with or without bone marrow transplantation is more effective in treating promyelocytic leukemia PURPOSE: Randomized phase III trial to compare the effectiveness of different combination chemotherapy regimens with or without bone marrow transplantation in treating patients who have promyelocytic leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002701
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Comparison of Three Treatment Regimens in Treating Patients With Relapsed or Refractory Acute Myelogenous Leukemia Condition(s): adult acute differentiated monocytic leukemia (M5b); adult acute myeloblastic leukemia without maturation (M1); adult acute minimally differentiated myeloid leukemia (M0); adult acute poorly differentiated monocytic leukemia (M5a); recurrent adult acute myeloid leukemia; adult acute erythroleukemia (M6); adult acute myelomonocytic leukemia (M4); adult acute myeloblastic leukemia with maturation (M2); adult acute megakaryocytic leukemia (M7); adult acute promyelocytic leukemia (M3) Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Eastern Cooperative Oncology Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Monoclonal antibodies such as gemtuzumab ozogamicin can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. Combining more than one drug or combining monoclonal antibody with chemotherapy may kill more cancer cells. It is not yet known which treatment regimen is more effective for acute myelogenous leukemia. PURPOSE: Randomized phase II trial to compare the effectiveness of three treatment regimens in treating patients who have relapsed or refractory acute myelogenous leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005962
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Filgrastim-Treated Donor Peripheral Stem Cell Transplantation in Treating Patients With Acute Leukemia Condition(s): adult acute lymphoblastic leukemia in remission; recurrent adult acute myeloid leukemia; acute undifferentiated leukemia; recurrent childhood acute myeloid leukemia; recurrent adult acute lymphoblastic leukemia; secondary acute myeloid leukemia; recurrent childhood acute lymphoblastic leukemia; childhood acute lymphoblastic leukemia in remission Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Fred Hutchinson Cancer Research Center Purpose - Excerpt: RATIONALE: Transplanted peripheral stem cells can sometimes be rejected by the body's tissues. Treating donor peripheral stem cells with filgrastim may increase the number of donor white blood cells. This may help to decrease the rejection of the transplanted cells in patients receiving them as treatment for acute leukemia. PURPOSE: Phase II trial to study the effectiveness of filgrastim-treated donor peripheral stem cells in treating patients with acute leukemia who are undergoing peripheral stem cell transplantation. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00025545
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Flavopiridol in Treating Patients With Chronic Lymphocytic Leukemia Condition(s): stage II chronic lymphocytic leukemia; stage IV chronic lymphocytic leukemia; refractory chronic lymphocytic leukemia; stage I chronic lymphocytic leukemia; stage III chronic lymphocytic leukemia; B-cell Chronic Lymphocytic Leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Cancer and Leukemia Group B Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of flavopiridol in treating patients who have chronic lymphocytic leukemia that has not responded to treatment with fludarabine. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003620
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flt3L in Treating Patients With Acute Myeloid Leukemia Condition(s): adult acute differentiated monocytic leukemia (M5b); adult acute myeloblastic leukemia without maturation (M1); adult acute minimally differentiated myeloid leukemia (M0); adult acute poorly differentiated monocytic leukemia (M5a); adult acute erythroleukemia (M6); adult acute myeloid leukemia in remission; adult acute myelomonocytic leukemia (M4); adult acute myeloblastic leukemia with maturation (M2); adult acute megakaryocytic leukemia (M7); adult acute promyelocytic leukemia (M3)
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Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Cancer and Leukemia Group B; Southwest Oncology Group; Eastern Cooperative Oncology Group Purpose - Excerpt: RATIONALE: Drugs such as flt3L may stimulate a person's immune system and help kill cancer cells. It is not yet known if flt3L is effective in treating acute myeloid leukemia. PURPOSE: Randomized phase III trial to determine the effectiveness of flt3L in treating patients who have acute myeloid leukemia that is in remission. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006223 ·
High Dose Chemotherapy, Peripheral Stem Cell Transplantation, and Interleukin-2 in Treating Patients With Acute Myeloid Leukemia Condition(s): adult acute myelomonocytic leukemia (M4); untreated adult acute myeloid leukemia; adult acute monocytic leukemia (M5); adult acute myeloblastic leukemia without maturation (M1); adult acute myeloblastic leukemia with maturation (M2); adult acute minimally differentiated myeloid leukemia (M0); secondary acute myeloid leukemia; adult acute megakaryocytic leukemia (M7); adult acute erythroleukemia (M6) Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Roswell Park Cancer Institute Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining chemotherapy with peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more cancer cells. Interleukin-2 may stimulate a person's white blood cells to kill leukemia cells. PURPOSE: Phase III trial to study the effectiveness of high-dose combination chemotherapy, peripheral stem cell transplantation, and interleukin-2 in treating patients who have acute myeloid leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002945
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Irinotecan and Cytarabine in Treating Patients With Refractory or Recurrent Acute Myeloid Leukemia or Chronic Myelogenous Leukemia Condition(s): Myeloid Leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): Roswell Park Cancer Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase I trial to study the effectiveness of combining irinotecan with cytarabine in treating patients who have refractory or recurrent acute myeloid leukemia or chronic myelogenous leukemia.
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Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00053144 ·
Monoclonal Antibody Therapy in Treating Patients With Chronic Lymphocytic Leukemia, Lymphocytic Lymphoma, Acute Lymphoblastic Leukemia, or Acute Myeloid Leukemia Condition(s): recurrent adult acute lymphoblastic leukemia; refractory chronic lymphocytic leukemia; stage III diffuse small lymphocytic/marginal zone lymphoma; noncontiguous stage II diffuse small lymphocytic/marginal zone lymphoma; stage IV diffuse small lymphocytic/marginal zone lymphoma; recurrent diffuse small lymphocytic/marginal zone lymphoma; recurrent adult acute myeloid leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): Arthur G. James Cancer Hospital & Richard J. Solove Research Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Monoclonal antibodies can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. PURPOSE: Phase I trial to study the effectiveness of monoclonal antibody therapy in treating patients who have chronic lymphocytic leukemia, lymphocytic lymphoma, acute lymphoblastic leukemia, or acute myeloid leukemia. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00017472
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Oblimersen in Treating Patients With Relapsed or Refractory Chronic Lymphocytic Leukemia Condition(s): stage II chronic lymphocytic leukemia; stage IV chronic lymphocytic leukemia; refractory chronic lymphocytic leukemia; stage I chronic lymphocytic leukemia; stage III chronic lymphocytic leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): Genta Purpose - Excerpt: RATIONALE: Biological therapies such as oblimersen may interfere with the growth of the cancer cells and slow or stop the growth of chronic lymphocytic leukemia. PURPOSE: Phase I/II trial to study the effectiveness of oblimersen in treating patients who have relapsed or refractory chronic lymphocytic leukemia. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00021190
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VNP40101M in Treating Patients With Relapsed or Refractory Leukemia or Myelodysplastic Syndrome Condition(s): acute leukemia; atypical chronic myeloid leukemia; chronic leukemia; Hairy Cell Leukemia; myelodysplastic and myeloproliferative disease; Prolymphocytic Leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): Vion Pharmaceuticals Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase I trial to study the effectiveness of VNP40101M in treating patients who have relapsed or refractory leukemia or myelodysplastic syndrome. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049686
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Diagnostic Study of Gene Alterations in Patients With Acute Myeloid Leukemia Condition(s): Leukemia Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI); Cancer and Leukemia Group B Purpose - Excerpt: RATIONALE: Diagnostic procedures, such as genetic testing, may improve the ability to detect acute myeloid leukemia and determine the extent of disease. PURPOSE: Diagnostic study to try to detect changes in the genes of patients who have acute myeloid leukemia. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003931
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Fludarabine and Busulfan Followed by Allogeneic Stem Cell Transplantation in Treating Older Patients With Acute Myeloid Leukemia in First Complete Remission Condition(s): adult acute monocytic leukemia; adult acute myeloid leukemia; secondary acute myeloid leukemia Study Status: This study is not yet open for patient recruitment. Sponsor(s): Cancer and Leukemia Group B; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy, such as fludarabine and busulfan, use different ways to stop cancer cells from dividing so they stop growing or die. Allogeneic stem cell transplantation may be able to replace immune cells that were destroyed by chemotherapy. PURPOSE: Phase II trial to study the effectiveness of combining fludarabine with busulfan before allogeneic stem cell transplantation in treating older patients who have acute myeloid leukemia that is in the first complete remission. Phase(s): Phase II Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00070135 ·
Gemcitabine in Treating Children With Relapsed or Refractory Acute Lymphoblastic Leukemia or Acute Myelogenous Leukemia Condition(s): recurrent childhood acute lymphoblastic leukemia; recurrent childhood acute myeloid leukemia Study Status: This study is suspended. Sponsor(s): Children's Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of gemcitabine in treating children who have relapsed or refractory acute lymphoblastic leukemia or acute myelogenous leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006462
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Gemtuzumab Ozogamicin With or Without Cytarabine in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia Condition(s): recurrent adult acute myeloid leukemia Study Status: This study is suspended. Sponsor(s): National Cancer Institute (NCI); Cancer and Leukemia Group B Purpose - Excerpt: RATIONALE: Monoclonal antibodies such as gemtuzumab ozogamicin can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. It is not yet known whether gemtuzumab ozogamicin is more effective with or without cytarabine in treating acute myeloid leukemia. PURPOSE: Randomized phase II trial to compare the effectiveness of gemtuzumab ozogamicin with or without cytarabine in treating patients who have relapsed or refractory acute myeloid leukemia. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006265
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STI571 Plus Combination Chemotherapy in Treating Patients With Chronic Myelogenous Leukemia or Acute Lymphocytic Leukemia Condition(s): recurrent adult acute lymphoblastic leukemia; relapsing chronic myelogenous leukemia; blastic phase chronic myelogenous leukemia Study Status: This study is completed. Sponsor(s): Jonsson Comprehensive Cancer Center; National Cancer Institute (NCI)
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Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. STI571 may stop the growth of leukemia cells. Combining chemotherapy and STI571 may kill more cancer cells. PURPOSE: Phase I/II trial to study the effectiveness of combination chemotherapy plus STI571 in treating patients who have chronic myelogenous leukemia or acute lymphocytic leukemia. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00015860 ·
Tipifarnib in Treating Patients With Leukemia or Myelodysplastic Syndrome Condition(s): Myeloid Leukemia; Refractory Anemia Study Status: This study is suspended. Sponsor(s): University of Maryland Greenebaum Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Tipifarnib may stop the growth of cancer cells by blocking the enzymes necessary for cancer cell growth. PURPOSE: Phase II trial to study the effectiveness of tipifarnib in treating patients who have leukemia or myelodysplastic syndrome and have not received previous therapy. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00027872
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “leukemia” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: ·
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON LEUKEMIA Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “leukemia” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on leukemia, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Leukemia By performing a patent search focusing on leukemia, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We
9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on leukemia: ·
Activated iododerivatives for the treatment of cancer and AIDS Inventor(s): Naicker; Selvaraj (Edmonton, CA), Yatscoff; Randall W. (Edmonton, CA), Foster; Robert T. (Edmonton, CA) Assignee(s): Isotechnika Inc. (Edmonton, CA) Patent Number: 6,511,988 Date filed: August 10, 2001 Abstract: A series of activated iodo-benzamide derivatives are described as antineoplastic and antiviral drug compounds. The compounds generally possess a chelating group, a thiol trapping group and an activating group. The presumptive mechanism of action in preventing cancer cell and virus replication is through inhibition of the binding of transcription factors to zinc finger binding domains. The compounds are effective in inhibiting growth of a variety of human and animal tumor and leukemia cell lines at low concentrations. Excerpt(s): This invention is related to synthesis of activated iodo derivatives and their use as antineoplastic and antiviral agents by targeting the zinc finger regions of metalloregulatory proteins such as p-ADPRT and nucleocapsid of HIV. A series of activated iodo-benzamide derivatives are described as antineoplastic and antiviral drug compounds. The compounds generally possess a chelating group, a thiol trapping group and an activating group. The presumptive mechanism of action in preventing cancer cell and virus replication is through inhibition of the binding of transcription factors to zinc finger binding domains. The compounds are effective in inhibiting growth of a variety of human and animal tumor and leukemia cell lines at low doses. In the past several years, a series of discoveries revealed that several proteins contain metal ions, particularly zinc ions (Zn.sup.2+), that play fundamental roles in stabilizing specific protein conformations (Berg, J. M., J. Biol. Chem., 265: 6513-6516, 1990; Berg. J. M., In Progress in Inorganic chemistry, 37: 143-190, 1989). Many of these metalloproteins are involved in nucleic acid binding and in gene regulation (Bravo, R., Cell Growth and Differentiation, 1: 305-309, 1990; Evans; R. M., and Hollenberg, S. M., Cell, 52: 1-3, 1988). 1. DNA repair--Shell, S., Advances in Radiation Biology, 11, 1, 1984; Clear, J. E. et al., Mutation Research, 257, 1, 1991. Web site: http://www.delphion.com/details?pn=US06511988__
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Antibodies to leukemia inhibitory factor and their use in immunoassays Inventor(s): Kim; Kyung Jin (San Francisco, CA) Assignee(s): Genentech, Inc. (South San Francisco, CA) Patent Number: 6,544,749 Date filed: May 28, 1999 Abstract: The invention relates to monoclonal antibodies to human leukemia inhibitory factor. The disclosed monoclonal antibodies are believed to recognize unique epitopes on hLIF and are useful in the treatment of conditions wherein the presence of hLIF causes or contributes to undesirable pathological effects, such as cachexia, dysregulated
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calcium metabolism, or excessive bone cell proliferation, and in the detection of hLIF, for example, in clinical samples or specimens. Excerpt(s): This application relates to hybrid cell lines (lymphocyte hybridomas) for the production of monoclonal antibodies to human leukemia inhibitory factor, to such homogeneous monospecific antibodies, and to the use of such antibodies for diagnostic and therapeutic purposes. Leukemia inhibitory factor (LIF) is a polypeptide with a broad range of biological effects. LIF was initially purified from mouse cells and identified on the basis of its ability to induce differentiation in and suppress the proliferation of the murine monocytic leukemia cell line M1. Tomida, et al., J. Biol. Chem. 259:10978-10982 (1984); Tomida, et al., FEBS Lett. 178:291-296 (1984). Human LIF (hLIF) subsequently was shown to have comparable effects on human HL60 and U937 cells, particularly when acting in collaboration with GM-CSF or G-CSF colony stimulating factors. Maekawa, et al. Leukemia 3:270-276 (1989). Depending upon its particular activity or effect, LIF has been referred to by various names, including differentiation-inducing factor (DIF, D-factor), hepatocyte-stimulating factor (HSF-II, HSF-III), melanoma-derived LPL inhibitor (MLPLI), and cholinergic neuronal differentiation factor (CDP). Hilton, et al., J. Cell. Biochem. 46:21-26 (1991). Web site: http://www.delphion.com/details?pn=US06544749__ ·
Antibody composition for debulking blood and bone marrow samples from CML patients Inventor(s): Eaves; Connie J. (Vancouver, CA), Thomas; Terry E. (Vancouver, CA) Assignee(s): StemCell Technologies Inc. (Vancouver, CA) Patent Number: 6,491,917 Date filed: July 30, 1999 Abstract: The present invention relates to an antibody composition which contains antibodies specific for glycophorin A, CD2, CD3, CD14, CD15, CD16, CD19, CD24, CD56, CD66b and IgE antigens. A negative selection process is also provided for use on blood and bone marrow samples from a patient with chronic myeloid leukemia to recover cell preparations depleted of lineage committed cells. The invention also relates to kits for carrying out this process and to the cell preparations prepared by the process. Excerpt(s): The present invention relates to a method of depleting normal and transformed lineage committed cells from a sample from a patient with chronic myeloid leukemia. Chronic myeloid leukemia (CML) is a monoclonal expansion of a transformed pluripotent stem cell (Fialkow et al., 63:125, 1977, American Journal of Medicine). Myeloid cells, erythroid cells and less frequently lymphocytes arise from the leukemic clone (Bakhshi et al., New Eng. J. Med. 309:826, 1983). CML is characterized in more than 90% of patients by the rearrangement between the break cluster region (BCR gene, located on chromosome 22) and the ABL gene (located on chromosome 9) (Bartran et al., Nature 306:277, 1983). Although patients with CML may have a prolonged course, the disease is invariably lethal. Bone marrow transplantation is the treatment of choice for this patient population with a curative rate of 90% in some centres. However, for 60% of patients this therapy may not be available either due to the lack of a suitable donor due to differences in human leukocyte antigens (HLA) or the age of the recipient. Web site: http://www.delphion.com/details?pn=US06491917__
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Anticancer activity of imino acid conjugates or methylglyoxal Inventor(s): Mukherjee; Rama (Gurgaon Haryana, IN), Ray; Manju (Kolkata, IN), Burman; Anand C. (London, GB), Jaggi; Manu (Gurgaon Haryana, IN), Singh; Anu T. (Delhi, IN), Prasad; Sudhanand (Delhi, IN), Kapoor; Kamal K. (Delhi, IN) Assignee(s): Dabur Research Foundation (Ghaziabad, IN) Patent Number: 6,613,793 Date filed: July 1, 2002 Abstract: The invention relates to the use of imino acid conjugates of methylglyoxal for the inhibition and/or treatment of cancer. The invention relates more specifically to the use imino acid conjugates of methylglyoxal for inhibition and/or treatment of cancer of the Colon, Prostate, Larynx, Kidney, Pancreas, Lung, Breast, Intestine, Oral cavity, Ovary, Glioblastoma, and Leukemia. The invention also relates to compositions and methods of inhibiting cancer using imino acid conjugates of methylglyoxal. Excerpt(s): The invention relates to the use of imino acid conjugates of methylglyoxal for the inhibition and/or treatment of cancer. The invention relates more specifically to the use imino acid conjugates of methylglyoxal for inhibition and/or treatment of cancer of the Colon, Prostate, Larynx, Kidney, Pancreas, Lung, Breast, Intestine, Oral cavity, Ovary, Glioblastoma, and Leukemia. The anticancer activity of the conjugates is attributed to the inhibition of the activity of glyceraldehyde 3 phosphate dehydrogenase enzyme. The invention also relates to compositions and methods of inhibiting cancer using imino acid conjugates of methyglyoxal. As early as 1913 it had been observed that ketoaldehydes such as, methylglyoxal could be converted to corresponding hydroxyl acids (methylglyoxal to D-lactate) by strong and ubiquitous enzyme present in various animal tissues. It was then widely held that methylglyoxal was a key intermediate of glucose breakdown. But with the elucidation of Embden-Meyerh of pathway of glycolysis, this idea was rejected. Although no definite enzyme was identified or isolated, several investigators time to time reported the formation of methylglyoxal in different organisms (Current Science 75, 103-113; 1998). Cooper and his co-investigators established that the enzyme methylglyoxal synthase which converts the glycolytic intermediate dihydroxyacetone phosphate to methylglyoxal is present in a variety of bacteria (Annu Rev Microbiol 38, 49-68; 1984). In the early 1980s, Ray and Ray began a thorough investigation of the enzymes involved in the synthesis and breakdown of methylglyoxal in a mammalian system. Mainly by their work and also by the investigations from other laboratories, the metabolic pathway of methylglyoxal in a mammalian system had been established. In the process, they had isolated, purified and partially characterized a battery of enzymes involved. Thereafter the pathway for methylglyoxal metabolism has been elucidated in yeast, bacteria and protozoa (Current Science 75, 103-113; 1998). Web site: http://www.delphion.com/details?pn=US06613793__
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BCR-ABL directed compositions and uses for inhibiting Philadelphia chromesome stimulated cell growth Inventor(s): Liu; Jiaxin (Bellaire, TX), Wu; Yun (Houston, TX), Lopez-Berestein; Gabriel (Bellaire, TX), Arlinghaus; Ralph B. (Bellaire, TX), Lu; Dai (Pearland, TX) Assignee(s): Board of Regents, The University of Texas Systems (Austin, TX) Patent Number: 6,537,804 Date filed: June 21, 1999 Abstract: The present invention provides methods for detecting and quantitating BCRABL gene products and other abnormal ABL gene products of Ph.sup.1 -positive leukemic cells. The invention further provides methods for determining the relative number of leukemic cells compared with normal ABL cells to assess the tumor burden of a patient. In another aspect, the methods of the present invention can be used to determine a specific phase of leukemia, particularly chronic-phase CML. Excerpt(s): The present invention relates generally to the field of malignant cell proliferation. More particularly, it provides compositions and methods to limit Bcr-Abl oncoprotein-driven malignant cell proliferation. Peptide and protein molecules are provided that inhibit various Bcr-Abl signal transduction pathways, e.g., activation of the Ras protein. Methods for reducing Philadelphia chromosome-positive cells in cell populations, including bone marrow culture, and methods of treating various leukemias are also provided. The Philadelphia chromosome (Ph.sup.1) is associated with the bulk of chronic myelogenous leukemia (CML) patients (more than 95%), 10-25% of acute lymphocytic leukemia (ALL) patients, and about 2-3% of acute myelogenous leukemias (AML). This abnormal chromosome fuses most of the ABL gene to the 5' two-thirds of the BCR gene. A number of different kinds of evidence support the contention that BcrAbl oncoproteins, such as p210 and p185 BCR-ABL, are causative factors in these leukemias (Campbell et al., 1991). The malignant activity is due in large part to the BcrAbl protein's highly activated protein tyrosine kinase activity and its abnormal interaction with protein substrates (Campbell et al., 1991, Arlinghaus et al., 1990). The Bcr-Abl oncoprotein p210 Bcr-Abl is associated with both CML and ALL, whereas the smaller oncoprotein, p185 BCR-ABL, is associated with ALL patients, although some CML patients also express p185 (Campbell et al., 1991). Web site: http://www.delphion.com/details?pn=US06537804__
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CD38 as a prognostic indicator in B cell chronic lymphocytic leukemia Inventor(s): Wasil; Tarun (St. John's, CA), Damle; Rajendra N. (Lynbrook, NY), Chiorazzi; Nicholas (Tenafly, NJ) Assignee(s): North Shore - Long Island Jewish Research Institute (Manhasset, NY) Patent Number: 6,506,551 Date filed: October 8, 1999 Abstract: The subject invention discloses a method for determining the prognosis and probable clinical course of a subject diagnosed with B-CLL. Specifically, the invention involves comparing CD38 expression in a biological sample from the subject containing B-CLL cells to a baseline level of CD38 expression, wherein an elevated level of CD38 expression in relation to the baseline level of CD38 expression may indicate poor prognosis or aggressive course of disease in the subject. Also disclosed is a method for
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determining whether the Ig V genes of the B-CLL cells of a B-CLL patient are mutated, comprising comparing CD38 expression in a biological sample from the subject containing B-CLL cells to a baseline level of CD38 expression, wherein a lower level of CD38 expression in relation to the baseline level indicates IG V gene mutation. Excerpt(s): B cell chronic lymphocytic leukemia (B-CLL) is the most common leukemia in the Western world (Rai K, Patel D: Chronic Lymphocytic Leukemia, in Hoffman R, Benz E, Shattil S, Furie B, Cohen H, Silberstein L (eds): Hematology: Basic Principles and Practice (ed 2nd). New York, Churchill Livingstone, 1995, p 1308). Around 7,500 individuals develop and 5,000 die from this disease each year (Landis S H, et al., CA Cancer J Clin 48:6, 1998). Age is an important factor, since the incidence of B-CLL increases linearly with each decade above the age of 40 (Ries L, et al: SEER cancer statistics review 1973-1991: Tables and graphs., in Ries L, et al (eds). Bethesda, NIH, 1994; Rai K R, Clin Geriatr Med 13:245, 1997). In addition, gender is relevant, since men outnumber women by an approximate 2:1 ratio (Catovsky D, et al., Br J Haematol 72:141, 1989) and may have a worse clinical outcome (Id.; Mandelli F, et al., J Clin Oncol 5:398, 1987). Patients with B-CLL follow heterogeneous clinical courses. Some survive for prolonged periods without definitive therapy, while others die rapidly despite aggressive treatment (Rai K, Patel D: Chronic Lymphocytic Leukemia, in Hoffman R, et al. (eds): Hematology: Basic Principles and Practice (ed 2nd). New York, Churchill Livingstone, 1995, p 1308; Zwiebel J A, Cheson B D, Semin Oncol 25:42, 1998). While various staging systems, most notably the Rai and Binet staging systems, have been developed to address this clinical heterogeneity (Rai K R, et al., Blood 46, 219, 1975; Binet J L, et al., Cancer 48:198, 1981; and Rai K: A critical analysis of staging in CLL, in Gail R, Rai K (eds): Chronic Lymphocytic Leukemia. Recent Progress and Future Directions. New York, Alan R Liss, 1987, p 253), they cannot accurately predict whether an early or intermediate stage patient will experience an indolent or aggressive course of disease. Specifically, since these systems consider gross manifestations of the disease, including the level of blood and marrow lymphocyte counts, the size and distribution of the lymph nodes, the spleen size, the degree of anemia and the patient's blood platelet count, they can only identify patients with poor prognostic outcome when the disease has progressed to a more advanced state. At the present time, there is no known treatment for B-CLL which has been shown to definitively increase life expectancy. Consequently, only patients classified in the advanced stages of B-CLL have been considered for aggressive treatment such as chemotherapy, radiation therapy, surgery, immunotherapy or transplantation. These treatments may exact a severe physical and emotional toll on the patient without necessarily improving outcome; in some instances, B-CLL patients may even succumb from the rigors of treatment rather than from the effects of B-CLL. Patients classified in the early stages of B-CLL, who may be in better physical condition to receive more aggressive or experimental treatment, generally receive no treatment as long as the condition remains stable. This is for two reasons. First, currently available therapies do not extend life span. Second, there are currently no reliable indicators of which early stage patients will do well and which will do poorly. Further, the unpredictable course of the disease can make interpreting the results of clinical trials difficult, as some early stage patients will follow an indolent course even without the benefit of treatment. Web site: http://www.delphion.com/details?pn=US06506551__
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Chemokine.beta.-4 polypeptides Inventor(s): Adams; Mark D. (North Potomac, MD), Li; Haodong (Gaithersburg, MD) Assignee(s): Human Genome Sciences, Inc. (Rockville, MD) Patent Number: 6,458,349 Date filed: March 3, 1999 Abstract: Human chemokine polypeptides and DNA (RNA) encoding such chemokine polypeptides and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemokine polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemokine polypeptides and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed. Diagnostic assays for identifying mutations in nucleic acid sequence encoding a polypeptide of the present invention and for detecting altered levels of the polypeptide of the present invention are also disclosed. Excerpt(s): This invention relates to newly identified polynucleotides, polypeptides encoded by such polynucleotides, the use of such polynucleotides and polypeptides, as well as the production of such polynucleotides and polypeptides. More particularly, the polypeptides of the present invention are human chemokine beta-4 and human chemokine beta-10, sometimes hereinafter referred to as "Ck.beta.-4" and "Ck.beta.-10", collectively referred to as "the chemokine polypeptides". The invention also relates to inhibiting the action of such polypeptides. Chemokines are an emerging super-family of small secreted cytokines that are structurally and functionally related. All chemokines exhibit 25 to 75% homology at the amino acid level and contain spatially conserved cysteine residues as do the polypeptides of the present invention. Members of the "C-XC branch" (according to the position of the first two cysteines in the conserved motif), also known as neutrophil-activating peptide (NAP)/IL-8 family, exert pro-inflammatory activity mainly through their action on neutrophils (e.g., IL-8 and NAP-2), whereas members of the "C--C branch" family appear to attract certain mononuclear cells. Members of the "C--C branch" include PF4, MIPs, MCPs, and the chemokine polypeptides of the present invention. Numerous biological activities have been assigned to this chemokine family. The macrophage inflammatory protein 1.alpha. and 1.beta. are chemotactic for distinct lymphocyte populations and monocytes (Schall, T. J., Cytokine, 3:165 (1991)), while MCP-1 has been described as a specific monocyte chemoattractant (Matsushima, K., et al., J. Exp. Med., 169:1485 (1989)). The common function of this chemokine family is their ability to stimulate chemotactic migration of distinct sets of cells, for example, immune cells (leukocytes) and fibroblasts. These chemokines are also able to activate certain cells in this family. Web site: http://www.delphion.com/details?pn=US06458349__
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Chromosome-specific staining to detect genetic rearrangements associated with chromosome 3 and/or chromosome 17 Inventor(s): Kallioniemi; Olli-Pekka (Tampere, FI), Pinkel; Daniel (Walnut Creek, CA), Gray; Joe W. (Livermore, CA), Kallioniemi; Anne (Tampere, FI), Sakamoto; Masaru (Tokyo, JP) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,475,720 Date filed: June 7, 1995 Abstract: Methods and compositions for staining based upon nucleic acid sequence that employ nudeic acid probes are provided. Said methods produce staining patterns that can be tailored for specific cytogenetic analyses. Said probes are appropriate for in situ hybridization and stain both interphase and metaphase chromosomal material with reliable signals. The nucleic acid probes are typically of a complexity greater than 50 kb, the complexity depending upon the cytogenetic application. Methods and reagents are provided for the detection of genetic rearrangements. Probes and test kits are provided for use in detecting genetic rearrangements, particularly for use in tumor cytogenetics, in the detection of disease related loci, specifically cancer, such as chronic myelogenous leukemia (CML), retinoblastoma, ovarian and uterine cancers, and for biological dosimetry. Methods and reagents are described for cytogenetic research, for the differentiation of cytogenetically similar but genetically different diseases, and for many prognostic and diagnostic applications. Excerpt(s): The invention relates generally to the field of cytogenetics, and more particularly, to the field of molecular cytogenetics. The invention concerns methods for identifying and classifying chromosomes. Still more particularly, this invention concerns nucleic acid probes which can be designed by the processes described herein to produce staining distributions that can extend along one or more whole chromosomes, and/or along a region or regions on one or more chromosomes, including staining patterns that extend over the whole genome. Staining patterns can be tailored for any desired cytogenetic application, including prenatal, tumor and disease related cytogenetic applications, among others. The invention provides for compositions of nucleic acid probes and for methods of staining chromosomes therewith to identify normal chromosomes and chromosomal abnormalities in metaphase spreads and in interphase nuclei. The probe-produced staining patterns of this invention facilitate the microscopic and/or flow cytometric identification of normal and abnormal chromosomes and the characterization of the genetic nature of particular abnormalities. The particular focus of this application is that wherein the abnormalities are genetic rearrangements. Although most of the examples herein concern human chromosomes and much of the language herein is directed to human concerns, the concept of using nucleic acid probes for staining or painting chromosomes is applicable to chromosomes from any source including both plants and animals. Chromosome abnormalities are associated with genetic disorders, degenerative diseases, and exposure to agents known to cause degenerative diseases, particularly cancer, German, "Studying Human Chromosomes Today," American Scientist, Vol. 58, pgs. 182-201 (1970); Yunis, "The Chromosomal Basis of Human Neoplasia," Science, Vol. 221, pgs. 227-236 (1983); and German, "Clinical Implication of Chromosome Breakage," in Genetic Damage in Man Caused by Environmental Agents, Berg, Ed., pgs. 65-86 (Academic Press, New York, 1979). Chromosomal abnormalities can be of several types, including: extra or missing individual chromosomes, extra or missing portions of a chromosome (segmental duplications or deletions), breaks, rings and chromosomal rearrangements, among
Patents 281
others. Chromosomal or genetic rearrangements include translocations (transfer of a piece from one chromosome onto another chromosome), dicentrics (chromosomes with two centromeres), inversions (reversal in polarity of a chromosomal segment), insertions, amplifications, and deletions. Web site: http://www.delphion.com/details?pn=US06475720__ ·
Composition and method of imparting resistivity to HIV superinfection to cells Inventor(s): Ferrari; Giuliana (Milan, IT), Verani; Paola (Rome, IT), Federico; Maurizio (Rome, IT), Mavilio; Fulvio (Milan, IT) Assignee(s): del Monte Tabor GenEra S.p.A. (Milan, IT), Fondaxione Centro San Raffaele (Milan, IT), Istituto Superiore Disanita' (Rome, IT) Patent Number: 6,429,009 Date filed: April 8, 1998 Abstract: The invention describes the expression of a human immunodeficiency virus (HIV) type 1 provirus (F12-HIV) cloned from a nonproducer, chronically-infected CD4 down-regulated Hut-78 cell clone (F12) which does not lead to the formation of viral particles and, upon transfection in HeLa CD4.sup.+ cells, confers resistance to HIV superinfection without affecting CD4 receptor exposure. A Moloney murine leukemia virus-based retroviral vector containing an F12-HIV genome lacking the 3' long terminal repeat (LTR) and part of the nef gene, expressed under the control of its 5' LTR, was constructed to facilitate the transfer of the anti-HIV properties of F12-HIV into human cells. The F12-HIV genome was inserted in an orientation opposite to that of the murine leukemia virus transcriptional unit and was designated the N2/F12-HIV nef.sup.antisense vector. Lymphoblastoid CEMss cells, as well as human peripheral blood lymphocytes, were successfully transduced by the recombinant retrovirus. CEMss clones expressing the F12-HIV nef.sup.- antisense vector were resistant to HIV superinfection even at the highest multiplicity of infection tested (10.sup.5 50% tissue culture infective doses per 10.sup.6 cells). Nonproducer, interfering HIV proviruses transduced into retroviral vectors may provide an alternative strategy for the protection of CD4.sup.+ human primary cells from HIV infection. Excerpt(s): The present invention relates to a composition and to a method of imparting resistivity to superinfection with HIV. More in particular the invention concerns a composition and a method to confer resistance to human cells, in particular T-cells, to the superinfection with a retrovirus, specifically the human immunodeficiency virus (HIV). Several experimental strategies aimed at blocking HIV replication in vivo have been proposed. So far, most have been based on immunotherapeutic or chemotherapeutic approaches, in which the anti-HIV mechanism of action is well known. However, none of the immunotherapeutic and chemotherapeutic approaches proposed thus far has been demonstrated to effect a resolutive anti-HIV therapy. Web site: http://www.delphion.com/details?pn=US06429009__
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Discalamide compounds and their use as anti-proliferative agents Inventor(s): Pomponi; Shirley A. (Ft. Pierce, FL), Gunasekera; Sarath P. (Vero Beach, FL), Longley; Ross E. (Vero Beach, FL), Isbrucker; Richard A. (Ontario, CA), Paul; Gopal K. (Ft. Pierce, FL) Assignee(s): Harbor Branch Oceanographic Institution, Inc. (Fort Pierce, FL) Patent Number: 6,476,065 Date filed: April 16, 2001 Abstract: The subject invention provides novel biologically active compounds which are useful for inhibiting cellular proliferation. Because of the biological activity of these compounds, they can be used for immunomodulation and/or treating cancer. In a preferred embodiment, the novel compounds, compositions and methods of use of the subject invention can advantageously be used to inhibit the growth of tumor cells in a mammalian host. More particularly, the subject compounds can be used for inhibiting in a human the growth of tumor cells, including cells of breast, colon, CNS, ovarian, renal, prostate, bone, gastrointestinal, stomach, testicular, or lung tumors, as well as human leukemia or melanoma cells. Specifically exemplified are discalamides A and B. Excerpt(s): Of great importance to man is the control of pathological cellular proliferation such as that which occurs in the case of cancer. Considerable research and resources have been devoted to oncology and antitumor measures including chemotherapy. While certain methods and chemical compositions have been developed which aid in inhibiting, remitting, or controlling the growth of, for example, tumors, new methods and antiproliferative chemical compositions are needed. In searching for new biologically active compounds, it has been found that some natural products and organisms are potential sources for chemical molecules having useful biological activity of great diversity. For example, the diterpene commonly known as Taxol, isolated from several species of yew trees, is a mitotic spindle poison that stabilizes microtubules and inhibits their depolymerization to free tubulin (Fuchs, D. A., R. K. Johnson [1978] Cancer Treat. Rep. 62:1219-1222; Schiff, P. B., J. Fant, S. B. Horwitz [1979] Nature (London) 22:665-667). Taxol is also known to have antitumor activity and has undergone a number of clinical trials which have shown it to be effective in the treatment of a wide range of cancers (Rowinski, E. K. R. C. Donehower [1995] N. Engl. J. Med 332:1004-1014). See also, e.g., U.S. Pat. Nos. 5,157,049; 4,960,790; and 4,206,221. Marine sponges have also proven to be a source of biologically active chemical molecules. A number of publications disclose organic compounds derived from marine sponges including Scheuer, P. J. (ed.) Marine Natural Products, Chemical and Biological Perspectives, Academic Press, New York, 1978-1983, Vol. I-V; Uemura, D., K. Takahashi, T. Yamamoto, C. Katayama, J. Tanaka, Y. Okumura, Y. Hirata [1985] J. Am. Chem. Soc. 107:4796-4798; Minale, L. et al. [1976] Fortschr. Chem. Org. Naturst. 33:1-72; Faulkner, D. J. [2001] Natural Products Reports 18:1-49; Gunasekera, S. P., M. Gunasekera, R. E. Longley and G. K. Schulte [1990] "Discodermolide: A new bioactive polyhydroxy lactone from the marine sponge Discodermia dissoluta" J. Org. Chem., 55:4912-4915; [1991] J. Org. Chem. 56:1346; Hung, Deborah T., Jenne B. Nerenberg, Stuart Schreiber [1994] "Distinct binding and cellular properties of synthetic (+)- and (-) discodermolides" Chemistry and Biology 1:67-71; Hung, Deborah T., Jie Cheng, Stuart Schreiber [1996] (+)Discodermolide binds to microtubules in stoichiometric ratio to tubulin dimers, blocks Taxol binding and results in mitotic arrest" Chemistry and Biology 3:287-293. U.S. Pat. No. 4,801,606 and 4,808,590 (T. Higa, S. Sakemi and S. Cross) disclose related onnamide compounds, having antiviral, antitumor, and antifungal properties, isolated from the marine sponge Theonella sp.
Patents 283
Web site: http://www.delphion.com/details?pn=US06476065__ ·
Human chemokine.beta.-9 Inventor(s): Li; Haodong (Gaithersburg, MD), Adams; Mark D. (North Potomac, MD), Li; Haodong (Gaithersburg, MD), Adams; Mark D. (North Potomac, MD) Assignee(s): Human Genome Sciences, Inc. (Rockville, MD), Human Genome Sciences, Inc. (Rockville, MD) Patent Number: 6,518,046 Date filed: May 19, 1997 Abstract: The present invention relates to Human Ck.beta.-9 polypeptides and DNA (RNA) encoding such chemolcine polypeptides. Moreover, a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such Ck.beta.-9 polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune diseases, fibrotic disorders, wound healing and psoriasis. Antagonists against such polypeptides and their use as a therapeutic agent to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective disease, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed. Diagnostic assays are also disclosed which detect the presence of mutations in the Ck.beta.-9 coding sequence and over-expression of the Ck.beta.-9 protein. Excerpt(s): This invention relates to newly identified polynucleotides, polypeptides encoded by such polynucleotides, the use of such polynucleotides and polypeptides, as well as the production of such polynucleotides and polypeptides. More particularly, the polypeptides of the present invention are human chemokine beta-9 sometimes hereinafter referred to as "Ck.beta.-9". The invention also relates to inhibiting the action of such polypeptides. This invention relates to newly identified polynucleotides, polypeptides encoded by such polynucleotides, the use of such polynucleotides and polypeptides, as well as the production of such polynucleotides and polypeptides. More particularly, the polypeptides of the present invention are human chemokine beta-9 sometimes hereinafter referred to as "Ck.beta.-9". The invention also relates to inhibiting the action of such polypeptides. Chemokines, also referred to as intercrine cytokines, are a subfamily of structurally and functionally related cytokines. These molecules are 8-10 kd in size. In general, chemokines exhibit 20% to 75% homology at the amino acid level and are characterized by four conserved cysteine residues that form two disulfide bonds. Based on the arrangement of the first two cysteine residues, chemokines have been classified into two subfamilies, alpha and beta. In the alpha subfamily, the first two cysteines are separated by one amino acid and hence are referred to as the "C--X--C" subfamily. In the beta subfamily, the two cysteines are in an adjacent position and are, therefore, referred to as the "C--C" subfamily. Thus far, at least eight different members of this family have been identified in humans. Chemokines, also referred to as intercrine cytokines, are a subfamily of structurally and functionally related cytokines. These molecules are 8-10 kd in size. In general, chemokines exhibit 20% to 75% homology at the amino acid level and are characterized by four conserved cysteine residues that form two disulfide bonds. Based on the arrangement of the first two cysteine residues, chemokines have been classified into two subfamilies, alpha and beta. In the alpha subfamily, the first two cysteines are separated by one amino acid and hence are referred to as the "C--X--C" subfamily. In the beta subfamily, the two cysteines are in an adjacent position and are, therefore, referred to as the "C--C" subfamily. Thus far, at least eight different members of this family have been identified in humans. The intercrine
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cytokines exhibit a wide variety of functions. A hallmark feature is their ability to elicit chemotactic migration of distinct cell types, including monocytes, neutrophils, T lymphocytes, basophils and fibroblasts. Many chemokines have pro-inflammatory activity and are involved in multiple steps during an inflammatory reaction. These activities include stimulation of histamine release, lysosomal enzyme and leukotriene release, increased adherence of target immune cells to endothelial cells, enhanced binding of complement proteins, induced expression of granulocyte adhesion molecules and complement receptors, and respiratory burst. In addition to their involvement in inflammation, certain chemokines have been shown to exhibit other activities. For example, macrophage inflammatory protein 1 (MIP-1) is able to suppress hematopoietic stem cell proliferation, platelet factor-4 (PF-4) is a potent inhibitor of endothelial cell growth, Interleukin-3 (IL-8) promotes proliferation of keratinocytes, and GRO is an autocrine growth factor for melanoma cells. The intercrine cytokines exhibit a wide variety of functions. A hallmark feature is their ability to elicit chemotactic migration of distinct cell types, including monocytes, neutrophils, T lymphocytes, basophils and fibroblasts. Many chemokines have pro-inflammatory activity and are involved in multiple steps during an inflammatory reaction. These activities include stimulation of histamine release, lysosomal enzyme and leukotriene release, increased adherence of target immune cells to endothelial cells, enhanced binding of complement proteins, induced expression of granulocyte adhesion molecules and complement receptors, and respiratory burst. In addition to their involvement in inflammation, certain chemokines have been shown to exhibit other activities. For example, macrophage inflammatory protein 1 (MIP-1) is able to suppress hematopoietic stem cell proliferation, platelet factor-4 (PF-4) is a potent inhibitor of endothelial cell growth, Interleukin-3 (IL-8) promotes proliferation of keratinocytes, and GRO is an autocrine growth factor for melanoma cells. Web site: http://www.delphion.com/details?pn=US06518046__ ·
Immune cell cytokine Inventor(s): Soppet; Daniel R. (Centreville, VA), Li; Yi (Gaithersburg, MD) Assignee(s): Human Genome Sciences, Inc. (Rockville, MD) Patent Number: 6,537,539 Date filed: February 17, 1999 Abstract: Human Immune Cell Cytokine-like Hormone polypeptide and DNA (RNA) encoding such polypeptide in a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such polypeptide for stimulating the proliferation and differentiation of stem cells of the immune system. Antagonists against such polypeptides are also disclosed. The antagonists include antibodies which may be employed as a therapeutic to treat leukemia and lymphoblastoma, may also be used as imaging agents and diagnostic agents for detecting expression levels of the protein. Also disclosed are diagnostic assays for detecting diseases related to mutations in the nucleic acid sequences and altered concentrations of the polypeptides. Excerpt(s): This invention relates to newly identified polynucleotides, polypeptides encoded by such polynucleotides, the use of such polynucleotides and polypeptides, as well as the production of such polynucleotides and polypeptides. The polypeptide of the present invention has been putatively identified as a cytokine, more particularly, the polypeptide of the present invention has been identified as an immune cell cytokine-like
Patents 285
potential hormone, sometimes hereinafter referred to as "HLHDC84". The invention also relates to inhibiting the action of such polypeptides. The cytokine family of proteins exhibit a wide variety of functions. A hallmark feature is their ability to elicit chemotactic migration of distinct cell types, including polymorphonuclear cells and macrophages. Many cytokines have pro-inflammatory activity and are involved in multiple steps during inflammatory reactions. In addition to their involvement in inflammation, cytokines have been shown to exhibit other activities. For example, interleukin-8 (IL-8) promotes proliferation of keratinocytes. In light of the diverse biological activities, it is not surprising that cytokines have been implicated in a number of physiological and disease conditions, including lymphocyte trafficking, wound healing, hematopoietic regulation and immunological disorders such as allergy, asthma and arthritis. Web site: http://www.delphion.com/details?pn=US06537539__ ·
Inhibition of abnormal cell proliferation with camptothecin and combinations including the same Inventor(s): Rubinfeld; Joseph (Danville, CA) Assignee(s): SuperGen, Inc. (Dublin, CA) Patent Number: 6,420,378 Date filed: April 20, 2000 Abstract: A method for treating diseases associated with abnormal cell proliferation comprises delivering to a patient in need of treatment a compound selected from the group consisting of 20(S)-camptothecin, analog of 20(S)-camptothecin, derivative of 20(S)-camptothecin, prodrug of 20(S)-camptothecin, and pharmaceutically active metabolite of 20(S)-camptothecin, in combination with an effective amount of one or more agents selected from the group consisting of alkylating agent, antibiotic agent, an alkylating agent, antibiotic agent, antimetabolic agent, hormonal agent, plant-derived agent, anti-angiogenesis agent and biologic agent. The method can be used to treat benign tumors, malignant or metastatic tumors, leukemia and diseases associated with abnormal angiogenesis. Excerpt(s): This invention relates to a method for treating diseases using a camptothecin, and more specifically a method for treating diseases associated with abnormal cell growth using a camptothecin alone or in combination with another drug. 20(S)camptothecin, a plant alkaloid, was found to have anticancer activity in the late 1950's. Wall, M. et al., Plant antitumor agents. I. The isolation and structure of camptothecin,. a novel alkaloidal leukemia and tumor inhibitor from Camptotheca acuminata, J. Am. Chem. Soc. 88: 3888-3890, (1966); Monroe E. Wall et al., Camptothecin: Discovery to Clinic, 803 Annals of the New York Academy of Sciences 1 (1996). These documents, and all documents (articles, patents, etc.) cited to herein, are incorporated by reference into the specification as if reproduced fully below. The chemical formula of camptothecin was determined to be C.sub.20 H.sub.16 N.sub.2 O.sub.4. 20(S)camptothecin itself is insoluble in water. However, during the sixties and seventies the sodium salt of 20(S)-camptothecin was derived from 20(S)-camptothecin through opening of the lactone ring using a mild base. Clinical trials were then conducted using this hydrosoluble, sodium salt derivative of 20(S)-camptothecin (20(S)-camptothecin Na+), which was administered intravenously. The studies were later abandoned because of the high toxicity and low potency of 20(S)-camptothecin Na+. Gottlieb, J. A., et al., Preliminary pharmacological and clinical evaluation of camptothecin sodium salt
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(NSC 100880), Cancer Chemother. Rep. 54:461-470 (1979); Muggia, F. M., et al., Phase I clinical trials of weekly and daily treatment with camptothecin (NSC 100880): Correlation with clinical studies, Cancer Chemother. Rep. 56:515-521 (1972); Gottlieb, J. A. et al., Treatment of malignant melanoma with camptothecin (NSC 100880), Cancer Chemother. Rep. 56:103-105 (1972); and Moertel, C. G., et al., Phase II study of camptothecin (NSC 100880) in type treatment of advanced gastrointestinal cancer, Cancer Chemother Rep. 56:95-101 (1972). Web site: http://www.delphion.com/details?pn=US06420378__ ·
Leukemic cell-adsorbing material cylindracea or jequirity plant seed
containing lectin
protein
from
Agrocybe
Inventor(s): Nakamura; Osamu (Tosu, JP), Yasuda; Seiji (Tosu, JP), Ohba; Hideki (Kitakyushu, JP), Sallay; Imre (Tosu, JP), Yagi; Fumio (Ijuhin-machi, JP), Moriwaki; Sawako (Fukuoka, JP) Assignee(s): Japan as represented by Secretary of Agency of Industrial Science and (Tokyo-to, JP) Patent Number: 6,420,171 Date filed: April 14, 2000 Abstract: An efficient method for therapeutic treatment of leukemia is provided in which a patient's body fluid during external circulation is brought into direct contact with an adsorbent material capable of specifically and selectively adsorbing leukemic cells in the body fluid. The leukemic cell-adsorbing material is a composite of a lectin protein coupled with a physiologically inert carrier material such as a galactan polysaccharide in the form of beads. The lectin protein may be obtained from a mushroom fungus such as Agrocybe cylindracea or a leguminous seed such as from the jequirity bean plant. The lectin protein and carrier material can be bound by forming chemical linkages between amino groups in the lectin protein and functional groups in the carrier material, and unreacted functional groups of the carrier material may be blocked with an amino acid. A leukemic cell-adsorbing column may be formed by filling the leukemic cell-adsorbing material into a tubular body to form an adsorbent bed. The tubular body may have an inner diameter of from 10 to 20 mm and a height of from 50 to 200 mm. Excerpt(s): The present invention relates to development of a suitable column to adsorb leukemic cells selectively from the blood of leukemic patients for the purpose of therapeutic treatment, and a leukemic cell-adsorbent material used therein. The current therapeutic treatment of leukemia is to undertake transplantation of a healthy marrow following the administration of anticancer agents and radiation. Anticancer agents are administered until leukemic cells disappear in blood, which in general exhibits strong side effects to the patient of leukemia. They must endure a very severe life under the medical care for a quite long time. In addition, it is sometimes not certain that the relapse into the disease can be fully prevented even by a prolonged administration of anticancer agents. On the other hand, a novel promising therapeutic way for leukemia has become highlighted by the discovery of lectin proteins derived from certain plants and animals which act as leukemic cell-capturing agents capable of recognizing leukemic cells specifically as reported in Japanese Patent Kokai 9-206096. This leukemic cell-capturing agent can discriminate leukemic cells.from normal cells in the blood by recognizing the sugar chains expressed on the cancer cells specifically so that the lectin protein is expected to remove leukemic cells from body fluids very efficiently.
Patents 287
Web site: http://www.delphion.com/details?pn=US06420171__ ·
Method and reagent for treatment of diseases by expression of the c-Myc gene Inventor(s): Thompson; James D. (Boulder, CO), Draper; Kenneth G. (Boulder, CO) Assignee(s): Ribozyme Pharmaceuticals, Inc. (Boulder, CO) Patent Number: 6,544,755 Date filed: February 7, 1994 Abstract: An enzymatic RNA molecule which cleaves mRNA associated with development or maintenance of Burkitt's lymphoma or acute lymphocytic leukemia. Excerpt(s): This invention relates to methods for inhibition of growth of transformed cells, and inhibition of progression to a transformed phenotype in pre-neoplastic cells. Transformation is a cumulative process whereby normal control of cell growth and differentiation is interrupted, usually through the accumulation of mutations affecting the expression of genes that regulate cell growth and differentiation. Scanlon WO91/18625, WO91/18624, and WO91/18913 describes a ribozyme effective to cleave oncogene RNA from the H-ras gene. This ribozyme is said to inhibit H-ras expression in response to exogenous stimuli. Reddy WO92/00080 describes use of ribozymes as therapeutic agents for leukemias, such as CML by targeting specific portions of the BCRABL gene transcript. Web site: http://www.delphion.com/details?pn=US06544755__
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Method of inducing formation of kidney epithelia from mesenchymal precursors Inventor(s): Barasch; Jonathan M. (New York, NY), Yang; Jun (New York, NY), Oliver; Juan A. (New York, NY) Assignee(s): The Trustees of Columbia University in the City of New York (New York, NY) Patent Number: 6,423,681 Date filed: May 4, 1999 Abstract: This invention provides methods of using a gpl3O receptor ligand, e.g. leukemia inhibitory factor, to induce the formation of kidney epithelia, to treat subjects suffering from kidney failure, and to preserve kidneys for transplantation. Excerpt(s): Throughout this application, various publications are referenced in parentheses by author and year. Full citations for these references may be found at the end of the specification immediately preceding the claims. The disclosures of these publications in their entireties are hereby incorporated by reference into this application to more fully describe the state of the art to which this invention pertains. The kidney develops from two components, the metanephric mesenchyme and the ureteric bud. The ureteric bud invades the mesenchyme, triggering both mesenchymal proliferation and the conversion of the mesenchyme into epithelia. This process has been termed induction of the mesenchyme (Grobstein, 1955; Saxen, 1987; Ekblom, 1989). The bud is known to produce factors which stimulate growth of the metanephric mesenchyme (Perantoni et al., 1995; Barasch et al., 1997), but the ureteric factors which convert mesenchyme into epithelia have been unknown. To date, induction of isolated metanephric mesenchyme in vitro has been obtained with living cells, including a number of embryonic tissues (Grobstein, 1955; Sariola et al., 1989; Herzlinger et al., 1994;
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Kispert et al., 1998), but not with purified molecules. To identify ureteric factors that trigger mesenchymal induction, we developed ureteric bud cell lines (UB cells; Barasch et al., 1996). These cells express a number of proteins in common with the embryonic ureteric bud at the time it invades the mesenchyme, including epithelial specific proteins (E-cadherin, ZO-1, cytokeratin, collagen IV, and laminin), receptor tyrosine kinases (c-ret and c-met), lectin (dolichos bifloris) binding sites (Barasch et al., 1996; Sakuri et al., 1997), as well as several monoclonal binding sites which cross react with the ureteric bud. In addition, UB cells secrete a number of metanephric mesenchymal growth factors (FGF-2, FGF-9, TIMP-1 and TIMP-2) that are also synthesized by the embryonic ureteric bud (Barasch et al, 1997; Barasch et al., 1999). We previously found that UB cells secrete factors (Barasch et al., 1997) that stimulate mesenchymal growth but cannot trigger metanephric mesenchymal conversion to epithelia. Web site: http://www.delphion.com/details?pn=US06423681__ ·
Method of screening apoptosis inducing substances Inventor(s): Fukushima; Naoshi (Gotemba, JP) Assignee(s): Chugai Seiyaku Kabushiki Kaisha (Tokyo, JP) Patent Number: 6,579,692 Date filed: September 8, 1998 Abstract: The present invention provides a method of screening substances having property of causing apoptosis, and relates to a method of screening substances having property of causing apoptosis characterized by using cells which are expressing IAP (Integrin Associated Protein), and the relates to above screening method, wherein the cells used are myeloid cells, and relates to pharmaceutical compositions containing as the active ingredient the substances obtained by the above method, and the present invention makes it possible to differentiate, identify and screen readily and highly efficiently the substances, such as antibodies and the like, that have property of causing apoptosis on myeloid cells by using cells which are expressing IAP while using specific binding reactions of the substances, and the above specific substances thus obtained can be used by virtue of their characteristics as the active ingredient of pharmaceutical compositions such as anticancer agents and medicines for myelocytic leukemia and the like. Excerpt(s): This Application is 35 USC.sctn.371 of PCT/JP97/00702, filed Mar. 6, 1997. The present invention relates to a method of screening substances having property of causing apoptosis and the like, in particular, relates to a novel screening method which makes it possible to screen readily and highly efficiently the substances, such as monoclonal antibodies and the like, that have property of causing apoptosis on myeloid cells by using cells which are expressing IAP (Integrin Associated Protein), and relates to the substances having property of causing apoptosis obtained by the above screening method, pharmaceutical compositions containing as the active ingredient the above substances, and relates to substances having property of causing apoptosis which have a specific binding activity to IAP, pharmaceutical compositions containing as the active ingredient the above substances. Granulocyte colony-stimulating factors, for example, recombinant granulocyte colony-stimulating factors (rG-CSF), have been known primarily as humoral factors to stimulate the differentiation and proliferation of granulocyte cells, and it has been reported in an experiment upon mice in vivo that the administration of rG-CSF enhances the hematopoiesis of the bone marrow and in addition causes remarkable extramedullary hematopoiesis in the spleen to proliferate
Patents 289
hematopoietic stem cells and all hematopoietic precursor cells in the spleen. And it has been thought as extramedullary hematopoietic mechanism in the spleen that hematopoiesis occurs due to a splenic hematopoietic microenvironment modifications according to the stimulation of rG-CSF to enhance hematopoietic potential. Web site: http://www.delphion.com/details?pn=US06579692__ ·
Methods and compositions for modulating cell proliferation and cell death Inventor(s): Wientjes; Guillaume (2287 Palmleaf Ct., Columbus, OH 43235), Au; Jessie L. -S. (2287 Palmleaf Ct., Columbus, OH 43235) Assignee(s): none reported Patent Number: 6,599,912 Date filed: June 5, 2000 Abstract: Methods and compositions for modulating the FGF effect on the sensitivity of malignant and normal cells to anticancer agents are provided. In particular, methods and compositions for inhibiting FGF-induced resistance to a broad spectrum of anticancer agents in solid and soft-tissue tumors, metastatic lesions, leukemia and lymphoma are provided. Preferably, the compositions include at least one FGF inhibitor in combination with a cytotoxic agents, e.g., antimicrotubule agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, mitotic inhibitors, alkylating agents, intercalating agents, agents capable of interfering with a signal transduction pathway (e.g., g., a protein kinase C inhibitor, e.g., an anti-hormone, e.g., an antibody against growth factor receptors), an agent that promotes apoptosis and/or necrosis, and interferon, an interleukin, a tumor necrosis factor, and radiation.In other embodiments, methods and composition for protecting a cell in a subject, from one or more of killing, inhibition of growth or division or other damage caused, e.g., by a cytotoxic agent, are provided. Preferably, the method includes: administering, to the subject, an effective amount of at least one FGF agonist, thereby treating the cell, e.g., protecting or reducing the damage to the dividing cell from said cytotoxic agent. Excerpt(s): Resistance of tumor cells to cancer therapy, limited efficacy of cancer therapy in metastatic disease, and undesired host toxicity of cancer therapy are three significant challenges in patient management. A common resistance mechanism to chemotherapy observed in preclinical studies is the overexpression of drug efflux proteins (Lum, B. L. et al. (1993) Cancer 72, 3502-3514; Barrand, M. A. et al. (1997) Gen. Pharmacol. 28, 639645; Fidler, I. J. (1999) Cancer Chemother. Pharmacol. 43:S3-S10.). However, at least some clinical studies show that inhibition of the drug efflux proteins does not significantly improve the effectiveness of chemotherapy in patients (Ferry, D. R., et al. (1996) Eur. J. Cancer 32:1070-1081; Broxterman, H. J., et al. (1996) Eur. J. Cancer. 32:10241033), suggesting the existence of other resistance mechanisms. Cancer therapy, such as chemotherapy and radiation, targets proliferating cells and thereby causes undesired toxicity to normal host tissues that undergo continuous renewal, including the hematopoietic cells, cells in the lining of the gastrointestinal tract, and hair follicles. Bone marrow suppression induced by cancer therapy is, at least in part, overcome by the use of hematopoietic growth factors, including erythropoietin, granulocytes colonystimulating factor, and granulocyte-macrophage colony-stimulating factor (Gabrilove, J. L. and Goldie, D. W. (1993) In: Cancer, Principles & Practice of Oncology (eds. DeVita, V. T. et al., J. B. Lippincott Co., Philadelphia). On the other hand, no treatment is available to overcome the gastrointestinal toxicity and alopecia induced by anticancer agents.
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Web site: http://www.delphion.com/details?pn=US06599912__ ·
Methods and compositions for the treatment of chronic lymphocytic leukemia Inventor(s): Nardella; Francis A. (Scottsdale, AZ) Assignee(s): Salmedix, Inc. (San Diego, CA) Patent Number: 6,573,292 Date filed: July 6, 2001 Abstract: Methods for the treatment of Chronic Lymphocytic Leukemia and B-cell and T-cell lymphomas are provided. These methods comprise administering to a patient in need of treatment an effective amount of certain indole and carbazole compounds, such as etodolac. Excerpt(s): The present invention relates to the use of indole derivatives characterized by having a 1,3,4,9-tetrahydropyrano [3,4-b]indole, 1,3,4,9-tetrahydrothiopyrano [3,4b]indole, 1,2,3,4-tetrahydro-4H carbazole or 2,3,4,9-tetrahydro-1H-carbazole nucleus, such as etodolac, in the treatment of chronic lymphocytic leukemia, and B-cell and T-cell lymphomas. Chronic lymphocytic leukemia (CLL) is a heterogeneous group of diseases characterized by different maturation states of the B-cells and T-cells, which are related to the aggressiveness of the disorder. Accordingly, CLL is commonly classified into separate categories, including B-cell chronic lymphocytic leukemia of classical and mixed-types, B-cell and T-cell prolymphocytic leukemia, hairy-cell leukemia and hairycell variant, splenic lymphoma with circulating villous lymphocytes, large granular lymphocytic leukemia, adult T-cell leukemia/lymphoma syndrome and leukemic phases of malignant lymphomas of both B-cell and T-cell types. B-cell chronic lymphocytic leukemia (B-CLL) is characterized by proliferation and accumulation of Blymphocytes that appear morphologically mature but are biologically immature. B-CLL typically occurs in persons over 50 years of age. This disorder accounts for 30% of leukemias in Western countries, with 10,000 new cases being diagnosed annually in the United States alone. The disorder is characterized by proliferation of biologically immature lymphocytes (lymphocytosis), which typically express low levels of surface immunoglobulins, which upon organ infiltration cause lymph-node enlargement and hepato-splenomegaly. In the advanced stages of the disease, bone marrow occupation by the abnormal lymphocytes causes bone marrow failure, resulting in anemia and thrombocytopenia. Web site: http://www.delphion.com/details?pn=US06573292__
Patents 291
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Methods for the detection of HTLV-II antibodies employing novel HTLV-II NRA envelope peptides Inventor(s): Rosenblatt; Joseph D. (Los Angeles, CA), Chen; Irvin S. Y. (Woodland Hills, CA), Guidinger; Peggy (Chicago, IL), Peterson; Bryan (Mundelein, IL), Tate; Cynthia (Chicago, IL), Edwards; Michelle (Kenosha, WI), Motley; Cheryl T. (Waukegan, IL), Lee; Helen H. (Lake Forest, IL), Swanson; Priscilla A. (Libertyville, IL), Robertson; Eugene (Grayslake, IL), Idler; Kenneth B. (Trevor, WI), Stephens; John E. (Gurnee, IL), Chan; Emerson W. (Libertyville, IL), Johnson; Joan E. (Libertyville, IL), Golde; David W. (New York, NY), Buytendorp; Mark H. (Cary, IL) Assignee(s): Abbott Laboratories (Abbott Park, IL) Patent Number: 6,406,841 Date filed: June 20, 1994 Abstract: The present invention relates generally to a novel human T-cell lymphotropic, or leukemia, virus type II (HTLV-II) isolate designated NRA. HTLV-II.sub.NRA was originally isolated from a patient with atypical hairy cell leukemia. Preliminary restriction analysis of this isolate demonstrated that it differs genetically from the prototypical HTLV-II isolate Mo. HTLV-II.sub.NRA proviral molecular clones were obtained and the entire nucleotide sequence of the virus ascertained. The claimed invention is particularly directed toward the gp46 and p21e envelope proteins encoded by the env gene. Methods and kits for the detection of HTLV-II antibodies employing these envelope proteins are also described. Excerpt(s): The present invention relates generally to an isolate of human T-cell lymphotropic virus type II ("HTLV-II") referred to as "NRA." More particularly, the invention relates to compositions derived from the NRA provirus, and to the use of such compositions in assays and kits to detect HTLV infection. Human T-cell lymphotropic virus type I ("HTLV-I") has been established as the etiologic agent of two diseases, adult T-cell leukemia ("ATL") [Poiesz et al., Proc. Natl. Acad. Sci. USA, 77:7415-7419 (1980); Uchiyama et al., Blood, 50:481-492 (1977)] and a neurologic disorder known either as HTLV-associated myelopathy ("HAM") [Tsujimoto et al., Mol. Biol. Med., 5:29-42 (1988)] or tropical spastic paraparesis ("TSP") [Gessain et al., Lancet, II:407-409 (1985)]. Genetic analysis of HTLV-I genomes has been performed. [Ratner et al., AIDS Res. and Human Retroviruses, 7:923-941 (1991); Goodenow et al., J. Acquired Immune Defic. Syndr., 2:344-352 (1989); Gray et al., Virology, 177:391-395 (1990)]. Genetic diversity within the HTLV-I genome has been reported to be associated with the geographical origin of the isolate. [Gessain et al., J. Virol., 66:2288-2295 (1992); Sherman et al., J. Virol, 66:2556-2563 (1992)]. Web site: http://www.delphion.com/details?pn=US06406841__
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Methods of treatment with compounds having RAR.alpha. receptor specific or selective activity Inventor(s): Duong; Tien T. (Irvine, CA), Teng; Min (Aliso Viejo, CA), Chandraratna; Roshantha A. (Mission Viejo, CA) Assignee(s): Allergan, Inc. (Irvine, CA) Patent Number: 6,610,744 Date filed: November 29, 2001
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Abstract: Retinoid compounds which act specifically or selectively on RAR.sub.alpha. receptor subtypes in preference over RAR.sub.beta. and RAR.sub.GAMMA. receptor subtypes, posses desirable pharmaceutical properties associated with retinoids, and are particularly suitable for treatment of tumors, such as acute monocytic leukemia, cervical carcinoma, myeloma, ovarian carcinomas and head and neck carcinomas, without having one or more undesirable side effects of retinoids, such as inducement of weight loss, mucocutaneous toxicity, skin irritation and teratogenecity. Excerpt(s): The present invention relates to the use of compounds which have specific or selective agonist like activity on RAR.sub.alpha. retinoid receptors for treatment of diseases and conditions which respond to treatment by such retinoids. More particularly the present invention is directed to the use of RAR.sub.alpha. receptor specific or selective agents for the treatment of tumors. Compounds which have retinoid-like activity are well known in the art, and are described in numerous United States and other patents and in scientific publications. It is generally known and accepted in the art that retinoid-like activity is useful for treating animals of the mammalian species, including humans, for curing or alleviating the symptoms and conditions of numerous diseases and conditions. In other words, it is generally accepted in the art that pharmaceutical compositions having a retinoid-like compound or compounds as the active ingredient are useful as regulators of cell proliferation and differentiation, and particularly as agents for treating skin-related diseases, including, actinic keratoses, arsenic keratoses, inflammatory and non-inflammatory acne, psoriasis, ichthyoses and other keratinization and hyperproliferative disorders of the skin, eczema, atopic dermatitis, Darriers disease, lichen planus, prevention and reversal of glucocorticoid damage (steroid atrophy), as a topical anti-microbial, as skin anti-pigmentation agents and to treat and reverse the effects of age and photo damage to the skin. Retinoid compounds are also useful for the prevention and treatment of cancerous and precancerous conditions, including, premalignant and malignant hyperproliferative diseases such as cancers of the breast, skin, prostate, cervix, uterus, colon, bladder, esophagus, stomach, lung, larynx, oral cavity, blood and lymphatic system, metaplasias, dysplasias, neoplasias, leukoplakias and papillomas of the mucous membranes and in the treatment of Kaposi's sarcoma. In addition, retinoid compounds can be used as agents to treat diseases of the eye, including, without limitation, proliferative vitreoretinopathy (PVR), retinal detachment, dry eye and other corneopathies, as well as in the treatment and prevention of various cardiovascular diseases, including, without limitation, diseases associated with lipid metabolism such as dyslipidemias, prevention of post-angioplasty restenosis and as an agent to increase the level of circulating tissue plasminogen activator (TPA). Other uses for retinoid compounds include the prevention and treatment of conditions and diseases associated with human papilloma virus (HPV), including warts and genital warts, various inflammatory diseases such as pulmonary fibrosis, ileitis, colitis and Krohn's disease, neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and stroke, improper pituitary function, including insufficient production of growth hormone, modulation of apoptosis, including both the induction of apoptosis and inhibition of T-cell activated apoptosis, restoration of hair growth, including combination therapies with the present compounds and other agents such as Minoxidil.sup.R, diseases associated with the immune system, including use of the present compounds as immunosuppressants and immunostimulants, modulation of organ transplant rejection and facilitation of wound healing, including modulation of chelosis. U.S. Pat. No. 4,740,519 (Shroot et al.), U.S. Pat. No. 4,826,969 (Maignan et al.), U.S. Pat. No. 4,326,055 (Loeliger et al.), U.S. Pat. No. 5,130,335 (Chandraratna et al.), U.S. Pat. No. 5,037,825 (Klaus et al.), U.S. Pat. No. 5,231,113 (Chandraratna et al.), U.S. Pat. No. 5,324,840 (Chandraratna), U.S. Pat. No.
Patents 293
5,344,959 (Chandraratna), U.S. Pat. No. 5,130,335 (Chandraratna et al.), Published European Patent Application Nos. 0 170 105 (Shudo), 0 176 034 A (Wuest et al.), 0 350 846 A (Klaus et al.), 0 176 032 A (Frickel et al.), 0 176 033 A (Frickel et al.), 0 253 302 A (Klaus et al.), 0 303 915 A (Bryce et al.), UK Patent Application GB 2190378 A (Klaus et al.), German Patent Application Nos. DE 3715955 A1 (Klaus et al.), DE 3602473 A1 (Wuest et al., and the articles J. Amer. Acad. Derm. 15: 756-764 (1986) (Sporn et al.), Chem. Pharm. Bull. 33: 404-407 (1985) (Shudo et al.), J. Med Chem. 1988 31, 2182-2192 (Kagechika et al.), Chemistry and Biology of Synthetic Retinoids CRC Press Inc. 1990 p 334-335, 354 (Dawson et al.), describe or relate to compounds which include a tetrahydronaphthyl moiety and have retinoid-like or related biological activity. Web site: http://www.delphion.com/details?pn=US06610744__ ·
Monoclonal antibodies for detection of friend murine leukemia virus Inventor(s): Robertson; Michael N. (Hamilton, MT), Chesebro; Bruce (Corvalis, MT), Miyazawa; Masaaki (Sendai, JP), Britt; William J. (Birmingham, AL) Assignee(s): The United States of America as represented by the Department of Health and (Washington, DC) Patent Number: 6,403,300 Date filed: May 2, 1991 Abstract: The present invention relates to Friend murine leukemia virus (F-MuLV) specific monoclonal antibodies, or binding fragments thereof, specific for an antigenic determinant of a gp85 envelope precursor protein characteristic of a methanol-fixed FMuLV infected cell. The invention also relates to hybridomas resulting from the fusion of myeloma cells and spleen cells, which hybridomas produce a Friend murine leukemia virus (F-MuLV) specific monoclonal antibody specific for an antigenic determinant of a gp85 envelope precursor protein characteristic of a methanol-fixed F-MuLV infected cell. The invention further relates to kits containing the above-described monoclonal antibodies. Excerpt(s): The present invention relates, in general, to monoclonal antibodies. In particular, the present invention relates to monoclonal antibodies that recognize Friend murine leukemia virus. Several monoclonal antibodies which react with the Friend murine leukemia virus (F-MuLV) and related retroviruses have been produced (CHESEBRO, B. et al. (1983a) Virology 127, 134-148). These antibodies have been used to titrate and distinguish a mixture of ecotropic F-MuLV and dual-tropic Friend mink cell focus-inducing (MCF) viruses in a focal infectivity assay (FIA) using indirect membrane immunofluorescence to detect foci of infected live cells (SITBON, M. et al. (1985) Virology 141, 110-118). However, with immunofluorescence microscopy it has often been difficult to find low power (10.times.) objectives with sufficient light gathering capacity to facilitate visualization of foci. Higher magnifications can be used, but this greatly increases the labor of scanning culture wells to count foci of viral infection. These problems can be overcome by using immunoperoxidase, rather than immunofluorescence in the detection of foci, but in this situation it is desirable to carry out tests on methanol-fixed cells both to eliminate endogenous peroxidase and to allow detection of antigens in the cytoplasm of infected cells. Furthermore, the use of fixed cells aids greatly in the convenience of performing assays since multiple assays can be prepared and stored for processing at a later time. However, monoclonal antibodies generated against protein antigens in their native state frequently will not recognize the viral antigens after fixation. The present invention provides monoclonal antibodies
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selected specifically for reactivity with methanol-fixed viral antigens. These monoclonal antibodies were shown to be highly effective in titration of virus by a focal infectivity assay using an indirect immunoperoxidase detection system. In addition, one of these antibodies was found to be very useful in immunohistochemical detection of viral antigen by light microscopy and immunoelectronmicroscopy. Web site: http://www.delphion.com/details?pn=US06403300__ ·
Monocyclic-7H-pyrrolo[2,3-d]pyrimidine compounds, compositions, and methods of use Inventor(s): Changelian; Paul S. (E. Greenwich, CT), Brown; Matthew F. (Pawcatuck, CT), Flanagan; Mark E. (Gales Ferry, CT), Blumenkopf; Todd A. (Old Lyme, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,635,762 Date filed: June 17, 1999 Abstract: Novel pyrrolo[2,3-d]pyrimidine compounds useful as inhibitors of the enzyme protein tyrosine kinases such as Janus Kinase 3 as well as immunosuppressive agents for organ transplants, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis, Type I diabetes and complications from diabetes, cancer, asthma, atopic dermatitis, autoimmune thyroid disorders, ulcerative colitis, Crohn's disease, Alzheimer's disease, Leukemia and other autoimmune diseases are described. Excerpt(s): The present invention relates to pyrrolo[2,3-d]pyrimidine compounds which are inhibitors of protein tyrosine kinases, such as the enzyme Janus Kinase 3 (hereinafter also referred to as JAK3) and as such are useful therapy as immunosuppressive agents for organ transplants, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis, Type I diabetes and complications from diabetes, cancer, asthma, atopic dermatitis, autoimmune thyroid disorders, ulcerative colitis, Crohn's disease, Alzheimer's disease, Leukemia and other indications where immunosuppression would be desirable. This invention also relates to a method of using such compounds in the treatment of the above indications in mammals, especially humans, and the pharmaceutical compositions useful therefor. with the proviso that the groups of formulas IV, V, VI or XIII do not contain two or more oxygens, sulfurs or combinations thereof in adjacent positions. Web site: http://www.delphion.com/details?pn=US06635762__
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Myeloid cell leukemia associated gene MCL-1 Inventor(s): Craig; Ruth W. (Hanover, NH) Assignee(s): Dartmouth College (Hanover, NH) Patent Number: 6,528,263 Date filed: October 12, 2000 Abstract: A gene, mc1-1, of the bc1-2 family is disclosed along with its nucleotide and amino acid sequence. Also disclosed are diagnostic and therapeutic methods of utilizing the mc1-1 nucleotide and polypeptide sequences.
Patents 295
Excerpt(s): The present invention relates generally to unique proto-oncogene polypeptides and specifically to a novel polypeptide of the bcl-2 family and its nucleic acid sequence. Advances in recombinant DNA technology have led to the discovery of normal cellular genes (proto-oncogenes and tumor suppressor genes, and apoptosis/cell death-related genes) which control growth, development, and differentiation. Under certain circumstances, regulation of these genes is altered and normal cells assume neoplastic growth behavior. In some cases, the normal cell phenotype can be restored by various manipulations associated with these genes. There are over 40 known protooncogenes and suppressor genes to date, which fall into various categories depending on their functional characteristics. These include, 1) growth factors and growth factor receptors, 2) messengers of intracellular signal transduction pathways, for example, between the cytoplasm and the nucleus, and 3) regulatory proteins influencing gene expression and DNA replication. Qualitative changes in the structure of protooncogenes or their products and quantitative changes in their expression have been documented for several cancers. With chronic myelogenous leukemia, for example, the abl oncogene is translocated to chromosome 22 in the vicinity of the bcr gene. A cancer specific fusion protein, qualitatively different from parent cell proteins, is produced and is an ideal cancer marker. Mutant ras genes have been implicated in the earliest stages of human leukemias and colon cancers. The detection of these mutations in defined premalignant states could provide valuable prognostic information for clinicians. Web site: http://www.delphion.com/details?pn=US06528263__ ·
Non-myeloablative/lymphoablative conditioning regimen to induce patient antidonor unresponsiveness in stem cell transplantation Inventor(s): Slavin; Shimon (Jerusalem, IL) Assignee(s): Hadash Medical Research Services and Development Ltd. (Jerusalem, IL), Baxter International Inc. (Deerfield, IL) Patent Number: 6,544,787 Date filed: November 14, 1997 Abstract: Serious hematologic malignancies are treated through high dose or lethal chemotherapy and/or radiation therapy conditioning regimens followed by rescue with allogeneic stem cell transplantation (allo-SCT) or autologous stem cell transplantation (ASCT). These myeloablative/lymphoablative (M/L) treatment regimens involve the elimination of both the patient's hematopoietic stem cells and T-lymphocytes, often leading to serious complications including graft versus host disease (GVHD). The claimed invention addresses some of these problems by providing a conditioning regimen that is designed to eliminate the patient's T-lymphocytes while retaining a functional population of hematopoietic stem cells (HSC). This nonmyeloablative/lymphoablative (-/L) conditioning regimen involves the administration of one or more agents such as purine analogs (e.g., fludarabine), alkylating agents (e.g., bisulfan, cyclophosphamide), or anti-leukocyte globulins (e.g., anti-T lymphocyte globulin). After this, a donor-derived allogeneic stem cell preparation is administered to the patient. Patients treated according to the claimed invention develop donor-specific unresponsiveness and relatively fewer complications as compared to standard M/L conditioning regimens. The claimed methodologies should prove useful in the treatment of a number of hematologic malignancies such as chronic myelogenous leukemia, acute myelogenous leukemia, acute lymphoblastic leukemia, and non-Hodgkin's lymphoma.
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Excerpt(s): High dose or lethal conditioning regimens using chemotherapy and/or radiation therapy followed by rescue with allogeneic stem cell transplantation (alloSCT) or autologous stem cell transplantation (ASCT) have been the treatments of choice for patients with a variety of hematologic malignancies and chemosensitive solid tumors resistant to conventional doses of chemotherapy. A common source of stem cells for such procedures has been the bone marrow. Recently, peripheral blood stem cells (PBSC) have also been used. As such, the terms "allogeneic bone marrow transplantation" (allo-BMT) and "autologous bone marrow transplantation" (ABMT) are widely used in the literature to refer to particular types of allo-SCT and ASCT, respectively, whether the rescue is with bone marrow or PBSC. Current procedures typically employ allo-SCT or ASCT after myeloablative/lymphoablative (M/L) conditioning. As the name implies, M/L conditioning involves elimination, through cell killing, blocking, and/or down-regulation, of substantially all the hematopoietic stem cells and lymphocytes of the patient. Patients treated by allo-SCT or ASCT can develop major complications due to the M/L conditioning. In addition, patients receiving alloSCT are susceptible to graft versus host disease (GVHD), as well as to graft rejection. Moreover, relapse is still a frequent problem in these patients. Several attempts to improve disease-free survival by increasing the intensity of the M/L conditioning have failed due to unacceptable toxicity. Furthermore, increasing the intensity of the M/L conditioning does not appear to improve the outcome by decreasing the rate of relapse. A wide variety of protocols of varying intensities have been used among greater than 30,000 transplants worldwide reported to the International Bone Marrow Transplant Registry. Despite these numerous attempts to vary the intensity of the conditioning regimens, there have not been any documented significant differences in the over-all patient outcomes. Web site: http://www.delphion.com/details?pn=US06544787__ ·
Oral formulation of methylglyoxal and its imino acid conjugates for human use Inventor(s): Khattar; Dhiraj (Ghaziabad, IN), Burman; Anand C. (Regents Park, GB), Mukherjee; Rama (Gurgaon, IN), Kumar; Mukesh (Delhi, IN) Assignee(s): Dabur Research Foundation (Ghaziabad, IN) Patent Number: 6,596,755 Date filed: July 1, 2002 Abstract: The invention relates to an oral formulation of methylglyoxal and/or its imino acid conjugates for human use and methods for preparing the compositions. Particularly, the invention relates to compositions comprising methylglyoxal and more particularly, imino acid conjugates of methylglyoxal. The present invention also relates to formulations of methylglyoxal and imino acid conjugates of methylglyoxal that can be used for the treatment and suppression of malignant diseases including but not limited to the cancers of Colon, Prostate, Pancreas, Lung, Oral cavity, Glioblastoma, and Leukemia. Excerpt(s): The invention relates to an oral formulation of methylglyoxal and/or its imino acid conjugates for human use and methods for preparing the compositions. Particularly, the invention relates to compositions comprising methylglyoxal and more particularly, imino acid conjugates of methylglyoxal. The present invention also relates to formulations of methylglyoxal and imino acid conjugates of methylglyoxal that can be used for the treatment and suppression of malignant diseases including but not limited to the cancers of Colon, Prostate, Pancreas, Lung, Oral cavity, Glioblastoma, and
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Leukemia. Methylglyoxal is a normal cellular metabolite with potential anticancer properties. Szent-Gyorgyi and his collaborators in their pioneering work on the biological role of methylglyoxal had put forward strong evidences of in vitro inhibitory effect of methylglyoxal on Sarcoma-180 cells [2]. Egyud and Szent-Gyorgyi showed that when methylglyoxal was injected into mice along with sarcoma 180 cells, no tumor developed and mice remained completely healthy [3]. Apple and Greenberg similarly demonstrated that methylglyoxal significantly inhibited sarcoma tumor growth [4,5]. Web site: http://www.delphion.com/details?pn=US06596755__ ·
Proteins suppressing proliferation of lympho-hematopoietic cells Inventor(s): Kincade; Paul W. (Oklahoma City, OK), Tomiyama; Yoshiaki (Hyogo, JP), Oritani; Kenji (Osaka, JP), Matsuzawa; Yuji (Hyogo, JP) Assignee(s): Center for Advanced Science and Technology Incubation, Ltd. (Chiyoda, JP), Oklahoma Medical Research Foundation (Oklahoma, OK) Patent Number: 6,518,043 Date filed: March 13, 2000 Abstract: A novel protein having the activity to suppress proliferation of lymphohematopoietic cells derived from BNS2.4 cells, its gene, a method for preparing them and their uses are provided. The novel protein has been identified from a stromal cell line BMS2.4 by expression cloning targeting mouse myelomonocytic leukemia cell line WEHI3. This protein and its gene are useful for treating lympho-hematopoietic disorders. Excerpt(s): This application claims benefit of foreign priority from Japan application 11/107246, filed Apr. 14, 1999. The present invention relates to a novel polypeptide derived from BMS2.4 cells, a gene thereof, a method for preparing the polypeptide and the gene, and uses thereof. Production of blood cells is strictly regulated by various stromal elements including adhesion molecules, extracellular matrix, and cytokines. Complex interactions between stromal and hematopoietic cells are essential for the movement of hematopoietic stem/progenitor cells within or from bone marrow, for the control of production of blood cells, and for the elimination of defective and harmful cells. Web site: http://www.delphion.com/details?pn=US06518043__
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Purging leukemia cells from hematopoietic stem cells Inventor(s): Schwarzenberger; Paul (New Orleans, LA), Kolls; Jay (New Orleans, LA) Assignee(s): Board of Supervisors of Louisiana State University and Agricultural and (Baton Rouge, LA) Patent Number: 6,461,869 Date filed: July 20, 1999 Abstract: A gene therapy system is disclosed that selectively kills leukemia cells in bone marrow, while leaving stem cells unaffected. All cells in a mixture of stem cells and leukemia cells are transfected with a high efficiency gene transfer vector. The vector carries a eukaryotic expression construct encoding a toxin gene. This toxin gene is expressed only in leukemia cells, not in stem cells. Differential expression of the toxin
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gene in leukemia cells and stem cells may be achieved by placing the coding sequence under the control of an appropriate promoter, such as the RSV promoter or the SV40 promoter. High gene expression has been demonstrated in a panel of transformed leukemia cell lines, but no gene expression in transformed, CD34-selected, primary human stem cells. The treatment will be useful not only for leukemia patients, but also for other cancer patients undergoing autologous bone marrow transplants (e.g., breast or lymphoma cancers). Excerpt(s): This invention pertains to a method and composition for purging leukemia cells from hematopoietic stem cells. For many leukemia patients, the only hope for cure or long term survival is a bone marrow transplant from a donor. The cells for these "allogeneic" transplants are generally obtained from a sibling or from an unrelated, HLA-matched donor. However only a small fraction of potential patients receive such transplants due to constraints such as advanced age or the lack of a matching donor. Therefore, "autologous" marrow transplants are also used at times, the re-infusion of cells from the patient's own bone marrow following chemotherapy or radiation therapy that otherwise destroys the patient's marrow. Bone marrow is taken from a patient prior to high dose chemotherapy or radiation therapy, and is later reinfused to "rescue" the patient following the otherwise lethal therapy. However, there is currently no effective procedure to completely remove contaminating leukemia cells from bone marrow or other stem cell preparations. On the one hand, an autologous transplant does not carry the risk of short- or long-term graft-versus-host-disease, since the patient receives back his or her own bone marrow. However, a major drawback of existing autologous techniques is the lack of an effective way to remove all contaminating cancer cells from the bone marrow ex vivo. Relapses frequently result from such contaminating cancer cells. In principle, autologous transplants should be superior to allogeneic transplants if a method could be found to completely purge the transplanted cells of contaminating leukemia cells, because the risk of host-versus-graft disease would be eliminated. Progress has been made in reducing relapse rates in autologous transplants. Various purging procedures have been used to selectively remove leukemia cells from bone marrow, such as ex vivo chemotherapy with 4-hydrocyclophosphamide, or fractionation of cells by size. The combination of these two techniques, ex vivo chemotherapy with fractionation of cells by size, would probably be considered the current state-of-the art purging procedure by most researchers. However, this combination therapy often does not completely purge leukemic cells from the transplanted material. Web site: http://www.delphion.com/details?pn=US06461869__ ·
Recombinant DNA encoding a reverse transcriptase derived from moloney murine leukemia virus Inventor(s): Sorensen; Matthew (Irvine, CA), Riggs; Michael G. (San Diego, CA) Assignee(s): Gen-Probe Incorporated (San Diego, CA) Patent Number: 6,593,120 Date filed: September 15, 1999 Abstract: A recombinant plasmid for expression of Moloney Murine Leukemia Virus (MMLV)-derived reverse transcriptase in E. coli cells deficient in the expression of RNAse activity, a method for purification of the recombinant enzyme, and a purified recombinant reverse transcriptase for suitable use in cDNA and nucleic acid amplification procedures are disclosed.
Patents 299
Excerpt(s): The invention relates to recombinant proteins, particularly to viral reverse transcriptase enzymes produced by recombinant DNA technology, and specifically relates to reverse transcriptase derived from Moloney Murine Leukemia virus (MMLV) that is expressed from recombinant DNA in a bacterial host cell and that includes multiple histidine residues. Retroviruses are a group of viruses whose genetic material consists of single-stranded RNA. Following adsorption and entry of retroviral RNA into the host cell, the viral RNA is used as a template for synthesis of a complementary DNA (cDNA) strand. The cDNA is then made double-stranded through the action of an enzyme having DNA polymerase activity; this double-stranded DNA integrates into the host genome. The RNA-directed DNA polymerase activity responsible for the synthesis of cDNA from the viral RNA template is commonly called reverse transcriptase ("RT"). A number of retroviruses have been implicated as the causative agents of various cancers, and other diseases. A retrovirus, human immunodeficiency virus-1 (HIV-1), is the causal agent of acquired immunodeficiency syndrome (AIDS). Also, reverse transcriptase enzymes have become important reagents in molecular biology because of their ability to make cDNA from almost any RNA template. Reverse transcriptase is commonly used to make nucleic acids for hybridization probes and to convert singlestranded RNA into a double-stranded DNA for subsequent cloning and expression. Web site: http://www.delphion.com/details?pn=US06593120__ ·
Therapeutic compounds Inventor(s): Uckun; Fatih M. (White Bear Lake, MN), Sudbeck; Elise A. (St. Paul, MN), Liu; Xing-Ping (Minneapolis, MN), Cetkovic; Marina (Maplewood, MN), Malaviya; Ravi (Shoreview, MN) Assignee(s): Parker Hughes Institute (St. Paul, MN) Patent Number: 6,469,013 Date filed: May 16, 2001 Abstract: The invention provides novel JAK-3 inhibitors that are useful for treating leukemia and lymphoma. The compounds are also useful to treat or prevent skin cancer, as well as sunburn and UVB-induced skin inflammation. In addition, the compounds of the present invention prevent the immunosuppressive effects of UVB radiation, and are useful to treat or prevent autoimmune diseases, inflammation, and transplant rejection. The invention also provides pharmaceutical compositions comprising compounds of the invention, as well as therapeutic methods for their use. Excerpt(s): Signal Transducers and Activators of Transcription (STATS) are a family of DNA binding proteins reside in the cytoplasm until they are activated by tyrosine phosphorylation. This phosphorylation event is catalyzed by members of the Janus family of tyrosine kinases, including JAK-3 (Ihle, J. N. Adv. Immunol. 60; 1 -35, 1995; Witthuhn, B. A., et. al., Leukemia and Lymphoma. 32: 289-297, 1999). The dual role of STATs as signaling molecules and transcription factors is reflected in their structure. All STATT proteins contains a DNA binding domain, an SH2 domain, and a transactivation domain necessaru for transcriptional induction. In unstimulated cells, latent forms of STATs are predominatantly localized in the cytoplasm. Ligan binding induces STAT proteins to bind with their SH2 domains to the tyrosine phosphorylated motifs in the intracellular domains of various transmembrane cell surface receptors (Horvath, C.M. and Darnell, J.E., Curr. Opin. Cell. Biol. 9(2):233-239., 1997; Levy, D.E. Cytokine Growth Factor Rev. 8(1): 81-90, 1997). Thus, JAK-3 is an important enzyme that plays an essential role in the function of lymphocytes, macrophages, and mast cells. Compounds which
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inhibit JAK-3 would be expected to be useful for treating or preventing diseases or conditions wherein the function of lymphocytes, macrophages, or mast cells is implicated, such as, leukemia, lymphoma, transplant rejection (e.g. pancreas islet transplant rejection, bone marrow transplant applications (e.g. graft-versus-host disease), autoimmune diseases (e.g. diabetes), and inflammation (e.g. asthma, inflammation associated with sun burn, and skin cancer). A continuing need exists for compounds and methods that are useful for the treatment and/or prevention of such conditions and diseases. Web site: http://www.delphion.com/details?pn=US06469013__ ·
Transcription factor, BP1 Inventor(s): Berg; Patricia E. (Accokeek, MD) Assignee(s): George Washington University (Washington, DC) Patent Number: 6,416,956 Date filed: August 11, 2000 Abstract: An isolated DNA of SEQ ID NO: 1 is provided that encodes the transcription factor BP1, which is believed to be a repressor of the.beta.-globin gene. A host cell that is transformed with a vector that contains the DNA may be used to produce BP1. Vectors having a controllable promoter operably connected to the BP1 open reading frame may be used to transform.beta.-globin producing cells of patients with sickle cell anemia, thereby providing a treatment. Because BP1 is overexpressed in leukemia and breast cancer cells, acute myeloid leukemia, acute lymphocytic leukemia, and breast cancer can be screened for and diagnosed by determining whether BP1 is overexpressed in cell samples of patients who may have these conditions. An antisense DNA or RNA to the DNA encoding BP1 may be used as a treatment for acute myeloid leukemia, acute lymphocytic leukemia, and breast cancer. Excerpt(s): The present invention relates to a DNA that encodes the transcription factor BP1, a vector containing the DNA and a host cell containing the DNA. The invention also relates to an antisense DNA or RNA to the DNA encoding BP1, methods for treating sickle cell anemia by administering an effective amount of BP1, and methods for screening for acute myeloid leukemia, acute lymphocytic leukemia, and breast cancer. Expression of globin genes in the.beta.-globin cluster is restricted to erythropoietic cells, with five different genes expressed during embryonic (.epsilon.), fetal (G.gamma. and A.gamma.) and adult (.delta. and.beta.) development. Transcriptional activation of globin genes occurs not only by binding of transcriptional activator proteins to the promoter of the gene being activated, but also by a regulatory element located 6-18 kb upstream of the.beta.-globin cluster, the Locus Control Region (LCR) (See, for example, Berg, P. E. and A. N. Schechter. 1992. Molecular genetics of disorders of hemoglobin. In T. Friedmann (ed), Molecular Genetic Medicine. Academic Press, San Diego.; Forrester, W. C., C. Thompson, J. T. Elder, and Groudine, M. 1986. A developmentally stable chromatin structure in the human.beta.-globin gene cluster. Proc. Natl. Acad. Sci. USA 83: 1359-1363.; and Tuan, D., W. Soloman, Q. Li, and I. M. London. 1985. The ".beta.-likeglobin" gene domain in human erythroid cells. Proc. Natl. Acad. Sci. USA 82: 63846388.). Sequential activation of the.beta.-globin cluster genes during ontogeny must be countered by repression of the globin genes inactive during a given developmental stage. Repression is caused by binding of repressor proteins to promoter/upstream DNA and, in the case of the adult.beta.-globin gene, is probably also due to lack of activation by the LCR (see, for example, Crossley, M. and S. H. Orkin. 1993. Regulation
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of the.beta.-globin locus. Curr. Opinion Gen. Dev. 3: 232-237.). While much is known about transcriptional activators that bind to DNA sequences near the.beta.-globin gene, little is known about the proteins that repress its transcription. As discussed below, BP1 is shown to bind to two silencer DNA sequences upstream of the.beta.-globin gene and therefore, there is strong evidence suggesting that BP1 protein is a repressor of the.beta.globin gene. The present invention provides for a DNA sequence that encodes BP1, and methods of using information derived from knowledge of the DNA sequence to screen for conditions such as breast cancer, acute myeloid leukemia and acute lymphocytic leukemia. The DNA sequence was found to be closely related to two other human genes, DLX4 and DLX7, described in Quinn, L. M., B. V. Johnson, J. Nicholl, G. R. Sutherland, and B. Kalionis. 1997. Isolation and identification of homeobox genes from human placenta including a novel member of the Distal-less family, DLX4. Gene 187: 5561 and Nakamura S, Stock DW, Wydner KL, Bollekens JA, Takeshita K, Nagai BM, Chiba , Kitamura T, Freeland TM, Zhao Z, Minowada J, Lawrence JB, Weiss KB, and Ruddle FH. Genomic analysis of a new mammalian Distal-less gene: D1x-7. Genomics 1996; 38: 314-324. Web site: http://www.delphion.com/details?pn=US06416956__ ·
Use of etodolac for the treatment of chronic lymphocytic leukemia Inventor(s): Adachi; Soichi (La Jolla, CA), Leoni; Lorenzo M. (San Diego, CA), Cottam; Howard B. (Escondido, CA), Carson; Dennis A. (Del Mar, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,545,034 Date filed: July 23, 1999 Abstract: A method of treating cancer is provided comprising administering an amount of etodolac to a subject afflicted with cancer that is effective to reduce the viability and/or to sensitize the cancer to an anti-cancer agent. Excerpt(s): Chronic lymphocytic leukemia (CLL) is the most common leukemia in the United States. CLL involves the cancerous proliferation of lymphocytes. It is most common among older adults; 90 percent of the cases are in people more than 50 years old. It occurs 1-3 times more often among men than among women. The onset of CLL tends to be insidious, with symptoms developing gradually. Because it involves an overproduction of mature, functional lymphocytes, persons with this disorder may survive for years. In contrast, in some, the disorder proceeds very rapidly, and requires immediate treatment. Currently, the adenine deoxynucleosides fludarabine (fludara) and 2-chlorodeoxyadenosine (2CdA) are the drugs of choice to treat the disease. However, clinical remissions are seldom induced, and patients eventually succumb from their leukemia. The number of nonsteroidal anti-inflammatory drugs (NSAIDs) has increased to the point where they warrant separate classification. In addition to aspirin, the NSAIDs available in the U.S. include meclofenamate sodium, oxyphenbutazone, phenylbutazone, indomethacin, piroxicam, sulindac and tolmetin for the treatment of arthritis; mefenamic acid and zomepirac for analgesia; and ibuprofen, fenoprofen and naproxen for both analgesia and arthritis. Ibuprofen, mefenamic acid and naproxen are used also for the management of dysmenorrhea. The clinical usefulness of NSAIDs is restricted by a number of adverse effects. Phenylbutazone has been implicated in hepatic necrosis and granulomatous hepatitis; and sulindac, indomethacin, ibuprofen and naproxen with hepatitis and cholestatic hepatitis. Transient increases in serum aminotransferases, especially alanine aminotransferase,
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have been reported. All of these drugs, including aspirin, inhibit cyclooxygenase, that in turn inhibits synthesis of prostaglandins, which help regulate glomerular filtration and renal sodium and water excretion. Thus, the NSAIDs can cause fluid retention and decrease sodium excretion, followed by hyperkalemia, oliguria and anuria. Moreover, all of these drugs can cause peptic ulceration. See, Remington's Pharmaceutical Sciences, Mack Pub. Co., Easton, Pa. (18th ed., 1990) at pages 1115-1122. Web site: http://www.delphion.com/details?pn=US06545034__ ·
UVC radiation therapy for chronic lymphocytic leukemia Inventor(s): Larcom; Lyndon L. (Clemson, SC), Smith; Samuel (Greenville, SC), Tuck; Amy (Piedmont, SC) Assignee(s): Clemson University (Clemson, SC) Patent Number: 6,585,676 Date filed: June 12, 2001 Abstract: Lymphocytes from chronic lymphocytic leukemia (CLL) patients have been found to be readily killed by ultra-violet light-C (UVC) radiation. Cells from healthy donors were minimally affected by doses of UVC 10 times higher than those which caused dramatic drops in the metabolism of CLL cells and eventual death.Irradiated cells from CLL patients and from healthy individuals all demonstrated a number of single strand DNA breaks and alkali-labile sites compared to unirradiated control cells. The extent of DNA damage to both healthy and CLL cells is dose dependent. However, the CLL cells demonstrated more extensive DNA fragmentation and an inability to undergo self-repair. The heightened sensitivity to UVC radiation of lymphocytes from CLL patients is used to provide an excorporeal treatment of CLL lymphocytes followed by the re-introduction of the treated lymphocytes to the patient. Excerpt(s): This invention is directed towards a therapeutic treatment for chronic lymphocytic leukemia. The lymphocytes from CLL patients have been found to be sensitive to ultraviolet radiation in the UVC range. It has been found possible to provide a UVC radiation exposure which will kill CLL cells without any measurable adverse effects on healthy lymphocytes taken from non-leukemia control patients. A treatment therapy in which a CLL patient's blood is treated extracorporeally with UVC radiation is provided which takes advantage of the CLL lymphocyte's sensitivity to UVC radiation. Chronic lymphocytic leukemia (CLL) is a hematological malignancy characterized by the clonal expansion of naive B-lymphocytes mainly in GO phase of the cell cycle. CLL results in the accumulation of mature immunologically defective lymphocytes in the GO phase. The disease is further characterized by the accumulation of B-lymphocytes in bone marrow, lymph nodes, spleen, and liver. In CLL patients, both the B and T cells are ineffective in their response to antigens and are associated with hypogammaglobulinemia and susceptibility to infectious diseases. The end stages of the disease results in the failure of production of myeloid and erythroid marrow elements as well as the presence of lymphoid masses. It is currently believed that the defective lymphocytes in CLL patients are produced at a normal rate as in healthy individuals, but fail to undergo appropriate apoptosis. Currently, existing therapies and treatment protocols for advanced clinical stages have met with only partial success. Traditional drug treatments have involved combinations of chlorambucil (an alkylating agent) and prednisone (corticoid steroid). More recently, the purine analog fludarabine has been shown to have positive effects on new and pre-treated CLL patients. However, such
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drug treatments pose undesirable side effect for some patients. Further, some patients develop resistance to a particular drug. Web site: http://www.delphion.com/details?pn=US06585676__
Patent Applications on Leukemia As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to leukemia: ·
Activated iododerivatives for the treatment of cancer and aids Inventor(s): Foster, Robert T.; (Edmonton, CA), Naicker, Selvaraj; (Edmonton, CA), Yatscoff, Randall W.; (Edmonton, CA) Correspondence: Mary Ann Dillahunty; BURNS, DOANE, SWECKER & MATHIS, L.L.P.; P.O. Box 1404; Alexandria; VA; 22313-1404; US Patent Application Number: 20030187015 Date filed: November 25, 2002 Abstract: A series of activated iodo-benzamide derivatives are described as antineoplastic and antiviral drug compounds. The compounds generally possess a chelating group, a thiol trapping group and an activating group. The presumptive mechanism of action in preventing cancer cell and virus replication is through inhibition of the binding of transcription factors to zinc finger binding domains. The compounds are effective in inhibiting growth of a variety of human and animal tumor and leukemia cell lines at low concentrations. Excerpt(s): This application was filed as PCT/IB98/00768 on Apr. 10, 1998 which is a continuation-in-part of U.S. provisional application No. 60/043,360, which are relied upon and incorporated by reference. This invention is related to synthesis of activated iodo derivatives and their use as antineoplastic and antiviral agents by targeting the zinc finger regions of metalloregulatory proteins such as p-ADPRT and nucleocapsid of HIV. A series of activated iodo-benzamide derivatives are described as antineoplastic and antiviral drug compounds. The compounds generally possess a chelating group, a thiol trapping group and an activating group. The presumptive mechanism of action in preventing cancer cell and virus replication is through inhibition of the binding of transcription factors to zinc finger binding domains. The compounds are effective in inhibiting growth of a variety of human and animal tumor and leukemia cell lines at low doses. In the past several years, a series of discoveries revealed that several proteins contain metal ions, particularly zinc ions (Zn.sup.2+), that play fundamental roles in stabilizing specific protein conformations (Berg, J. M., J. Biol. Chem., 265: 6513-6516, 1990; Berg, J. M., In Progress in Inorganic chemistry, 37: 143-190, 1989). Many of these metalloproteins are involved in nucleic acid binding and in gene regulation (Bravo, R., Cell Growth and Differentiation, 1: 305-309, 1990; Evans; R. M., and Hollenberg, S. M., Cell, 52; 1-3, 1988). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
10
This has been a common practice outside the United States prior to December 2000.
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Anti-CD80 antibody having ADCC activity for ADCC mediated killing of B cell lymphoma cells alone or in combination with other therapies Inventor(s): Hanna, Nabil; (Rancho Santa Fe, CA), Hariharan, Kandasamy; (San Diego, CA) Correspondence: Pillsbury Winthrop LLP; Intellectual Property Group; P.O. Box 10500; McLean; VA; 22102; US Patent Application Number: 20030180290 Date filed: November 12, 2002 Abstract: Methods for treating B cell malignancies, in particular B cell leukemia and lymphoma, using an anti-CD80 antibody alone or in combination with an anti-CD20 antibody or chemotherapy is provided. These methods result in a synergistic anti-tumor response. Excerpt(s): This application claims priority to provisional application U.S. Serial No. 60/331,187 filed Nov. 9, 2001 which is incorporated by reference in its entirety herein. Additionally, this application is a continuation-in-part of U.S. Ser. No. 09/758,173 filed Jan. 12, 2001 which is a divisional of U.S. Ser. No. 09/383,916 filed Aug. 26, 1999 which is a divisional of U.S. Ser. No. 08/487,950 filed Jun. 7, 1995, now U.S. Pat. No. 6,113,898 all of which are incorporated by reference in their entirety herein. The present invention relates to the discovery that a PRIMATIZED.RTM. IgG.sub.1 antibody that shows specificity to the human CD80 molecule and which is referred to by the subject assignee, IDEC Pharmaceuticals Corporation, as IDEC-114 possesses antibody dependent cellular cytotoxicty (ADCC) against CD80 positive cells, especially CD80 positive cells of B cell lineage, and more particularly B cell lymphoma cells. (The sequence of this PRIMATIZED.RTM. antibody is disclosed in U.S. Pat. No. 6,113,898 which is incorporated by reference in its entirety herein). (This primatized antibody is referred to as 16C10 therein). The present invention also relates to the discovery that the use of IDEC-114 in combination with Rituxan.RTM., a chimeric anti-CD20 antibody approved by the FDA for treatment of non-Hodgkin's lymphoma, and/or chemotherapy yields a synergistic anti-tumor response against B cell lymphoma in vivo. IDEC-114 or 16C10 as it is referred to in an earlier patent and applications by the inventors is a PRIMATIZED.RTM. anti-CD80 IgG.sub.1 lambda monoclonal antibody (mAb) containing human constant regions and primate (cynomolgus macaque) variable regions. This antibody binds specifically to human CD80 (B7.1), which is membraneassociated 60 KDa glycoprotein expressed an activated B cells, activated antigen presenting cells, and activated T cells. (Freeman et al., J. Immunol. 1043:2714-22 (1989); Razi-Wolf et al., Proc. Natl Acad. Sci., USA 89:4210-4 (1992); and Azuma et al., J. Exp. Med. 177:845-50 (1993)) As noted above, the DNA and amino acid sequences that contain the variable heavy and light regions of IDEC-114 are disclosed in U.S. Pat. No. 6,113,898, which are identified therein as the 16C10 and heavy and light variable sequences, and which patent is incorporated by reference in its entirety herein. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Anti-HLA-DR antibodies and the methods of using thereof Inventor(s): Green, Jennifer McPhate; (Belmont, CA), Tso, J. Yun; (Menlo Park, CA) Correspondence: HOWREY SIMON ARNOLD & WHITE, LLP; BOX 34; 301 RAVENSWOOD AVE.; MENLO PARK; CA; 94025; US Patent Application Number: 20030138862 Date filed: October 10, 2002 Abstract: This invention provides anti-HLA-DR antibodies and the methods of use thereof for the treatment of leukemia or lymphomas, or solid tumors such as ovarian cancer or melanoma. Excerpt(s): This application claims the benefit of priority of the U.S. provisional application U.S. Ser. No. 60/329,178 filed Oct. 11, 2001 and the U.S. provisional application U.S. Ser. No. 60/331,965, filed Nov. 21, 2001, each of which is incorporated by reference in its entirety. The leukemias are a heterogeneous group of neoplasm arising from the malignant transformation of hematopoietic (blood forming) cells. Leukemic cells proliferate primarily in bone marrow and lymphoid tissues where they interfere with normal hematopoiesis and immunity. Ultimately, they emigrate into the peripheral blood and infiltrate other tissues. Leukemias are classified according to the cell types primarily involved (myloid and lymphoid) and as acute or chronic based upon the natural history of the disease. Acute leukemias, including acute lymphocytic leukemia (ALL) and acute myelogenous leukemia (AML), have a rapid clinical course and often result in death within a matter of months without effective treatment. In contrast, chronic leukemias have a more prolonged natural history. Chronic leukemias include chronic lymphocytic leukemia (CCL), chronic myelogenous leukemia (CML) and hairy cell leukemia. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Antiviral activity of shiga toxin Inventor(s): Bohach, Carolyn H.; (Moscow, ID), Ferens, Witold A.; (Moscow, ID) Correspondence: CHRISTENSEN, O'CONNOR, JOHNSON, KINDNESS, PLLC; 1420 FIFTH AVENUE; SUITE 2800; SEATTLE; WA; 98101-2347; US Patent Application Number: 20030152593 Date filed: December 18, 2002 Abstract: The present invention provides methods and compositions for eliminating virally-infected cells by administering a Shiga-toxin composition, and the present invention provides methods and compositions for suppressing bovine leukemia-related cell proliferation. In the methods, a Shiga-toxin composition is administered in an amount effective to suppress bovine leukemia-related cell proliferation. The Shiga-toxin composition can include a Shiga-toxin polypeptide; a probiotic microorganism expressing a Shiga-toxin polypeptide; or a transgenic plant expressing a Shiga-toxin polypeptide. In one embodiment, the Shiga-toxin polypeptide is Stx1A and, in another embodiment, the Shiga-toxin polypeptide is Stx1 holotoxin. In yet a further embodiment, the Shiga-toxin polypeptide comprises Stx2. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 09/615,179, filed Jul. 13, 2000, incorporated herein by reference in its entirety. The present invention relates to methods and compositions for eliminating virally-infected
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cells using a Shiga-toxin polypeptide and to methods and compositions for suppressing bovine leukemia virus-related lymphocyte proliferation using a Shiga-toxin polypeptide. Bovine Leukemia Virus (BLV) is an oncogenic retrovirus responsible for the enzootic form of bovine lymphosarcoma, the most frequent malignancy of domestic cattle (Ferrer (1980 Adv. Vet. Sci. Comp. Med. 24:1-68). BLV infection results in a 1-8 year long asymptomatic period (Ferrer et al. (1979) J. Am. Vet. Med. Assoc. 175(7):705-8), followed by development of persistent lymphocytosis (PL) in approximately 30% of infected cattle with progression to a malignant lymphosarcoma in fewer than 10% of the animals (Ferrer et al. (1979) J. Am. Vet. Med. Assoc. 175(7):705-8). The PL stage is a benign neoplasia of B lymphocytes, which are the predominant or exclusive targets of BLV (Esteban et al. (1985) Cancer Res. 45(7):3225-30). This stage of infection is associated with an increased percentage of peripheral B lymphocytes containing provirus as well as increased viral gene expression (Mirsky et al. (1996) J. Virol. 70(4):2178-83). The development of PL markedly enhances the probability of transmission (Mammerickx et al. (1987) Leuk Res. 11:353-58). The critical importance of PL to transmission of this blood-borne disease was demonstrated by experiments showing that it required significantly less blood from cattle with persistent lymphocytosis to transmit BLV than blood from infected cattle which did not have persistent lymphocytosis (Mammerickx et al. (1987) Leuk. Res. 11:353-58). Moreover, vertical transmission from BLV-infected dams to their calves has been shown to be strongly correlated with persistent lymphocytosis (Agresti et al. (1993) Amer. J. Vet. Res. 54:373-78). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
BAALC expression as a diagnostic marker for acute leukemia Inventor(s): de la Chapelle, Albert; (Delaware, OH), Tanner, Stephan Markus; (Columbus, OH) Correspondence: CALFEE HALTER & GRISWOLD, LLP; 800 SUPERIOR AVENUE; SUITE 1400; CLEVELAND; OH; 44114; US Patent Application Number: 20030119043 Date filed: November 12, 2002 Abstract: Overexpression of the gene, BAALC, in biological samples from a patient is prognostic for tumor aggressiveness and unfavorable patient outcome. The present invention provides polynucleotide primers and probes for assaying for overexpression of BAALC transcripts. Kits containing the primers and probes are also provided. Also provided are antibodies for assaying for overexpression of BAALC proteins as well as peptide immunogens for producing the anti-BAALC antibodies. The present invention also provides methods for characterizing acute myelogenous leukemia, chronic myelogenous leukemia and prostate cancer in a patient, base on detection of BAALC overexpression. Excerpt(s): This application claims priority to U.S. Provisional Application S/ No. 60/348,210, filed Nov. 9, 2001, which is incorporated herein in its entirety. Leukemias comprise approximately 2% of adult cancers and are a heterogeneous group. There are two broad categories of leukemias. Acute leukemias arise when there is a block in the normal differentiation of cells to mature blood cells that results in large accumulations of immature cells or blasts in the blood. Examples of such cancers are acute myelogenous leukemia (AML; other names are acute myeloid leukemia and acute nonlymphocytic leukemia) and acute lymphoblastic leukemia (ALL). In chronic leukemia, on the other hand, there is unregulated proliferation of cells that have
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differentiated to mature blood cells. Examples of such cancers are chronic lymphocytic leukemia (CLL) and chronic myelogenous leukemia (CML). CML has a chronic phase which then progresses to a phase called blast crisis where immature, blast cells are present in the blood. Both acute and chronic leukemias involve the myeloid cells of the bone marrow, including white cells, red cells, megakaryocytes and cells of the lymphoid lineage. The cytogenetics of many leukemias are characterized by balanced chromosomal translocations that give rise to gene rearrangements. In acute myeloid leukemia (AML) for example, about 55% of adult de novo cases have clonal cytogenetic abnormalities, many of which are specific translocations. However, in the remaining cases, no visible cytogenetic abnormalities are found, although genetic changes are detected methods other than cytogenetics. In adult acute lymphoblastic leukemia (ALL), the proportion of patients with no cytogenetic abnormality is about 31%. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Binding-specific peptides, binding-specific carrier molecules, and uses thereof Inventor(s): Preisler, Harvey D.; (Chicago, IL) Correspondence: FOLEY & LARDNER; 150 EAST GILMAN STREET; P.O. BOX 1497; MADISON; WI; 53701-1497; US Patent Application Number: 20030134342 Date filed: January 31, 2002 Abstract: The present invention provides peptides that bind cells differentially that are capable of discriminating between normal and malignant cells, and uses of such peptides and specific carrier molecules for screening the binding reactivity of peptides from leukemia cells. Excerpt(s): This application claims priority from U.S. Provisional Patent Application No. 60/278,465, filed Mar. 24, 2001, the contents of which are hereby incorporated by reference. The present invention provides materials and methods using peptides that bind cells. In particular the present invention provides peptides that bind to malignant eukaryotic cells, including leukemic cells. In normal hematopoeisis, pluripotent stem cells in the bone marrow proliferate (they are capable of self-renewal) and differentiate into either myeloid progenitor cells or lymphoid progenitor cells. These progenitor cells retain the capacity for self-renewal, but they are committed to one of those two major hematopoietic lineages. Depending on the types and amounts of cytokines present, the myeloid and lymphoid cells generate various more mature progenitor cells which proliferate, become committed and further differentiate into the various types of blood cells. Lymphoid cells mature into the T and B cells of the immune system. Myeloid stem cells mature into granulocytes, monocytes, platelets, erythrocytes and eosinophils. Among the cytokines that regulate hematopoiesis are granulocyte colony-stimulating factor (G-CSF), macrophage colony-stimulating factor (M-CSF), several interleukins (IL; in particular IL-3 and IL-6), stem cell factor (SCF), granulocyte-macrophage colonystimulating factor (GM-CSF), erythropoietin (Epo) and thrombopoietin (Tpo). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Combinations comprising N-{5-[4-(4-methyl-piperazino-methyl)-benzoylamido]- -2methylphenyl}-4-(3-pyridyl)-2-pyrimidine-amine and at least one telomerase inhibitor Inventor(s): Tauchi, Tetsuzo; (Kanagawa, JP) Correspondence: THOMAS HOXIE; NOVARTIS, CORPORATE INTELLECTUAL PROPERTY; ONE HEALTH PLAZA 430/2; EAST HANOVER; NJ; 07936-1080; US Patent Application Number: 20030166660 Date filed: October 17, 2002 Abstract: The invention relates to a method of treating a warm-blooded animal, especially a human, having a proliferative disease comprising administering to the animal a combination which comprises (a) N-{5-[4-(4-methyl-piperazino-methyl)benzoylamido]-2-methylphenyl}-4-(3-p- yridyl)-2-pyrimidine-amine and (b) at least one telomerase inhibitor, to a combination comprising (a) and (b) as defined above and optionally at least one pharmaceutically acceptable carrier for simultaneous, separate or sequential use, in particular for the delay of progression or treatment of a proliferative disease and finally to the use of at least one telomerase inhibitor for the preparation of a medicament for the delay of progression or treatment of Imatinib-resistant leukemia. Excerpt(s): The invention relates to a method of treating a warm-blooded animal, especially a human, having a proliferative disease comprising administering to the animal a combination which comprises (a) N-{5-[4-(4-methyl-piperazino-methyl)benzoylamido]-2-methylphenyl}-4-(3-p- yridyl)-2-pyrimidine-amine and (b) at least one telomerase inhibitor, especially as defined herein; a combination comprising (a) and (b) as defined above and optionally at least one pharmaceutically acceptable carrier for simultaneous, separate or sequential use, in particular for the delay of progression or treatment of a proliferative disease, especially a tumor disease and leukemia; a pharmaceutical composition comprising such a combination; the use of such a combination for the preparation of a medicament for the delay of progression or treatment of a proliferative disease, and finally to the use of at least one telomerase inhibitor for the preparation of a medicament for the delay of progression or treatment of an Imatinib-resistant leukemia; and to a commercial package or product comprising such a combination. The preparation of N-{5-[4-(4-methyl-piperazino-methyl)benzoylamid- o]-2-methylphenyl}-4-(3-pyridyl)-2-pyrimidine-amine and the use thereof, especially as an antiproliferative agent, are described in EP-A-0 564 409, which was published on Oct. 6, 1993 and in equivalent applications in numerous other countries. This compound is also known and hereinafter referred to as Imatinib [International Non-proprietary Name]. Telomerase is a DNA polymerase with an endogenous RNA template, on which the nascent telomeric repeats are synthesized. It is known that approximately 85-90% of all human cancers are positive for telomerase, both in cultured tumor cells and primary tumor tissue, whereas most somatic cells appear to lack detectable levels of telomerase. This finding has been extended to a wide range of human tumors (see, for example, Hiyama et al., "Correlating telomerase activity levels with human neuroblastoma outcomes," Nature Medicine, 1:249-255, 1995a.). Therefore, Human telomerase is now considered as a novel and potentially highly selective target for antitumor drug design, and many new promising telomerase inhibitors have been discovered (Anne E. Pitts and David R. Corey.sup.A, "The telomerase challenge--an unusual problem in drug discovery"; Drug Discovery Today 1999, 4:155-161). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 309
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Compositions and methods for WT1 specific immunotherapy Inventor(s): Carter, Darrick; (Seattle, WA), Mossman, Sally P.; (Seattle, WA), Gaiger, Alexander; (Seattle, WA), Smithgall, Molly D.; (Seattle, WA), Cheever, Martin A.; (Mercer Island, WA), Sutherland, R. Alec; (Bothell, WA), Evans, Lawrence S.; (Seattle, WA), McNeill, Patricia D.; (Federal Way, WA), Swanson, Ryan M.; (Seattle, WA) Correspondence: SEED INTELLECTUAL PROPERTY LAW GROUP PLLC; 701 FIFTH AVE; SUITE 6300; SEATTLE; WA; 98104-7092; US Patent Application Number: 20030198622 Date filed: July 12, 2002 Abstract: Compositions and methods for the therapy of malignant diseases, such as leukemia and cancer, are disclosed. The compositions comprise one or more of a WT1 polynucleotide, a WT1 polypeptide, an antigen-presenting cell presenting a WT1 polypeptide, an antibody that specifically binds to a WT1 polypeptide; or a T cell that specifically reacts with a WT1 polypeptide. Such compositions may be used, for example, for the prevention and treatment of metastatic diseases. Excerpt(s): The present invention relates generally to the immunotherapy of malignant diseases such as leukemia and cancers. The invention is more specifically related to compositions for generating or enhancing an immune response to WT1, and to the use of such compositions for preventing and/or treating malignant diseases. Cancer and leukemia are significant health problems in the United States and throughout the world. Although advances have been made in detection and treatment of such diseases, no vaccine or other universally successful method for prevention or treatment of cancer and leukemia is currently available. Management of the diseases currently relies on a combination of early diagnosis and aggressive treatment, which may include one or more of a variety of treatments such as surgery, radiotherapy, chemotherapy and hormone therapy. The course of treatment for a particular cancer is often selected based on a variety of prognostic parameters, including an analysis of specific tumor markers. However, the use of established markers often leads to a result that is difficult to interpret, and the high mortality continues to be observed in many cancer patients. Immunotherapies have the potential to substantially improve cancer and leukemia treatment and survival. Recent data demonstrate that leukemia can be cured by immunotherapy in the context of bone marrow transplantation (e.g., donor lymphocyte infusions). Such therapies may involve the generation or enhancement of an immune response to a tumor-associated antigen (TAA). However, to date relatively few TAAs are known and the generation of an immune response against such antigens has, with rare exception, not been shown to be therapeutically beneficial. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Conditioned culture media Inventor(s): Moreadith, Randall; (Chapel Hill, NC), Schoonjans, Luc; (Wilsele, BE) Correspondence: Barbara E. Johnson; Webb Ziesenheim Logsdon Orkin & Hanson; 700 Koppers Building; 436 Seventh Avenue; Pittsburgh; PA; 15219; US Patent Application Number: 20030124720 Date filed: January 4, 2002
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Abstract: A novel medium for maintaining and growing pluripotent and germ line competent mammalian stem cells. The medium is conditioned by a fibroblast cell clone that produces leukemia inhibitory factor. The cells are placed in the medium so that, over a period of time, the leukemia inhibitory factor accumulates in the medium. A portion of the medium is then removed, and the quantity removed is replaced with unconditioned medium. Excerpt(s): This is a continuation-in-part application of U.S. patent application Ser. No. 09/894,913, filed Jun. 28, 2001, which is a continuation-in-part of U.S. patent application Ser. No. 09/628,883, filed Jul. 31, 2000, which is a continuation-in-part application of U.S. patent application Ser. No. 08/810,945, filed Feb. 27, 1997, now U.S. Pat. No. 6,103,523, issued Aug. 14, 2000, and which is incorporated herein by reference, as combined with U.S. Provisional Patent Application Serial No. 60/214,859, filed on Jun. 28, 2000, which is also incorporated herein by reference. The present invention relates to improved methods for the derivation of pluripotent embryonic stem (ES) cell lines and their use for germ line transmission and for the generation of genetically modified animals. Embryonic stem (ES) cell lines are cell lines isolated from the inner cell mass (ICM) of blastocyst-stage embryos which, under specific conditions, can be maintained in culture for many passages, i.e., replating of cells onto new cell culture dishes at regular time intervals, without loss of their pluripotency. They maintain a normal karyotype and when reintroduced into a host blastocyst they can colonize the germ line. Such cell lines may provide an abundance of pluripotent cells that can be transformed in vitro with DNA, and selected for recombination (homologous or non-homologous) of exogenous DNA into chromosomal DNA, allowing stable incorporation of the desired gene. To date, germ line transmission, i.e., the transmission of the ES genome to the next generation, has however only been achieved with ES cells of certain mouse strains. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Crystal form of N-(4-trifluoromethylphenyl)-5-methylisoxazole-4-carboxamid- e Inventor(s): Paulus, Erich; (Eppstein, DE), Westenfelder, Uwe; (Frankfurt, DE), Hedtmann, Udo; (Frankfurt, DE), Faasch, Holger; (Hochheim, DE) Correspondence: FINNEGAN, HENDERSON, FARABOW, GARRETT & DUNNER; LLP; 1300 I STREET, NW; WASHINGTON; DC; 20005; US Patent Application Number: 20030166945 Date filed: November 25, 2002 Abstract: The invention relates to a crystal modification of the compound of the formula I 1and the processes for the preparation of and use that crystal modifications 1. The invention is used for treating acute immunological episodes, such as sepsis, allergies, graft-versus-host and host-versus-graft-reactions, autoimmune diseases, in particular rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, psoriasis, atopic dermatitis, asthma, urticaria, rhinitis, uveitis, type II diabetes, liver fibrosis, cystic fibrosis, colitis, cancers, such as lung cancer, leukemia, ovarian cancer, sarcomas, Kaposi's sarcoma, meningioma, intestinal cancer, lymphatic cancer, brain tumors, breast cancer, pancreatic cancer, prostate cancer, or skin cancer. Excerpt(s): This case claims benefit under 35 U.S.C.sctn.119 of German priority document 19734438.0 filed on Aug. 8, 1997. This document, as well as German priority document 19756093.8, filed Dec. 17, 1997, are hereby incorporated by reference. The compound of formula I crystallizes in the first crystal modification in the space group
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P2.sub.1/c with 8 molecules in the unit cell. Molecules of the compound of formula I are present as dimers which originate from the individual molecules by formation of a -C.dbd.O. HN hydrogen bridge bond (2.938.ANG.), the two molecular levels being virtually perpendicular to one another (91.2.degree.). The two molecules have very different conformations. The angles made by the five- and six-membered rings with the central carbonyl group are 5.4.degree. and 2.1.degree. and 23.4.degree. and 23.1.degree., respectively. The latter twist creates the steric preconditions permitting the hydrogen bridge bond between the two molecules. Lines of strong intensity: 16.70; 18.90; 23.00; 23.65; and 29.05 degrees. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Cytostatic agents Inventor(s): Drummond, Alan Hastings; (Oxford, GB), Pratt, Lisa Marie; (Oxford, GB), Ayscough, Andrew Paul; (Oxford, GB) Correspondence: GREENBERG TRAURIG, LLP; 885 3RD AVENUE; NEW YORK; NY; 10022; US Patent Application Number: 20030149084 Date filed: December 10, 2002 Abstract: This invention provides a method of inhibiting proliferation of tumor cells in a subject by administering to the subject an effective amount of ester and thioester compounds containing an N-formyl hydroxylamine group.The compounds with which this invention is concerned thus represent a selection of a subclass from the compounds known in the art as MMP inhibitors, for a specific and previously unrecognized pharmaceutical utility in the inhibition of proliferation of rapidly dividing cells, including such tumor cells as lymphoma, leukemia, myeloma, adenocarcinoma, carcinoma, mesothelioma, teratocarcinoma, choriocarcinoma, small cell carcinoma, large cell carcinoma, melanoma, retinoblastoma, fibrosarcoma, leiomyosarcoma or endothelioma cells by a mechanism other than MMP inhibition. Excerpt(s): The present invention relates to N-formyl hydroxylamine derivatives, to processes for their preparation, to pharmaceutical compositions containing them, and to the use of such compounds in medicine. In particular, the compounds are inhibitors of the proliferation of a range of rapidly dividing tumour cells, for example melanoma and/or lymphoma cells. There is a need in cancer therapy for therapeutic compounds which are inhibitors of the proliferation of tumour cells. One compound which is known to have such activity is 5-fluorouracil (5FU). Patent publication WO 98/11063 describes and claims the use of certain hydroxamic acid derivatives as inhibitors of tumour cell proliferation, and also describes and claims certain novel hydroxamic acids useful for that purpose. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Deuterated rapamycin compounds, method and uses thereof Inventor(s): Yatscoff, Randall W.; (Edmonton, CA), Foster, Robert T.; (Edmonton, CA), Naicker, Selvaraj; (Edmonton, CA) Correspondence: Mary Ann Dillahunty; BURNS, DOANE, SWECKER & MATHIS, L.L.P.; P.O. Box 1404; Alexandria; VA; 22313-1404; US Patent Application Number: 20030139440 Date filed: November 20, 2002 Abstract: The synthesis of deuterated analogues of rapamycin is disclosed together with a method for use for inducing immunosupression and in the treatment of transplantation rejection, graft vs host disease, autoimmune diseases, diseases of inflammation leukemia/lymphoma, solid tumors, fungal infections, hyperproliferative vascular disorders. Also described is a method for the synthesis of water soluble deuteratred rapamycin compounds and their use as described above. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 09/148,623, which is based on provisional patent application No. 60/057,632, both of which are relied on and incorporated herein by reference. This invention relates to deuterated derivatives of rapamycin and a method for using them in the treatment of transplantation rejection, host vs. graft disease, graft vs. host disease, leukemia/lymphoma, hyperproliferative vascular disorders, autoimmune diseases, diseases of inflammation, solid tumors, and fungal infections. Rapamycin, known as sirolimusis, is a 31-membered macrolide lactone, C.sub.51H.sub.79NO.sub.13, with a molecular mass of 913.6 Da. In solution, sirolimus forms two conformational trans-, cisisomers with a ratio of 4:1 (chloroform) due to hindered rotation around the pipecolic acid amide bond. It is sparingly soluble in water, aliphatic hydrocarbons and diethyl ether, whereas it is soluble in alcohols, halogenated hydrocarbons and dimethyl sulfoxide. Rapamycin is unstable in solution and degrades in plasma and low-, and neuteral -pH buffers at 37.degree. C. with half-life of <10 h. the structures of the degradation products have recently been characterized. Rapamycin is a macrocyclic triene antibiotic produced by Streptomyces hygroscopicus, which was found to have antifungal activity, particularly against Candida albicans, both in vitro and in vivo (C. Vezina et al., J. Antibiot. 28, 721 (1975); S. N. Seh{overscore (g)}al et al., J. Antibiot. 28, 727 (1975); H. A. Baker et al., J. Antibiot. 31, 539 (1978); U.S. Pat. No. 3,929,992; and U.S. Pat. No. 3,993,749]. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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EPOTHILONE DERIVATIVES, METHOD FOR PRODUCING SAME AND THEIR PHARMACEUTICAL USE Inventor(s): BUCHMANN, BERND; (NEUENDORR, DE), SCHWEDE, WOLFGANG; (BERLIN, DE), KLAR, ULRICH; (BERLIN, DE), SKUBALLA, WERNER; (BERLIN, DE) Correspondence: MILLEN WHITE ZELANO & BRANIGAN; ARLINGTON COURTHOUSE PLAZA I; 2200 CLARENDON BOULEVARD; SUITE 1400; ARLINGTON; VA; 22201; US Patent Application Number: 20030144523 Date filed: May 3, 2000
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Abstract: This invention relates to the new epothilone derivatives of general formula I, 1in whichsubstituents Y, Z R.sup.2a, R.sup.2b, R.sup.3, R.sup.4a, R.sup.4b, D--E, R.sup.5, R.sup.6, R.sup.7, R.sup.8 and X have the meanings that are indicated in more detail in the description.The new compounds interact with tubulin by stabilizing microtubuli that are formed. They are able to influence the cell-splitting in a phasespecific manner and are suitable for treating malignant tumors, for example, ovarian, stomach, colon, adeno-, breast, lung, head and neck carcinomas, malignant melanomas, acute lymphocytic and myelocytic leukemia. In addition, they are suitable for antiangiogenesis therapy as well as for treatment of chronic inflammatory diseases (psoriasis, arthritis). To avoid uncontrolled proliferation of cells and for better compatibility of medical implants, they can be applied or introduced into polymer materials.The compounds according to the invention can be used alone or to achieve additive or synergistic actions in combination with other principles and classes of substances that can be used in tumor therapy. Excerpt(s): Epothilone A (R=H), Epothilone B (R=CH.sub.3) in, e.g., Angew. Chem. [Applied Chem.], 1996, 108, 1671-1673. Because of their in-vitro selectivity for breast cell lines and intestinal cell lines and their significantly higher activity against Pglycoprotein-forming multiresistant tumor lines in comparison to taxol as well as their physical properties that are superior to those of taxol, e.g., a water solubility that is higher by a factor of 30, this novel structural class is especially advantageous for the development of a pharmaceutical agent for treating malignant tumors. The natural products are not sufficiently stable either chemically or metabolically for the development of pharmaceutical agents. To eliminate these drawbacks, modifications to the natural product are necessary. Such modifications are possible only with a totalsynthesis approach and require synthesis strategies that make possible a broad modification of the natural product. The purpose of the structural changes is also to increase the therapeutic range. This can be done by improving the selectivity of the action and/or reducing undesirable toxic side-effects and/or increasing active strength. The total synthesis of epothilone A is described by Schinzer et al. in Chem. Eur. J. 1996, 2, No. 11, 1477-1482 and in Angew. Chem. 1997, 109, No. 5, pp. 543-544). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Euphorbia antiquorum extract, a pharmaceutical composition containing the same and methods for treatment of cancers Inventor(s): Cheng, Wen-Ching; (Taipei, TW), Lin, Chih-Hui; (Taichung, TW) Correspondence: LaRiviere, Grubman & Payne, LLP; P.O. Box 3140; Monterey; CA; 93942; US Patent Application Number: 20030165579 Date filed: February 27, 2002 Abstract: An herbal extract of Euphorbia antiquorum is provided. The herbal extract of the invention demonstrates in vitro inhibition of growth of hepatoma cells, colorectal adenocarcinoma cells, monocyte-like lymphoma and leukemia cells. This invention also provides a pharmaceutical composition containing the same and a method for treatments for cancers. Excerpt(s): This invention relates to herbal extracts from Euphorbia antiquorum, and more particularly, to a single-herb based pharmaceutical composition and method having therapeutic effects for treating cancers. According to the invention, the extracts
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from Euphorbia antiquorum have been found to show inhibitory effect on several different cancer cell lines. The extracts are useful in effective treatment of cancers, particularly hepatoma, colon cancer, leukemia and lymphocytoma. Cancer is the second leading cause of death in the United States (CA Cancer J. Clin. 43:7). The occurrence of cancer for any one individual is correlated with numerous risk factors. Some risk factors are believed to include age, genetics, diet and environmental exposure (e.g., to mutagenic chemicals, radiation, transforming viruses, etc.). According to an estimation by World Health Organization, about 10 million new cancer cases are now occurring annually around the world. The number is expected to reach 15 million by the year 2015, with two thirds of these new cases occurring in developing countries (World Health 48:22, 1995). For example, Hepatoma is much more prevalent in many of the developing countries than in the industrialized world. Although relatively uncommon in the Western world, an estimated 300 cases will occur annually in Missouri, USA. Statistics show that about 20,000 new patients are diagnosed every year in United States. It is not known exactly what causes hepatoma. However, certain risk factors have been identified. The risk factors are: a history of cirrhosis of the liver, certain types of viral hepatitis infection, chronic inflammatory conditions, exposure to the following substances aflatoxin, vinyl chloride, thorium dioxide, arsenic, long-term use of anabolic steroids and tabacco. In general, surgical resection is the treatment of choice for patients with hepatoma and can be curative, provided the tumor is confined to the liver and is completely removed. Unfortunately, many patients are not candidates for resection due to large tumor size, multiple tumors or severe cirrhosis of the liver. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Genes abnormally expressed in myeloid leukemia cells with an MLL-AF9 fusion Inventor(s): Wang, San Ming; (Chicago, IL), Chen, Jianjun; (Chicago, IL), Zhou, Guolin; (Chicago, IL), Rowley, Janet D.; (Chicago, IL), Lee, Sanggyu; (Chicago, IL) Correspondence: MARSHALL, GERSTEIN & BORUN; 6300 SEARS TOWER; 233 SOUTH WACKER; CHICAGO; IL; 60606-6357; US Patent Application Number: 20030165949 Date filed: December 23, 2002 Abstract: The invention provides materials and methods for the analysis of gene expression in hematopoietic cells, such as hematopoietic stem/precursor cells of mammals. Materials of the invention include microarrays of polynucleotides collectively characterizing gene expression in hematopoietic cells, as well as a vector comprising at least one such polynucleotide and a host cell containing such a vector. Methods of the invention include diagnostic methods for identifying or detecting expression products collectively characteristic of normal, or abnormal, hematopoietic cells. Other methods of the invention include therapeutic methods for the treatment or prevention of an abnormality such as a disease or condition of a hematopoietic cell, comprising delivery of an effective amount of a suitable material, such as a pharmaceutical composition of the invention, to a cell or patient in need thereof. Excerpt(s): The invention generally is related to leukemia. More specifically, the invention is directed to materials and methods for determining gene expression in leukemic cells. In particular, the invention provides genes abnormally expressed in leukemic cells with an MLL-AF9 fusion. Chromosomal rearrangements are consistently associated with acute myeloid leukemias (AMLs). The generation of chimeric genes and fusion proteins via chromosomal translocation events frequently results in the
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deregulation of myeloid differentiation since one of the two affected genes is often a transcription factor involved in the regulation of hematopoietic differentiation. The MLL (mixed-lineage leukemia) gene is an important regulatory gene located on chromosome band 11q23. The MLL gene is frequently involved in de novo and treatment-related leukemia, in reciprocal chromosome translocations with other genes, which results in breaks in MLL and the partner genes, and the formation of new fusion genes. Nearly 40 different partner genes have been shown to be involved in this translocation (Zieminvan der Poel, et al., Proc. Natl. Acad. Sci., 88(23), 10735-10739, 1991; Gu, et al., Cell, 71, 701-708, 1992). The MLL-AF9 fusion, which results from a (9;11) chromosome translocation, is one of the most common examples. The disruption of the wild-type genes and formation of the fusion genes will likely alter the normal expression pattern of other genes. Abnormally expressed genes, both those whose expression is increased, as well as those whose expression is decreased, likely change the cell behavior, and eventually lead to the development of leukemia. At present, there is a need to identify the abnormally expressed genes that are unique to the t(9;11). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
High efficiency retroviral vector which contains genetically engineered cellular noncoding sequence harboring splicing acceptor Inventor(s): Yu, Seung-Shin; (Seoul, KR), Lee, Jun-Tae; (Jeonrabuk-do, KR), Kim, SunYoung; (Seoul, KR) Correspondence: Anderson Kill & Olick; 1251 Avenue of the Americas; New York; NY; 10020-1182; US Patent Application Number: 20030166251 Date filed: May 1, 2002 Abstract: The present invention provides a safe and highly efficient retroviral vector derived from the MLV (murine leukemia virus) for use in gene therapy, which lacks viral coding sequences but contains the genetically engineered EF I.alpha. non-coding sequence harboring splicing acceptor. Excerpt(s): This application is a continuation of International Application PCT/KR01/01515, with an international filing date of Sep. 8, 2001, now abandoned. The present invention relates to a highly efficient and safe retroviral vector for gene therapy, derived from murine leukemia virus (MLV), which contains a mutated heterologous splicing acceptor and lacks MLV coding sequences. Retroviral vectors derived from murine leukemia virus (MLV) have been employed in more than 50% of approved clinical gene therapy trials (Wiley--The Journal of Gene Medicine Website; http://www.wiley.co.uk/gene- therapy). However, one of the major limiting factors hindering a wider use of these vectors is that the level of gene expression is does not get high enough to give clear therapeutic effects. The present inventors previously constructed retroviral vectors that contains no viral coding sequence and harbors a heterologous splicing acceptor sequence from cellular or other viral genes (KR Patent Laid-Open Publication No. 2000-6334). One of the vectors contains a splicing acceptor from the human EF1.alpha. gene. This vector gives a significantly higher level of gene expression than the control vector lacking such a splicing acceptor sequence. However one problem with this vector was that viral titer varied depending on the packaging lines used. For example, when the NIH3T3-based PG13 line was used, viral titer decreased about 10 folds. In FLYA13 derived from HT1080 cells, there was a 3-fold decrease in viral titer. Results from RNA analysis indicated that low viral titer is due to
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highly efficient splicing of the genomic size transcript containing the packaging signal sequence. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Human chemokine beta-10 mutant polypeptides Inventor(s): Li, Haodong; (Gaithersburg, MD), Li, Yuling; (Germantown, MD), Parmelee, David; (Rockville, MD), White, John R.; (Coatesville, PA), Alderson, Ralph; (Gaithersburg, MD), Gentz, Solange H.L.; (Belo Horizonte, BR), Adams, Mark D.; (Rockville, MD), Olsen, Henrik S.; (Gaithersburg, MD), Salcedo, Theodora; (East Syracuse, NY), Appelbaum, Edward R.; (Blue Bell, PA) Correspondence: HUMAN GENOME SCIENCES INC; 9410 KEY WEST AVENUE; ROCKVILLE; MD; 20850 Patent Application Number: 20030171319 Date filed: October 3, 2002 Abstract: Human Chemokine Beta-10 polypeptides and DNA (RNA) encoding such chemokine polypeptides and a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such chemokine polypeptides for the treatment of leukemia, tumors, chronic infections, autoimmune disease, fibrotic disorders, wound healing and psoriasis. Antagonists against such chemokine polypeptides and their use as a therapeutic to treat rheumatoid arthritis, autoimmune and chronic inflammatory and infective diseases, allergic reactions, prostaglandin-independent fever and bone marrow failure are also disclosed. Excerpt(s): This application claims priority under 35 U.S.C.sctn. 120 as a continuation-inpart to International Application No. PCT/US01/18046, filed Jun. 5, 2001, which claims benefit under 35 U.S.C.sctn. 119(e) to U.S. Provisional Application No. 60/209,578, filed Jun. 6, 2000; this application also claims priority under 35 U.S.C.sctn. 120 as a continuation-in-part to U.S. patent application Ser. No. 10/125,451, filed Apr. 19, 2002, which is a divisional of and claims priority under 35 U.S.C.sctn. 120 to U.S. patent application Ser. No. 09/479,729, filed Jan. 7, 2000, now U.S. Pat. No. 6,391,589, which claims benefit under 35 U.S.C.sctn. 119(e) to U.S. Provisional Application No. 60/115,439, filed Jan. 8, 1999; U.S. patent application Ser. No. 09/479,729 also is a continuation-in-part of and claims priority under 35 U.S.C.sctn. 120 to U.S. patent application Ser. No. 08/462,967, filed Jun. 5, 1995, now abandoned, which is a continuation-in-part of and claims priority under 35 U.S.C.sctn. 120 to U.S. patent application Ser. No. 08/458,355, filed Jun. 2, 1995, now U.S. Pat. No. 5,981,230, both of which claim priority under 35 U.S.C.sctn. 120 to International Application No. PCT/US 94/09484, filed Aug. 23, 1994; all of the above are hereby incorporated by reference in their entirety. The present invention relates to deletion and substitution mutant polypeptides of human chemokine beta-10 (Ck.beta.-10), as well as nucleic acid molecules encoding such polypeptides and processes for producing such polypeptides using recombinant techniques. In one aspect, the invention also relates to uses of the full-length and mature forms of Ck.beta.-10, as well as deletion and substitution mutants, in medical treatment regimens. In particular, the Ck.beta.-10 polypeptides described herein may be employed to treat a variety of conditions, including rheumatoid arthritis, inflammation, respiratory diseases, allergy, and IgE-mediated allergic reactions. Ck.beta.-10 is also known as MCP-4. Chemokines, also referred to as intercrine cytokines, are a subfamily of structurally and functionally related cytokines. These molecules are 8-14 kd in size. In general chemokines exhibit 20% to 75%
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homology at the amino acid level and are characterized by four conserved cysteine residues that form two disulfide bonds. Based on the arrangement of the first two cysteine residues, chemokines have been classified into two subfamilies, alpha and beta. In the alpha subfamily, the first two cysteines are separated by one amino acid and hence are referred to as the "C--X--C" subfamily. In the beta subfamily, the two cysteines are in an adjacent position and are, therefore, referred to as the --C--C-- subfamily. Thus far, at least eight different members of this family have been identified in humans. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Identification of rearrangements in nucleic acid molecules Inventor(s): Lastrucci, Rusla Marianne Dubreuil; (Huntsville, AL) Correspondence: STERNE, KESSLER, GOLDSTEIN & FOX PLLC; 1100 NEW YORK AVENUE, N.W.; WASHINGTON; DC; 20005; US Patent Application Number: 20030157527 Date filed: December 3, 2002 Abstract: Disclosed are methods and compositions for detecting a chromosomal rearrangement in a sample of nucleic acids. In an exemplary method, a first nucleic acid comprising a portion of a first chromosome, which may be detectably labeled, is attached to a substrate; a first portion of a test nucleic acid is hybridized to the first nucleic acid; a second nucleic acid comprising all or a portion of a second chromosome, which may be detectably labeled, is hybridized to a second portion of the test nucleic acid, thereby forming a trimolecular sandwich, and the hybridization of the test nucleic acid to both of the first and second nucleic acids is detected as an indication that the test nucleic acid comprises a chromosomal rearrangement. In particular embodiments, the first and second nucleic acids are derived from the same chromosome. In a related method, the test nucleic acid is used as a template for nucleic acid synthesis, and primers derived from a first and a second chromosome or from the same chromosome, which are distinctly labeled with first and second labels, respectively, are used to prime nucleic acid synthesis. A synthesized nucleic acid comprising each of the first and second primers is detected as an indication that the test nucleic acid comprises a chromosomal rearrangement. Also disclosed are kits for detecting chromosomal rearrangements. Such methods and kits can be used, for example, in the diagnosis or identification of disease-associated chromosomal rearrangements, e.g., cancers such as leukemia. Excerpt(s): This application claims priority under 35 U.S.C.sctn.119(e) from U.S. provisional application Nos. 60/334,531; 60/341,863; and 60/357,631, filed Dec. 3, 2001; Dec. 21, 2001; and Feb. 20, 2002; respectively, each of which is incorporated herein by reference. The present invention relates to methods and compositions for identifying chromosomal rearrangements. The rearrangement of nucleic acid molecules (e.g., chromosomal rearrangements such as translocations, deletions, inversions, or fusions) can result in disorders such as cancers, including solid tumors and non-solid cancers such as leukemias and lymphomas. For example, the Philadelphia chromosome (Ph) in chronic myeloid leukemia (CML) involves a reciprocal translocation, t(9;22)(q34;q11), bringing the 3' c-abl proto-oncogene sequences of chromosome 9 adjacent to the 5' sequences of the 5.8 kb breakpoint cluster region (BCR) on chromosome 22. This hybrid gene is transcribed into two forms of 8.5 kb chimeric BCR-abl mRNA, which differ by 75 bp. These mRNAs are translated into a chimeric 210 kd-protein product that is considered essential to the pathogenesis of CML. Other cancers, including other
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leukemias and lymphomas, can also result from chromosomal translocations. Several examples of cancer-associated chromosomal translocations are described herein. Conventional methods for identifying chromosomal translocations include classical cytogenetic analysis, fluorescence in situ hybridization (FISH), and PCR. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Immune cell cytokine Inventor(s): Soppet, Daniel R.; (Centreville, VA), Li, Yi; (Sunnyvale, CA) Correspondence: HUMAN GENOME SCIENCES INC; 9410 KEY WEST AVENUE; ROCKVILLE; MD; 20850 Patent Application Number: 20030143227 Date filed: February 3, 2003 Abstract: Human Immune Cell Cytokine-like Hormone polypeptide and DNA (RNA) encoding such polypeptide in a procedure for producing such polypeptides by recombinant techniques is disclosed. Also disclosed are methods for utilizing such polypeptide for stimulating the proliferation and differentiation of stem cells of the immune system. Antagonists against such polypeptides are also disclosed. The antagonists include antibodies which may be employed as a therapeutic to treat leukemia and lymphoblastoma, may also be used as imaging agents and diagnostic agents for detecting expression levels of the protein. Also disclosed are diagnostic assays for detecting diseases related to mutations in the nucleic acid sequences and altered concentrations of the polypeptides. Excerpt(s): This application is a Divisional of U.S. Application Ser. No. 09/251,330, filed Feb. 17, 1999, which is a Divisional of U.S. Application Ser. No. 08/780,370 filed Jan. 9, 1997, now U.S. Pat. No. 5,962,268, which claims benefit under 35 U.S.C. section 119(e) to U.S. Provisional Application Ser. No. 60/009,890, filed Jan. 11, 1996. This invention relates to newly identified polynucleotides, polypeptides encoded by such polynucleotides, the use of such polynucleotides and polypeptides, as well as the production of such polynucleotides and polypeptides. The polypeptide of the present invention has been putatively identified as a cytokine, more particularly, the polypeptide of the present invention has been identified as an immune cell cytokine-like potential hormone, sometimes hereinafter referred to as "HLHDC84". The invention also relates to inhibiting the action of such polypeptides. The cytokine family of proteins exhibit a wide variety of functions. A hallmark feature is their ability to elicit chemotactic migration of distinct cell types, including polymorphonuclear cells and macrophages. Many cytokines have pro-inflammatory activity and are involved in multiple steps during inflammatory reactions. In addition to their involvement in inflammation, cytokines have been shown to exhibit other activities. For example, interleukin-8 (IL-8) promotes proliferation of keratinocytes. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Immunotherapy of B-cell malignancies using anti-CD22 antibodies Inventor(s): Goldenberg, David M.; (Mendham, NJ) Correspondence: FOLEY AND LARDNER; SUITE 500; 3000 K STREET NW; WASHINGTON; DC; 20007; US Patent Application Number: 20030124058 Date filed: December 9, 2002 Abstract: B-cell malignancies, such as the B-cell subtype of non-Hodgkin's lymphoma and chronic lymphocytic leukemia, are significant contributors to cancer mortality. The response of B-cell malignancies to various forms of treatment is mixed. Traditional methods of treating B-cell malignancies, including chemotherapy and radiotherapy, have limited utility due to toxic side effects. Immunotherapy with anti-CD20 antibodies have also provided limited success. The use of antibodies that bind with the CD22 or CD19 antigen, however, provides an effective means to treat B-cell malignancies such as indolent and aggressive forms of B-cell lymphomas, and acute and chronic forms of lymphatic leukemias. Moreover, immunotherapy with anti-CD22 and/or anti-CD19 antibodies requires comparatively low doses of antibody protein, and can be used effectively in multimodal therapies. Excerpt(s): The present application is a continuation-in-part application of U.S. patent application Ser. No. 09/038,995. The present invention relates to immunotherapeutic methods for treating B-cell malignancies. In particular, this invention is directed to methods for treating B-cell malignancies by administering comparatively low doses of antibody that binds to the CD22 antigen or antibody that binds to the CD19 antigen. The present invention also is directed to multimodal therapeutic methods in which antiCD22 or anti-CD19 administration is supplemented with chemotherapy, or by administration of therapeutic proteins, such as immunoconjugates and antibody fusion proteins. B-Cell lymphomas, such as the B-cell subtype of non-Hodgkin's lymphoma, are significant contributors to cancer mortality. The response of B-cell malignancies to various forms of treatment is mixed. For example, in cases in which adequate clinical staging of non-Hodgkin's lymphoma is possible, field radiation therapy can provide satisfactory treatment. Still, about one-half of the patients die from the disease. Devesa et al., J. Nat'l Cancer Inst. 79:701 (1987). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Induction of apoptosis in cancer cells Inventor(s): Dawson, Marcia J.; (Los Altos, CA), Fontana, Joseph A.; (West Bloomfield, MI), Zhang, Xiao-kun; (San Diego, CA), Jong, Ling; (Sunnyvale, CA), Hobbs, Peter D.; (Moss Beach, CA), Leid, Mark; (Corvallis, OR) Correspondence: SCHWEGMAN, LUNDBERG, WOESSNER & KLUTH, P.A.; P.O. BOX 2938; MINNEAPOLIS; MN; 55402; US Patent Application Number: 20030176506 Date filed: December 2, 2002 Abstract: The present invention provides compounds that are inducers or inhibitors of apoptosis or apoptosis preceded by cell-cycle arrest. In addition, the present invention provides pharmaceutical compositions and methods for treating mammals with
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leukemia or other forms of cancer or for treating disease conditions caused by apoptosis of cells. Excerpt(s): This application claims priority from U.S. Provisional Patent Application No. 60/334,081, filed, Nov. 30, 2001, and U.S. Provisional Patent Application No. 60/406,252, filed, Aug. 26, 2002, which are incorporated herein by reference. Acute myelogenous leukemia (AML) is a heterogeneous disease composed of numerous sub-classifications displaying a wide spectrum of phenotypes. (See Berman, E., Curr. Opin. Hematol., 4: 205-11 (1999) and Bruservd, O. et al., Stem Cells, 18: 157-65 (2000).) The major therapeutic approach to this disease has been the use of chemotherapeutic agents with associated life-threatening toxicity. Although non-specific in their effects, these regimens have significantly increased the survival of AML patients. (See Saez, R. A., Cancer Control, 4: 399-406 (1997); Bruservd, O. et al., Stem Cells, 18: 343-351 (2000); and Stein, A. S. et al., Leukemia, 14: 1191-1196 (2000).) Recently, more targeted therapy has been developed. Treatment of acute promyelocytic leukemia (APL) patients with transretinoic acid (tRA) results in the differentiation of the cells with 90 percent of the patients achieving a complete remission. (See Chen, Z. X. et al., Blood, 78: 1413-1419 (1991); Castaigne, S. et al., Blood, 76: 1704-1709 (1990); and Warrell, R. P. et al., N. Engl. J. Med., 324: 1385-1393 (1991). tRA exerts its effect by modulating gene expression through its role as a ligand to the retinoic acid nuclear receptors (RARs) with the subsequent binding of this complex to the RARE consensus sequences located in the regulatory regions of retinoid-responsive genes. The selective sensitivity of APL cells to tRAmediated differentiation resides in their specific expression of a unique PMLRAR.alpha. fusion product with subsequent maturation arrest of these cells at the promyelocyte stage; exposure of these cells to a micromolar concentration of tRA allows for the degradation of the PML-RAR.alpha. fusion product and restitution of normal RAR.alpha. receptor function with subsequent maturation of the APL cells. Z. M. Shao et al.(1995) have recently shown that the retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]2-naphthalenecarboxylic acid (AHPN) is a potent inducer of apoptosis in a number of cell types. Both natural and synthetic retinoids exert their biological action through their binding to and activation of specific RARs and retinoic acid X nuclear receptors (RXRs). These receptors complexed with ligand and bound to specific regions in the promoters of genes designated as retinoid response elements (RAREs and RXREs) modulate gene expression. AHPN does not bind to the RXRs, is an extremely poor binder and transactivator of the RAR subtype.alpha., but at 1.mu.M binds and transactivates RAR.beta. and RAR.gamma. Whether AHPN induces apoptosis through activation of these receptors is still controversial. AHPN exposure results in apoptosis of the human leukemia cell line HL-60R, which lacks functional RARs, and the cell line K562, which is resistant to the antiproliferative actions of tRA. These results suggest that AHPN induces cell death at least in myeloid leukemia cells through a novel pathway that does not involve its direct interaction with the retinoid receptors. AHPN also causes the rapid activation of the MAPK kinase pathway by inducing the activation of the p38 and JNK kinases within 1 hour. Activation of these kinases is not observed following exposure of the cells to standard retinoids that function through classical RAR/RXR-signaling pathways. JNK activation has been implicated as a major player in the induction of apoptosis by a number of agents and has recently been shown to result in p53 activation and subsequent p53-mediated-apoptosis in sympathetic neurons. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Inhibition of chronic myelogenous leukemic cell growth by liposomal-antisense oligodeoxy-nucleotides targeting to Grb2 or Crk1 Inventor(s): Tari, Ana M.; (Houston, TX), Arlinghaus, Ralph B.; (Bellaire, TX), LopezBerestein, Gabriel; (Bellaire, TX) Correspondence: FULBRIGHT & JAWORSKI L.L.P.; 600 CONGRESS AVE.; SUITE 2400; AUSTIN; TX; 78701; US Patent Application Number: 20030153526 Date filed: December 20, 2002 Abstract: The present invention provides novel compositions and methods for use in the treatment of cancer, specifically, in the treatment of chronic myelogenous leukemia (CML). The compositions contain antisense oligonucleotides that hybridize to Grb2 and Crkl nucleic acids, the gene products of which are known to interact with the tumorigenic protein bcr-abl. Used alone, in conjunction with each other, and even in conjunction with antisense oligonucleotides directed to bcr-abl nucleic acids, these compositions inhibit the proliferation of CML cancer cells. Excerpt(s): The present invention relates to the field of cancer therapy, specifically, the treatment of chronic myelogenous leukemia. More particularly, these treatments involve the use of antisense oligonucleotides and liposomal formulations thereof. Chronic myelogenous leukemia (CML) is a hematologic malignancy in which uncontrolled proliferation of granulocytes occurs. It often is characterized by the reciprocal translocation of chromosomes 9 and 22, which relocates the Ableson (abl) protooncogene onto the 3'-end of the breakpoint cluster region (bcr). This produces a chimeric bcr-abl gene encoding a p210.sup.bcr-abl fusion protein, which is tumorigenic and is necessary for the growth of CML cells (Szczylik et al., 1991; Skorski et al., 1994; Tari et al., 1994; McGahon et al., 1994; Bedi et al., 1994). The bcr-abl protein can autophosphorylate at the 177 tyrosine amino acid found within the first exon of bcr. When phosphorylated, the bcr domain of the bcr-abl protein binds to the SH2 domain of the growth factor receptor-bound protein 2 (Grb2) adaptor protein. Through the SH3 domain, Grb2 binds to the human Son of sevenless 1 (hSos1) GDP/GTP exchange factor resulting in ras protein activation. The bcr-abl protein can also transphorylate the 177 tyrosine amino acid found within the normal bcr protein. It is believed that when the normal bcr protein becomes tyrosine phosphorylated at amino acid 177, it also will complex with Grb2. When the bcr-abl protein is expressed, the p46 and p52 Shc (Puil et al., 1994) proteins become tyrosine phosphorylated as well. These Shc proteins have also been shown to form stable complexes with Grb2. Therefore, Grb2 appears to play a very important role in the tumorigenicity mediated by the bcr-abl protein (Puil et al., 1994; Pendergast et al., 1993). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for examining wt1-related disease Inventor(s): Sugiyama, Haruo; (Mino-shi, JP) Correspondence: SUGHRUE MION, PLLC; 2100 PENNSYLVANIA AVENUE, N.W.; WASHINGTON; DC; 20037; US Patent Application Number: 20030138863 Date filed: November 22, 2002
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Abstract: The invention provides a method for testing a WT1-related disease, such as leukemia, a solid cancer, or an atypia, for diagnosing the disease, evaluating the course of cure and the prognosis of the disease more simply with high reliability, the method comprises measuring the amount of antibody against WT1 in a sample and using the measurement value and the time course of the value as a clinical marker for the testing. Excerpt(s): This invention relates to an examination method for WT1-related disease and more particularly to a method of testing for the presence of such a disease and of evaluating the progression, course of cure, and prognosis of the disease. WT1 gene is a zinc finger transcription factor isolated as a gene etiologically associated with Wilms' tumor and its gene product (WT1 protein) has a structure comprising a repression domain, an activation domain, and a zinc finger. The inventors previously reported that the expression level of WT1 gene is high in acute leukemia, that this expression level is inversely correlated with the prognosis of the disease, and that the MRD (minimal residual disease) of acute leukemia can be detected by measuring said expression level [Blood, Vol.84, No.9, p3071 (1994)]. Furthermore, the inventors found that by measuring the expression level of WT1 gene, various types of solid cancer and tissue atypia can be detected (WO97/39354). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Method for inducing differentiation of embryonic stem cells into functioning cells Inventor(s): Gu, Yanjun; (Sakyo-ku, JP), Inoue, Kazutomo; (Sakyo-ku, JP), Kim, Dohoon; (Sakyo-ku, JP), Ishii, Michiyo; (Kamigyo-ku, JP) Correspondence: BIRCH STEWART KOLASCH & BIRCH; PO BOX 747; FALLS CHURCH; VA; 22040-0747; US Patent Application Number: 20030162290 Date filed: January 25, 2002 Abstract: The present invention provides a 4-step method for inducing differentiation of embryonic stem cells into functioning cells comprising 1) expanding ES cells; 2) inducing Embryoid Bodies in the presence of leukemia Inhibitor factor and basic FGF; 3) selection expanding of the EBs and 4) differentiation. According to the present invention, ES cells can be differentiated into either insulin producing pancreatic islet like cell clusters or nerve like cells. Thus obtained functioning cells may be potential sources of donor cells in cell transplant therapy for many patients. Excerpt(s): The present invention relates to a method for inducing differentiation of mammalian embryonic stem cells into functioning cells. The present invention also relates to the functioning cells obtained by the present invention and a method for treatment of a patient by implanting functioning cells to the patient. Pluripotent stem cells have been derived from two embryonic sources. Embryonic stem (ES) cells are derived from the inner cell mass of preimplantation embryos, and embryonic germ (EG) cells are derived from primordial germ cells (PGCs). Both ES and EG cells are pluripotent and demonstrate germ-line transmission in experimentally produced chimeras. Mouse ES and EG cells share several morphological characteristics such as high levels of intracellular alkaline phosphatase (AP), and presentation of specific cell surface glycolipids and glycoproteins. These properties are characteristic of, but not specific for, pluripotent stem cells. Other important characteristics include growth as multicellular colonies, normal and stable karyotypes, the ability to be continuously passaged, and the capability to differentiate into cells derived from all three embryonic
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germ layers. Pluripotent stem cell lines that share most of these characteristics also have been reported for chicken, mink, hamster, pig, rhesus monkey, and common marmoset. Also a stem cell is a cell that has the ability to divide (self-replication) for indefinite periods--often throughout the life of the organism. Under the right conditions, or given the right signals, stem cells can give rise (differentiate) to the many different cell types that make up the organism. Recently, S. H. Lee et al. (Nature Biotechnology 18, 675-679 (2000), the disclosure of the publication is herein incorporated by reference) disclosed to generate CNS progenitor populations from ES cells, to expand these cells and to promote their differentiation into dopaminergic and serotonergic neurons in the presence of mitogens and specific signaling molecules. The differentiation and maturation of neuronal cells was completed after mitogen withdrawal from the growth medium. This experimental system provides a powerful tool for analyzing the molecular mechanisms controlling the functions of these neurons in vitro and in vivo, and potentially for understanding and treating neurodegenerative and psychiatric diseases. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Method for the rapid and ultra-sensitive detection of leukemic cells Inventor(s): Sacchi, Nicoletta; (Gaithersburg, MD), Nisson, Paul E.; (Gaithersburg, MD) Correspondence: STERNE, KESSLER, GOLDSTEIN & FOX PLLC; 1100 NEW YORK AVENUE, N.W.; WASHINGTON; DC; 20005; US Patent Application Number: 20030170715 Date filed: March 24, 2003 Abstract: An improved method is disclosed for diagnosing the presence of a chromosomal translocation characteristic of acute myelogenous leukemia. Nucleic acid molecules that may be used in this improved method are described. Excerpt(s): The invention relates to improved methods for diagnosing the presence or onset of acute myelogenous leukemia (AML) in an individual. The invention also pertains to nucleic acid probes that are capable of recognizing a chromosomal translocation that is characteristic of AML. Leukemia is a progressive, malignant disease of the blood-forming organs, characterized by the abnormal proliferation and development of leukocytes, and their precursors in the blood and bone marrow. The disease is classified clinically on the basis of (1) whether the condition is acute or chronic, (2) whether it involves myeloid (i.e. myelogenous), lymphoid (nonmyelogenous) or monocytic cells, and (3) whether it is associated with an increase in the concentration of abnormal cells in the blood. A characteristic of leukemia is the presence of specific chromosomal abnormalities which are considered to be involved in tumor development (Rabbitts, T., Cell 67:641-644 (1991); Cleary, M. L., Cell 66:619-622 (1991), both herein incorporated by reference). In acute leukemia, such chromosomal abnormalities frequently activate transcription factors. These factors are often important in differentiation. Thus, for example, the activation of the c-myc gene, is associated with T-cell acute leukemia. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for treating chronic myelogenous leukemia Inventor(s): Lyons, John; (Moraga, CA) Correspondence: WILSON SONSINI GOODRICH & ROSATI; 650 PAGE MILL ROAD; PALO ALTO; CA; 943041050 Patent Application Number: 20030147813 Date filed: February 7, 2002 Abstract: Methods, compositions and kits are provided for treating cancer associated with protein tyrosine kinase activity such as chronic myelogenous leukemia. In particular, a treatment method is provided comprising: administering to a patient having chronic myelogenous leukemia and a degree of resistance to imatinib mesylate, a therapeutically effective amount of a DNA methylation inhibitor which mitigates the imatinib mesylate resistance. Excerpt(s): The invention relates to methods, compositions, and kits for treating cancer associated with protein tyrosine kinase activity, and more particularly for treating chronic myelogenous leukemia. Chronic Myelogenous Leukemia (CML) is a myeloproliferative disorder of a pluripotent hematopoietic stem cell with a particular cytogenetic abnormality, the Philadelphia chromosome. Faderl et al (1999) Ann. Intern. Med. 131: 207-219. In childhood, it accounts for only 2 to 5% of all malignant disorders and presents as either of two distinct clinical entities, adult-type CML and juvenile CML. Adult-type CML of childhood is indistinguishable from that seen in older patients. However, juvenile CML is restricted to children and is Philadelphia chromosome negative. Grier and Civin (1998) in (Nathan and Oski, eds) Hematology of Infancy and Childhood, volume 2, 5th ed, W. B. Saunders Company, 34:1286-1459. CML is a progressive, uniformly fatal disease in untreated patients. It is characterized by three distinct phases: a chronic phase lasting three to five years; an acute or accelerated phase lasting three to six months; and a brief blastic crisis phase. The progression of the disease to blast crisis results in rapid death due to infections, bleeding and leukemic organ infiltration. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of isolating extract from the euphorbaciae obesa plant and methods for using the same Inventor(s): Newman, Robert A.; (Sugarland, TX), McMurray, John S.; (Houston, TX), Sample, David C.; (Porter, TX), Perez, Margot; (Houston, TX), Donato, Nicholas D.; (San Marcos, CA), Donato, Nicholas J.; (Sugarland, TX) Correspondence: FOLEY & LARDNER; P.O. BOX 80278; SAN DIEGO; CA; 92138-0278; US Patent Application Number: 20030118677 Date filed: December 12, 2001 Abstract: The present invention is directed to a process of isolating an extract from a Euphorbaciae obesa (EO) plant by: preparing a sample of said plant comprising removal of the latex material; dissolving said sample with first solvent to form a solution; seperating said solution into a liquid and a pulp fraction; and purifying said pulp fraction. The isolated EO extract induces apoptosis and inhibits growth of a cancerous cell. Thus, the present invention is also directed to a method for inducing apoptosis and
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growth inhibition of a cancerous cell by contacting the cell with an effective amount of the EO extract by the process of the invention. Preferably, the extract is administered both to the tumor directly and intravenously. The preferred lines of cancerous cells are melanoma, non-small cell lung cancer, prostate cancer, breast carcinoma, ovarian cancer, lymphoma and leukemia cells. Excerpt(s): This invention generally relates to compounds for treating cancer that are derived from plants and, in particular, the isolation and use of an extract from a Euphorbaciae obesa plant having anti-tumor effects on a variety of cancerous cells. Plants and marine organisms provide a rich source of compounds that have been investigated and exploited for a variety of medicinal and biological applications. The Euphorbiaceae family is one of the largest families of plants with about 300 genera and 7,500 species, mostly monoecious herbs, shrubs and trees, sometimes succulent and cactus-like, that are further frequently characterized by a milky sap or latex material. Members of the Euphorbiaceae family have been investigated as providing potential treatments for cancers, tumors and warts. Active components found in members of this plant family may be common to several genera or species of the family or may be limited to a particular genus or species. Certain Euphorbiaceae species have been shown to synthesize phorbol ester and diterpene diester compounds having therapeutic effects on certain cancers. For instance, the isolation and characterization of antileukemic properties from Euphorbia esula L and Croton tiglium L. have been reported. S. M. Kupchan et al., Science 191: 571-572 (1976). The fractionation of an active extract led to the characterization of the antileukemic component from Euphorbia esula L as a diterpene diester. Fractionation of croton oil led to the characterization of the active component known as a phorbol diester, phorbol 12-tiglate 13-decanoate. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Method of screening apoptosis inducing substances Inventor(s): Fukushima, Naoshi; (Gotemba-shi, JP), Fukushima, Naoshi; (Gotemba-shi, JP) Correspondence: OBLON, SPIVAK, MCCLELLAND, MAIER & NEUSTADT, P.C.; 1940 DUKE STREET; ALEXANDRIA; VA; 22314; US, OBLON, SPIVAK, MCCLELLAND, MAIER & NEUSTADT, P.C.; 1940 DUKE STREET; ALEXANDRIA; VA; 22314; US Patent Application Number: 20030157577 Date filed: March 6, 2003 Abstract: The present invention provides a method of screening substances having property of causing apoptosis, and relates to a method of screening substances having property of causing apoptosis characterized by using cells which are expressing IAP (Integrin Associated Protein), and the relates to above screening method, wherein the cells used are myeloid cells, and relates to pharmaceutical compositions containing as the active ingredient the substances obtained by the above method, and the present invention makes it possible to differentiate, identify and screen readily and highly efficiently the substances, such as antibodies and the like, that have property of causing apoptosis on myeloid cells by using cells which are expressing IAP while using specific binding reactions of the substances, and the above specific substances thus obtained can be used by virtue of their characteristics as the active ingredient of pharmaceutical compositions such as anticancer agents and medicines for myelocytic leukemia and the like.
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Excerpt(s): The present invention relates to a method of screening substances having property of causing apoptosis and the like, in particular, relates to a novel screening method which makes it possible to screen readily and highly efficiently the substances, such as monoclonal antibodies and the like, that have property of causing apoptosis on myeloid cells by using cells which are expressing IAP (Integrin Associated Protein), and relates to the substances having property of causing apoptosis obtained by the above screening method, pharmaceutical compositions containing as the active ingredient the above substances, and relates to substances having property of causing apoptosis which have a specific binding activity to IAP, pharmaceutical compositions containing as the active ingredient the above substances. The present invention relates to a method of screening substances having property of causing apoptosis and the like, in particular, relates to a novel screening method which makes it possible to screen readily and highly efficiently the substances, such as monoclonal antibodies and the like, that have property of causing apoptosis on myeloid cells by using cells which are expressing IAP (Integrin Associated Protein), and relates to the substances having property of causing apoptosis obtained by the above screening method, pharmaceutical compositions containing as the active ingredient the above substances, and relates to substances having property of causing apoptosis which have a specific binding activity to IAP, pharmaceutical compositions containing as the active ingredient the above substances. Granulocyte colony-stimulating factors, for example, recombinant granulocyte colonystimulating factors (rG-CSF), have been known primarily as humoral factors to stimulate the differentiation and proliferation of granulocyte cells, and it has been reported in an experiment upon mice in vivo that the administration of rG-CSF enhances the hematopoiesis of the bone marrow and in addition causes remarkable extramedullary hematopoiesis in the spleen to proliferate hematopoietic stem cells and all hematopoietic precursor cells in the spleen. And it has been thought as extramedullary hematopoietic mechanism in the spleen that hematopoiesis occurs due to a splenic hematopoietic microenvironment modifications according to the stimulation of rG-CSF to enhance hematopoietic potential. Granulocyte colony-stimulating factors, for example, recombinant granulocyte colony-stimulating factors (rG-CSF), have been known primarily as humoral factors to stimulate the differentiation and proliferation of granulocyte cells, and it has been reported in an experiment upon mice in vivo that the administration of rG-CSF enhances the hematopoiesis of the bone marrow and in addition causes remarkable extramedullary hematopoiesis in the spleen to proliferate hematopoietic stem cells and all hematopoietic precursor cells in the spleen. And it has been thought as extramedullary hematopoietic mechanism in the spleen that hematopoiesis occurs due to a splenic hematopoietic microenvironment modifications according to the stimulation of rG-CSF to enhance hematopoietic potential. Hence, the present inventors have noted splenic stromal cells administered rG-CSF with a view to clarifying the hematopoietic potential in the spleen, and established a hematopoietic stromal cell line (CF-1 cells) from the spleen of a mouse administered rG-CSF with a view to attempting the analysis of the enhancement of-the hematopoietic potential by stromal cells with rG-CSF, and examined the potential effect on hematopoiesis using the hematopoietic stromal cells, and as a result, colony-stimulating activities in vitro and potency supportive of hematopoietic stem cells in vivo have been recognized [Blood, 80, 1914 (1992)]. Hence, the present inventors have noted splenic stromal cells administered rG-CSF with a view to clarifying the hematopoietic potential in the spleen, and established a hematopoietic stromal cell line (CF-1 cells) from the spleen of a mouse administered rG-CSF with a view to attempting the analysis of the enhancement of-the hematopoietic potential by stromal cells with rG-CSF, and examined the potential effect on hematopoiesis using the hematopoietic stromal cells, and as a result, colony-
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stimulating activities in vitro and potency supportive of hematopoietic stem cells in vivo have been recognized [Blood, 80, 1914 (1992)]. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Method of treatment Inventor(s): Bucci, Tamara Ann Michelle; (Victoria, AU), Bartlett, Perry Francis; (Brisbane, AU), Kilpatrick, Trevor John; (Victoria, AU), Butzkueven, Helmut; (Victoria, AU), Shipham, Kylie Ann-Maree; (Victoria, AU) Correspondence: Edward W Grolz; Scully Scott Murphy & Presser; 400 Garden City Plaza; Garden City; NY; 11530; US Patent Application Number: 20030162700 Date filed: April 9, 2003 Abstract: The present invention relates generally to a method of treatment and to agents useful for same. More particularly, the present invention contemplates a method for the treatment and/or prophylaxis of a nervous system disease, demyelinating disease and/or an inflammatory disease of either the central or peripheral nervous system such as but not limited to an encephalopathic condition and even more particularly an encephalomyelopathic condition. The present invention further provides the use of leukemia inhibitory factor or derivatives, homologous or analogues thereof in the manufacture of a medicament for the treatment and/or prophylaxis of a nervous system disease, demyelinating disease and/or an inflammatory disease of either the central or peripheral nervous system such as but not limited to an encephalopathic and more particularly an encephalomyelopathic condition. Leukemia inhibitory factor may be used alone or in combination with one or more other therapeutic molecules such as but not limited to other cytokines. The method of the present invention enables the development of a therapeutic protocol for conditions such as multiple sclerosis, optic neuritis and other single episodes of central demyelination, transverse myelitis, HIVinduced leucoencephalopathy or chemotherapy induced leucoencephalopathy. Excerpt(s): The present invention relates generally to a method of treatment and to agents useful for same. More particularly, the present invention contemplates a method for the treatment and/or prophylaxis of a nervous system disease, demyelinating disease and/or an inflammatory disease of either the central or peripheral nervous system such as but not limited to an encephalopathic condition and even more particularly an encephalomyelopathic condition. The present invention further provides the use of leukemia inhibitory factor or derivatives, homologous or analogues thereof in the manufacture of a medicament for the treatment and/or prophylaxis of a nervous system disease, demyelinating disease and/or an inflammatory disease of either the central or peripheral nervous system such as but not limited to an encephalopathic and more particularly an encephalomyelopathic condition. Leukemia inhibitory factor may be used alone or in combination with one or more other therapeutic molecules such as but not limited to other cytokines. The method of the present invention enables the development of a therapeutic protocol for conditions such as multiple sclerosis, optic neuritis and other single episodes of central demyelination, transverse myelitis, HIVinduced leucoencephalopathy or chemotherapy induced leucoencephalopathy. Reference to any prior art in this specification is not, and should not be taken as, an acknowledgment or any form of suggestion that this prior art forms part of the common general knowledge in Australia or any other country. Bibliographic details of the publications numerically referred to in this specification are collected at the end of the
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description. Leukemia inhibitory factor (LIF) is a cytokine which exhibits a range of activities on a number of different cell types. For example, LIF is capable of maintaining embryonic stem (ES) cells in culture while retaining pluripotency. LIF is also capable of stimulating bone formation. Furthermore, LIF exhibits activity within the nervous and immune systems. For example, LIF promotes the survival of oligodendrocytes, the cells responsible for myelinating the central nervous system (CNS). It also acts as an antinflammatory and analgesic cytokine with the capacity to modulate expression of the pro-inflammatory cytokine, tumor necrosis factor-.alpha. (TNF-.alpha.), as well as interleukin-6 (I-6). LIF is, therefore, a pleiotropic molecule. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Methods and compositions relating to fortilin, an anti-apoptotic molecule, and modulators of fortilin Inventor(s): Yeh, Edward T.H.; (Houston, TX), Fujise, Ken; (Houston, TX) Correspondence: FULBRIGHT & JAWORSKI L.L.P.; A REGISTERED LIMITED LIABILITY PARTNERSHIP; SUITE 2400; 600 CONGRESS AVENUE; AUSTIN; TX; 78701; US Patent Application Number: 20030172388 Date filed: October 30, 2001 Abstract: The polypeptide Fortilin (also known as Translationally Controlled Tumour Protein, TCTP) specifically interacts with p53, a tumor suppressor involved in the induction of apoptosis and the normal growth regulation of a cell. Fortilin also specifically binds MCL1 (Myeloid Cell Leukemia 1). Fortilin has the ability to prevent apoptosis, which may be unregulated in hyperproliferative cells. The present invention is directed at compositions and methods involving a Fortilin modulator, which can induce apoptosis, for the prevention, treatment, or diagnosis of hyperproliferative diseases and conditions, including cancer and atherosclerosis. It is directed also at compositions and methods involving Fortilin, which can inhibit apoptosis, for the treatment of diseases and condition characterized by apoptosis, including certain vascular conditions. Excerpt(s): The present application claims priority to co-pending U.S. Provisional Patent Application Serial No. 60/244,416 filed on Oct. 30, 2000. The entire text of the abovereferenced disclosure is specifically incorporated herein by reference without disclaimer. The government may own rights in the present invention pursuant to grant number 1KO8HL04015 from the National Institutes of Health. The present invention relates generally to the fields of biochemistry, molecular biology, and diagnosis and therapy for hyperproliferative cell diseases and conditions, such as cancer and atherosclerosis. More particularly, it concerns a Fortilin polypeptide, the gene or transcript encoding it, modulators of Fortilin and their relevance to cancer and vascular diseases. Heart disease and cancer are the leading causes of death, respectively, in the United States. In 1997, 41.2 percent of deaths in the United States (953,110 lives) were caused by a cardiovascular disease, and cancer caused 539,377 deaths (americanheart.org). More than a million Americans are expected to have a heart attack a year, while cancer strikes one in two men and one in three women (Landis, 1998). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods of treating leukemia Inventor(s): Kantarjian, Hagop; (Houston, TX), Giles, Francis; (Houston, TX), Jolivet, Jacques; (Laval, CA) Correspondence: MILLEN, WHITE, ZELANO & BRANIGAN, PC; 2200 CLARENDON BLVD; SUITE 1400; ARLINGTON; VA; 22201; US Patent Application Number: 20030125305 Date filed: November 4, 2002 Abstract: The present invention provides a novel method for treating leukemia in a host that has been previously treated with a Brc-Abl tyrosine kinase inhibitor comprising administering to the host a therapeutically effective amount of a compound having the formula I: 1wherein B is cytosine or 5-fluorocytosine and R is selected from H, monophosphate, diphosphate, triphosphate, carbonyl substituted with a C.sub.1-6 alkyl, C.sub.2-6 alkenyl, C.sub.2-6 alkynyl, C.sub.6-10 aryl, and 2wherein each Rc is independently selected from the group comprising H, C.sub.1-6 alkyl, C.sub.2-6 alkenyl, C.sub.2-6 alkynyl an hydroxy protecting group. Excerpt(s): This application claims the benefit of U.S. Provisional Application Serial No. 60/330,891 filed Nov. 2, 2001 which is hereby incorporated in its entirety. The present invention relates to methods for treating leukemia, and more particularly, to the use of nucleoside analogues as an effective treatment for acute or chronic myelogenous leukemia. Leukemia is a malignant cancer of the bone marrow and blood. It is characterized by the uncontrolled growth of blood cells. The common types of leukemia are divided into four categories: acute or chronic myelogenous, involving the myeloid elements of the bone marrow (white cells, red cells, megakaryocytes) and acute or chronic lymphocytic, involving the cells of the lymphoid lineage. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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MLL translocations specify a distinct gene expression profile, distinguishing a unique leukemia Inventor(s): Armstrong, Scott A.; (Wayland, MA), Korsmeyer, Stanley J.; (Weston, MA), Golub, Todd R.; (Newton, MA) Correspondence: HAMILTON, BROOK, SMITH & REYNOLDS, P.C.; 530 VIRGINIA ROAD; P.O. BOX 9133; CONCORD; MA; 01742-9133; US Patent Application Number: 20030134300 Date filed: July 17, 2002 Abstract: The present invention relates to the diagnosis of mixed lineage leukemia (MLL), acute lymphoblastic leukemia (ALL), and acute myelogenous leukemia (AML) according to the gene expression profile of a sample from an individual, as well as to methods of therapy and screening that utilize the genes identified herein as targets. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/306,103 filed on Jul. 17, 2001. The entire teachings of the above application are incorporated herein by reference. A subset of human acute leukemias with a decidedly unfavorable prognosis possess a chromosomal translocation involving the Mixed Lineage Leukemia (MLL, HRX, AU-1) gene on chromosome segment 11q23. The leukemic cells, which typically have a lymphoblastic morphology, have been classified as Acute Lymphoblastic Leukemia (ALL). However, unlike the majority of childhood
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ALL, the presence of the MLL translocations often results in an early relapse after chemotherapy. As MLL translocations are typically found in leukemias of infants and chemotherapy-induced leukemia, it has remained uncertain whether host related factors or tumor-intrinsic biological differences are responsible for the poor survival in patients with the translocations. Lymphoblastic leukemias with either rearranged or germline MLL are similar with respect to most morphological and histochemical characteristics. Immunophenotypic differences associated with lymphoblasts bearing an MLL translocation include the lack of the early lymphocyte antigen CD 10, expression of the proteoglycan NG2, and the propensity to co-express the myeloid antigens CD15 and CD65. This prompted the corresponding disease to be called Mixed Lineage Leukemia and suggested models, largely unresolved, in which the leukemia reflects disordered cell fate decisions or the transformation of a more multi-potential progenitor. Generally, therapeutic treatment is more successful when tailored to the specific type of leukemia. Thus, a need exists for accurate and efficient methods for diagnosis of leukemia and identification of subclasses of leukemias. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Modulating lymphoid commitment and survival Inventor(s): Aster, Jon C.; (Lexington, MA), Pear, Warren S.; (Philadelphia, PA), Izon, David J.; (Wembley, AU), Allman, David; (Havertown, PA), He, Yiping; (Philadelphia, PA) Correspondence: Evelyn H. McConathy; Dilworth Paxson LLP; 3200 Mellon Bank Center; 1735 Market Street; Philadelphia; PA; 19103; US Patent Application Number: 20030181380 Date filed: March 10, 2003 Abstract: Provided are methods for manipulating aspects of lymphopoiesis by modulating and controlling Notch signaling, thereby providing treatment for diseases of the immune system. Accordingly, there are provided methods for selectively modulating T cell fate commitment of a common lymphoid progenitor at the expense of B cell fate commitment, and in the converse for selectively modulating B cell fate commitment of a common lymphoid progenitor at the expense of T cell fate commitment. Also provided are methods for treating patients suffering from a disease or disorder of T cell origin, or conversely of B cell origin. Further provided are methods for selectively killing B cells in a committed population of B cells, such as in a patient suffering from B cell leukemia or lymphoma; as well as methods for selectively killing T cells in a committed population of T cells such as in a patient suffering from diseases of T cell origin. Excerpt(s): This application claims priority to U.S. Provisional Application Nos. 60/363,018, filed Mar. 8, 2002, and 60/277,422, filed Mar. 21, 2001, the content of which is herein incorporated by reference. The present invention relates to compositions and methods useful in the treatment and prevention of diseases of the immune system, such as leukemias, specifically relating to controlling the effect of Notch signaling on lymphoid differentiation and cell fate decisions. B cell development begins in the bone marrow (BM), where the earliest B cells derive from a common lymphocyte progenitor, that is also capable of producing T and NK cells (Kondo et al., Cell 91:661-672. (1997); Izon et al., J. Immunol. 167:1387-1392. (2001b); Gounari et al., Nat. Immunol. 3:489-96. (2002); Igarashi et al., Immunity 17:117-130. (2002)). B cell development in the BM occurs in successive stages during which the immunoglobulin (Ig) genes are rearranged and
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expressed to produce a naive B cell that expresses surface immunoglobulin of a single antigen specificity (Hardy et al., Immunol. Rev 175:23-32. (2002); Janeway et al., (2001) Immunobiology, 5th ed., New York: Garland Publishing; Rolink et al., Curr. Opin. Immunol. 13:202-207. (2001)). The earliest B lineage cells, originating from a subset of hematopoietic stem cells known as early lymphoid progenitors (ELPs), are termed pro-B cells, and it is in these cells that Ig rearrangement begins (Igarashi et al., 2002). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Monoclonal antibody inducing apoptosis Inventor(s): Fukushima, Naoshi; (Gotemba-shi, JP), Uno, Shinsuke; (Gotemba-shi, JP) Correspondence: FOLEY AND LARDNER; SUITE 500; 3000 K STREET NW; WASHINGTON; DC; 20007; US Patent Application Number: 20030157100 Date filed: March 10, 2003 Abstract: The monoclonal antibodies of this invention are antibodies that specifically recognize human Integrin Associated Protein, and the antigens that induce apoptosis of nucleated blood cells having human Integrin Associated Protein. Accordingly, they are useful as antibodies that recognize human Integrin Associated Protein for its distinction and identification, while also having an action of inducing apoptosis of nucleated blood cells; these properties can be utilized to prepare useful therapeutic agents in the field of treatment for myeloid leukemia and lymphoid leukemia. Excerpt(s): This invention relates to novel monoclonal antibodies having the property of inducing apoptosis of nucleated blood cells with Integrin Associated Protein (IAP), as well as to their fragments, peptides and low molecular compounds, and to hybridomas that produce the monoclonal antibodies. The novel antibodies are useful as therapeutic agents for myeloid leukemia and lymphoid leukemia. Granulocyte colony-stimulating factors, such as recombinant granulocyte colony-stimulating factor (rG-CSF), have been known in the prior art as humoral factors that stimulate differentiation and proliferation of granulocytes. Reports based on in vivo experiments with mice have shown that administration of rG-CSF results in not only accelerated myelopoiesis in bone marrow but also notable extramedullary hemopoiesis in the spleen, and proliferation of all hemopoietic precursor cells, including hemopoietic stem cells, in the spleen. The mechanism of such extramedullary hemopoiesis in the spleen has been believed that stimulation by rG-CSF alters the hemopoietic microenvironment of the spleen and promotes the hemopoiesis supporting ability thereof, thus inducing hemopoiesis. In order to elucidate the hemopoietic function in the spleen, the present inventors have previously focused on stromal cells of the spleen following repeated administration of rG-CSF. The inventors have made efforts to examine how the hemopoietic function is promoted by rG-CSF via stromal cells, and have established a hemopoietic stromal cell line (CF-1 cells) from mouse spleen by-repeated administration of rG-CSF. The inventors have studied the hemopoiesis-supporting ability of the hemopoietic stromal cells and confirmed the colony-stimulating activity in vitro and the hemopoietic stem cellsupporting ability in vivo [Blood, 80, 1914-(1992)]. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Mouse model for HIV infection utilizing a chimeric HIV/MLV Gag protein that permits efficient assembly from murine cells Inventor(s): Chen, Benjamin K.; (Brookline, MA), Kim, Peter S.; (Bryn Mawr, PA) Correspondence: HAMILTON, BROOK, SMITH & REYNOLDS, P.C.; 530 VIRGINIA ROAD; P.O. BOX 9133; CONCORD; MA; 01742-9133; US Patent Application Number: 20030177509 Date filed: September 4, 2002 Abstract: Functional chimeric proteins that comprise HIV Gag protein and a Gag protein of non HIV origin (e.g., of viral or retroviral origin other than HIV origin) and overcome the block to HIV assembly in non human cells. One embodiment of the present invention is chimeras between HIV Gag protein and a Gag protein from a murine virus, such as Moloney Murine Leukemia Virus (MLV) Gag protein, that overcome the block to HIV assembly in mouse cells. Excerpt(s): This application claims the benefit of the filing date of U.S. Provisional Application No. 60/316,999, filed Sep. 4, 2001 and entitled Mouse Model for HIV Infection Utilizing a Chimeric HIV/MLV Gag Protein That Permits Efficient Assembly From Murine Cells, by Benjamin K. Chen and Peter S. Kim and U.S. Provisional Application No. 60/340,619, filed Dec. 10, 2001 and entitled Mouse Model for HIV Infection Utilizing a Chimeric HIV/MLV Gag Protein That Permits Efficient Assembly From Murine Cells, by Benjamin K. Chen and Peter S. Kim The teachings of these referenced applications are expressly incorporated herein by reference. The present invention relates to functional chimeras comprising HIV Gag protein and Gag protein of non HIV origin (e.g., of viral origin or retroviral origin other than HIV origin) that overcome the block to HIV assembly in non human cells. The functional chimeras can additionally comprise further components, as described herein The functional chimeras can comprise a.) complete HIV Gag protein or less than the complete HIV Gag protein and b.) complete Gag protein of non HIV origin or less than a complete Gag protein of non HIV origin. The functional chimeras can comprise, for example, HIV Gag protein and a Gag protein from a murine virus, such as Moloney Murine Leukemia Virus (MLV) Gag protein. A functional chimera can comprise. for example, complete HIV Gag protein and a portion of MLV Gag protein such as MLV Gag matrix (MA) protein, or MLV Gag MA protein and MLV p12 protein Alternatively, functional chimeras of the present invention comprise less than a complete HIV Gag protein and Gag protein of non HIV origin or a portion of a Gag protein of non HIV origin. In specific embodiments, functional chimeras of the present invention comprise a.) HIV Gag protein that lacks the HIV Gag MA domain or a portion of the MA domain and b.) all or a portion of the MA domain of a Gag protein of non HIV origin, such as the MA domain of MLV. In these embodimdents, the MA domain(s) or MA domain portions present must be of sufficient composition (amino acid residues) to overcome the block to HIV assembly that occurs in non human cells. For example, a functional chimera can comprise a.) HIV Gag protein that lacks the HIV Gag MA domain and b.) a complete MA domain of non HIV origin, such as the MA domain of MLV. Alternatively, a functional chimera can comprise a.) HIV Gag protein that includes a partial HIV Gag MA domain and b.) a complete MA domain of non HIV origin, such as the MA domain of MLV. In additional embodiments, the functional chimeras can comprise a.) HIV Gag protein that lacks the HIV Gag MA domain and b.) a portion of a MA domain of non HIV origin, such as the MA domain of MLV or can comprise a.) HIV Gag protein that includes a partial EMV Gag MA domain and b.) a complete MA domain of non HIV origin, such as the MA domain of MLV. In specific embodiments of the present
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invention, HIV p17 MA is replaced with p15 of MLV Gag. In further embodiments, the functional chimeras additionally comprise MLV p12 protein or a sufficient portion to overcome the block to HIV assembly in non human cells. In these embodiments, for example, a functional chimera can comprise a.) HIV Gag protein that lacks the HIV Gag MA domain and b.) a complete MA domain of non HIV origin, such as the MA domain of MLV, and MLV p12 protein or a sufficient portion to overcome the block to HIV assembly in non human cells. Alternatively, a functional chimera can comprise a.) HIV Gag protein that includes a partial HIV Gag MA domain and b.) a complete MA domain of non HIV origin, such as the MA domain of MLV and MLV p12 protein or a sufficient portion to overcome the block to HIV assembly in non human cells. In additional embodiments, the functional chimeras can comprise a.) HIV Gag protein that lacks the HIV Gag MA domain and b.) a portion of a MA domain of non HIV origin, such as the MA domain of MLV or can comprise a.) HIV Gag protein that includes a partial HIV Gag MA domain and b.) a complete MA domain of non HIV origin, such as the MA domain of MLV, and MLV p12 protein or a sufficient portion to overcome the block to HIV assembly in non human cells. In specific embodiments, HIV p17 MA is replaced with the p15 MA domain and the p12 domain of MLV Gag. Functional HIV Gag protein-MLV Gag protein chimeras are referred to herein as functional HIV-MLV Gag chimeras; functional chimeric HIV particles and functional HIV Gag protein-MLV Gag protein chimeras. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Novel transcription factor, BP1 Inventor(s): Berg, Patricia E.; (Accokeek, MD) Correspondence: ANTONELLI, TERRY, STOUT & KRAUS, LLP; 1300 NORTH SEVENTEENTH STREET; SUITE 1800; ARLINGTON; VA; 22209-9889; US Patent Application Number: 20030171273 Date filed: May 14, 2002 Abstract: An isolated DNA of SEQ ID NO:1 is provided that encodes the transcription factor BP1, which is believed to be a repressor of the.beta.-globin gene. A host cell that is transformed with a vector that contains the DNA may be used to produce BP1. Vectors having a controllable promoter operably connected to the BPl open reading frame may be used to transform.beta.-globin producing cells of patients with sickle cell anemia, thereby providing a treatment. Because BP1 is overexpressed in leukemia and breast cancer cells, acute myeloid leukemia, acute lymphocytic leukemia, and breast cancer can be screened for and diagnosed by determining whether BP1 is overexpressed in cell samples of patients who may have these conditions. An antisense DNA or RNA to the DNA encoding BP1 may be used as a treatment for acute myeloid leukemia, acute lymphocytic leukemia, and breast cancer. Excerpt(s): The present application claims the benefit of the filing date of U.S. Provisional Application No. 60/148,940, filed Aug. 13, 1999. The provisional application is incorporated by reference herein. Work described herein was supported by NIH grant R01DK53533. The U.S. Government has certain rights in the invention. The present invention relates to a DNA that encodes the transcription factor BP1, a vector containing the DNA and a host cell containing the DNA. The invention also relates to an antisense DNA or RNA to the DNA encoding BP1, methods for treating sickle cell anemia by administering an effective amount of BP1, and methods for screening for acute myeloid leukemia, acute lymphocytic leukemia, and breast cancer.
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Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Proteins with a high immunoreactivity and a method for the production thereof Inventor(s): Benes, Ivan; (Forch, CH), Thomsen-Bosslet, Silke; (Berlin, DE) Correspondence: HENRY M FEIEREISEN; 350 FIFTH AVENUE; SUITE 3220; NEW YORK; NY; 10118; US Patent Application Number: 20030171548 Date filed: October 4, 2002 Abstract: The invention relates to (glyco-) proteins, in particular monoclonal antibodies, which have an immunoreactivity of >81%, preferably >90%. The inventive monoclonal antibodies are produced using a fluidized bed reactor in conjunction with a conventional protein-chemical purification method or preferably with a purification method involving less column chromatography. The monoclonal antibodies thus produced are suitable, in gamma-irradiated form, e.g. Tc-99m labelled, for the in vivo diagnosis of inflammatory diseases and bone marrow metastases. In alpha - or betairradiated form, e.g. astatine or Re-188 or Y-90 labelled form, the inventive monoclonal antibodies can be used, for example, in the treatment of leukemia. Excerpt(s): The invention relates to preparations of immunoreactive proteins and in particular in purified form and having a high percentage of immunoreactive molecules relative to the total number of molecules. These proteins can be obtained through fermentation in a fluidized reactor of a host cell, which is capable of expressing the immunoreactive protein and production of the protein from the host cell respectively from the culture medium used for culturing the cells. The protein preparations according to the invention are outstandingly suitable for producing diagnostic and therapeutic compositions. Diagnostic and therapeutic proteins can be expressed in prokaryotic cells, such as for example E. coli (Houston et al., U.S. Pat. No. 5,132,405) as well as in eukaryotic cell systems, (for example Pichia pastoris, baby hamster kidney (BHK) cells, Chinese hamster Ovary (CHO-)cells, hybridomas, transgenic animals and plants (Meade et. al., U.S. Pat. No. 4,873,316) and can be purified by protein-chemical methods. With prokaryotic cell systems, a cost efficient production of small carbohydrate-free proteins can be realized due to the simple culture media and the fast growth of the microorganisms in relatively simple fermentation systems. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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RAF-MEK-ERK pathway inhibitors to treat cancer Inventor(s): Bollag, Gideon; (Hercules, CA), Lyons, John F.; (Moraga, CA) Correspondence: Gregory Giotta, Ph.D.; Vice President and Chief Legal Counsel; ONYX Pharmaceuticals, Inc.; 3031 Research Drive; Richmond; CA; 94806; US Patent Application Number: 20030125359 Date filed: December 3, 2002 Abstract: Materials and methods for treating certain cancers are described, preferably cancers that result from the up-regulation of the RAF-MEK-ERK pathway, and more preferably chronic myelogenous leukemia, and which cancer is preferably resistant to the inhibition of the Bcr-Abl tyrosine kinase, imatinib.
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Excerpt(s): The invention described herein is in the field of cancer therapy, and preferably for the treatment of chronic myelogenous leukemia. A goal of modem cancer therapy is to identify molecules in signal transduction pathways that affect cell growth, and particularly those that cause a normal cell to become cancerous. One such pathway is the RAF-MEK-ERK pathway, and the up-regulation of one or more of its members is thought to be responsible for a number of cancers. For example, patients with chronic myelogenous leukemia, herein after referred to as CML, who are in either the chronic or blast phase typical achieve remissions in response to the marketed drug Gleevec.TM., also referred to as imatinib or STI571 (N. Eng. J. Med. 244, 1031 [2001]; N. Eng. J. Med 244, 1038 [2001]). CML is characterized by the Philadelphia chromosomal translocation (Ph+) resulting in a Bcr-Abl fusion protein. Imatinib treats CML by blocking Bcr-Abl kinase activity. While the remissions achieved with imatinib during the chronic phase of CML are durable, patients with remissions achieved during the blast phase usually relapse within 2-6 months (N. Eng. J. Med. 244, 1038 [2001]). Resistance to Imatinib results in reactivation of Bcr-Abl kinase activity. Recently, it has been shown that these relapses are usually due to imatinib-resistance that occur either by over-expression of the translocated Bcr/Abl gene, or mutation of the imatinib target gene, namely the Abl kinase (Science 293, 876 [2001]). Resistance often correlates with mutations in the Abl kinase domain, including T315I and E255K. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Soluble tumor necrosis factor receptor treatment of medical disorders Inventor(s): Pluenneke, John D.; (Parkville, MO) Correspondence: IMMUNEX CORPORATION; LAW DEPARTMENT; 51 UNIVERSITY STREET; SEATTLE; WA; 98101 Patent Application Number: 20030148955 Date filed: December 9, 2002 Abstract: The invention pertains to methods and compositions for reducing resistance to STI 571 in a chronic myelogenous leukemia patient by administering a TNF.alpha. inhibitor, such as recombinant TNFR:Fc to such patient. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 09/778,403, filed Feb. 7, 2001, which is a continuation-in-part of Ser. No. 09/726,781, filed Nov. 29, 2000, which is a continuation-in-part of Ser. No. 09/602,351, filed Jun. 23, 2000, which is a continuation-in-part of PCT/US00/10565, filed Apr. 19, 2000, (claiming the benefit of priority from U.S. provisional applications 60/184,864, filed Feb. 25, 2000, and 60/164,676, filed Nov. 10, 1999), which is a continuation-in-part of 09/373,828, filed Aug. 13, 1999 (claiming the benefit of priority from U.S. provisional applications 60/148,234, filed Aug. 11, 1999; 60/143,959, filed Jul. 15, 1999; 60/134,320, filed May 14, 1999; and 60/130,074, filed Apr. 19, 1999). The invention pertains to methods for treating various medical disorders that are characterized by abnormal or excessive TNF.alpha. levels by administering a TNF.alpha. antagonist, such as a soluble TNF.alpha. The TNF.alpha. inhibitor may be administered in combination with other biologically active molecules. The pleiotropic cytokine tumor necrosis factor alpha (TNF.alpha.) is associated with inflammation and binds to cells through membrane receptor molecules, including two molecules having molecular weights of approximately 55 kDa and 75 kDa (p55 and p75). In addition to binding TNF.alpha., the p55 and p75 TNF.alpha. receptors mediate the binding to cells of homotrimers of TNF.beta., which is another cytokine associated with inflammation and which shares structural similarities with TNF.alpha.
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(e.g., see Cosman, Blood Cell Biochem 7:51-77, 1996). TNF.beta. is also known as lymphotoxin-.alpha. (LT.alpha.). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Strategy for leukemia therapy Inventor(s): Wang, Jean Y J; (San Diego, CA), Vigneri, Paolo; (Catania, IT) Correspondence: Colleen J McKiernan; James W McClain; Brown Martin Haller & McClain; 1660 Union Street; San Diego; CA; 92101-2926; US Patent Application Number: 20030162740 Date filed: December 27, 2002 Abstract: The chimeric Bcr-Abl oncoprotein is the molecular hallmark of chronic myelogenous leukemia (CML). In the cytoplasm, the protein transduces a growth signal that is responsible for overexpansion of cells. In the nucleus, the protein induces apoptosis. The invention is a method of treating cancer/killing Bcr-Abl expressing cells by inducing the translocation of Bcr-Abl to the nucleus to activate the apoptotic pathway in cancer cells. Excerpt(s): This application claims the benefit of priority of U.S. provisional application Ser. No. 60/215,595 filed Jun. 30, 2000 which is incorporated herein by reference in its entirety. Chronic myeloid leukemia (CML) is a hematological stem cell disorder characterized by excessive proliferation of cells of the myeloid lineage. The hallmark of CML is the Philadelphia chromosome, which arises from a reciprocal translocation between chromosomes 9 and 22 (Rowley, 1973). The molecular consequence of this translocation is the replacement of the first exon of c-Abl with sequences from the Bcr gene resulting in a Bcr-Abl fusion gene whose protein product shows enhanced tyrosine kinase activity (Bartram, et al., 1983; Ben-Neriah, et al., 1986; Heisterkamp et al, 1983; Konopka, et al., 1984; Shtivelman et al., 1985). The Bcr-Abl oncoprotein in CML is a 210kD protein that contains 902 or 927 amino acids of Bcr fused to the expression product of exons 2-11 of c-Abl (Ben-Neriah, et al., 1986; Shtivelman et al., 1985). Found in 95% of patients with CML, p210 Bcr-Abl is also present in approximately 5-10% of adults with acute leukemia for whom there is no evidence of antecedent CML (Kruzrock, et al., 1988). Another Bcr-Abl fusion protein of 185 kD containing Bcr sequences from exon 1 (426 amino acids) fused to exons 2-11 of c-Abl, occurs in 10% of adult cases and 5-10% of pediatric cases of acute lymphoblastic leukemia (ALL), but not in CML (Clark, et al., 1988; Hermans et al., 1987). It is believed that this single chromosomal rearrangement is sufficient to initiate the development of these diseases and may be the only molecular abnormality in early stage disease. A kinase inhibitor, STI-571 (4-[(4-methylpiperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyrodnyl)-2pyrimidinyl]amin]phenyl]benzamide methanesul-fonate; Glivec, Novartis, Basel, Switzerland) was initially identified in a screen for inhibitors of the platelet derived growth factor receptor (PDGFR) (Buchdunger et al., 1995). This ATP analog of the class 2-phenylaminopyrimidine, was found to have some selectivity for specific kinases including cdc2/cyclin B, c-FGR, protein kinase C.gamma. and v-Abl. As the constitutive activation of v-Abl is believed to be sufficient for the development of CML, it was seen as an ideal target for validating the clinical utility of protein kinase inhibitors in the treatment of cancer. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Targeting leukemia cells Inventor(s): Yang, Lijun; (Gainesville, FL) Correspondence: Stanley A. Kim, Ph. D., Esq.; Akerman, Senterfitt & Eidson, P.A.; 222 Lakeview Avenue, Suite 400; P.O. Box 3188; West Palm Beach; FL; 33402-3188; US Patent Application Number: 20030124127 Date filed: December 6, 2002 Abstract: A molecule is targeted to a leukemia cell by first contacting the cell with a retinoid in an amount effective to increase the expression of a marker in the cell, and the contacting the cell with an agent that specifically binds the marker. For directing a molecule to an acute promyelocytic leukemia cell, the cell is contacted with all-trans retinoic acid to induce or increase expression of CD52 on the cell. The cell is then contacted with a molecule, such as an anti-CD52 antibody, that specifically binds the CD52 expressed on the cell. Excerpt(s): This application claims priority from U.S. provisional patent application serial No. 60/338,373, filed Dec. 6, 2001. The invention relates to the fields of medicine, immunology and oncology. More particularly, the invention relates to an improved method for treating leukemia. Acute promyelocytic leukemia (APL) is a rapidly progressive cancer of the blood that is characterized by the uncontrolled proliferation of an immature form of a white blood cell termed a promyelocyte. Overproduction of these cells crowds the bone marrow, radically reducing the body's ability to form other normal and necessary blood cells. APL is a lethal leukemia and accounts for more than 10% of all acute myeloid leukemia cases (Powell B L, Curr. Opin. Oncol. 13:8-13, 2001). The disease is characterized by distinctive and unique clinico-pathologic features including: (1) the accumulation in the bone marrow of tumor cells blocked at the promyelocytic stage of myeloid differentiation, (2) translocations involving chromosomes 15 and 17, (3) sensitivity of APL blasts to the differentiating action of retinoic acid, (4) young age of onset, (5) frequent presentation with low white blood cell counts, and (6) severe consumptive coagulopathy with a high incidence of early fatal hemorrhages (Falanga A et al., Acta Hematol. 106:43-51, 2001). Without treatment, an APL patient's life expectancy is approximately a month or even less. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Therapeutic compounds Inventor(s): Fatih, M. Uckun; (White Bear Lake, MN) Correspondence: MERCHANT & GOULD PC; P.O. BOX 2903; MINNEAPOLIS; MN; 55402-0903; US Patent Application Number: 20030149045 Date filed: August 2, 2002 Abstract: The invention provides novel JAK-3 inhibitors that are useful for treating leukemia and lymphoma. The compounds are also useful to treat or prevent skin cancer, as well as sunburn and UVB-induced skin inflammation. In addition, the compounds of the present invention prevent the immunosuppressive effects of UVB radiation, and are useful to treat or prevent autoimmune diseases, inflammation, and transplant rejection. The invention also provides pharmaceutical compositions comprising compounds of the invention, as well as therapeutic methods for their use.
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Excerpt(s): This application is a continuation-in-part, claiming priority under 35 U.S.C.sctn.120, of U.S. application Ser. No. 09/812,098, filed Mar. 19, 2001 which is a continuation of U.S. application Ser. No. 09/378,093 filed Aug. 20, 1999, now U.S. Pat. No. 6,313,129, and claims priority under 35 U.S.C.sctn.119(e) from U.S. Provisional application No. 60/309,557 and from U.S. Provisional application No. 60/309,558, each filed Aug. 2, 2001, the disclosures of which are hereby incorporated by reference. Bone marrow transplantation (BMT) has become one of the standard treatment modalities offered to high-risk leukemia patients. Very intensive "supralethal" myeloablative chemotherapy or radiochemotherapy regimens can be applied in the context of BMT with a curative intent to overcome the drug resistance of residual leukemia cells of certain leukemia patients who are unlikely to be cured by standard chemotherapy. In addition, leukemia patients undergoing allogeneic BMT may benefit from the graftversus-leukemia (GVL) effect of the marrow allograft. Graft-Versus-Host Disease (GVHD), a donor T-cell initiated highly complex pathologic condition that frequently follows allogeneic BMT, especially in the context of a major-HLA disparity, is associated with significant morbidity and mortality. Severe GVHD remains a major obstacle to a more successful outcome of allogeneic BMT using HLA-matched unrelated donors as well as partially HLA-mismatched related donors. Therefore, GVHD prophylaxis aimed at reducing the risk of severe GVHD is an integral component of all BMT programs. On the other hand, there is a widely accepted notion in the BMT community that leukemia patients who develop GVHD after BMT have a reduced risk of relapse indicating that alloreactive T cells participating in GVHD are major contributors of the GVL function of the marrow allografts. In certain subsets of leukemia patients who relapsed after BMT (e.g. chronic myelogenous leukemia patients), infusions of donor T-cells resulted in remissions, thereby providing direct evidence that host leukemia cells can be killed by alloreactive T-cells. Therefore, several groups involved in the treatment of leukemia patients are currently exploring alternative methods of inducing mixed chimerism with non-myeloablative conditioning regimens followed by donor lymphocyte infusions to achieve a GVL effect without severe GVHD. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Thiazolidinedione derivatives for the treatment of diabetes and other diseases Inventor(s): Al-Shamma, Hussien A.; (Encinitas, CA), Pfahl, Magnus; (Solana Beach, CA), Tachdjian, Catherine; (San Diego, CA), Spruce, Lyle W.; (Chula Vista, CA), Fanjul, Andrea; (San Diego, CA), Pleynet, David P.M.; (San Diego, CA) Correspondence: MURPHY, MARK; NEEDLE & ROSENBERG P.C.; 1200 CANDLER BLDG.; 127 PEACHTREE N.E.; ATLANTA; GA; 30303; US Patent Application Number: 20030153606 Date filed: December 31, 2002 Abstract: The present invention relates to certain substituted heterocycles of Formula (I) which are useful in the treatment of diseases related to lipid and carbohydrate metabolism, such as type 2 diabetes, adipocyte differentiation, uncontrolled proliferation, such as lymphoma, Hodgkin's Disease, leukemia, breast cancer, prostate cancer or cancers in general; and inflammation, such as osteoarthritis, rheumatoid arthritis, Crohn's Disease or Inflammatory Bowel Disease. 1 Excerpt(s): This application is a continuation application claiming priority to U.S. patent application Ser. No. 09/652,810, filed Aug. 31, 2000, which status is now allowed, which claimed priority to U.S. provisional application Serial No. 60/151,670, filed Aug. 31,
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1999, the priority of which is also claimed hereby. The disclosure of both parent applications are hereby incorporated herein in their entirety by this reference. Type 2 diabetes, also referred to as non-insulin dependent diabetes mellitus (NIDDM), afflicts between 80 and 90% of all diabetic patients in developed countries. In the United States alone, approximately 15 million people, and more than 100 million worldwide, are affected. Because this disorder is a late onset disease and occurs often in overweight persons it can be expected that the number of patients suffering from this disease will increase further. Patients suffering from type 2 diabetes usually still produce insulin but become increasingly resistant to their own insulin and to insulin therapy. A promising new class of drugs has been recently introduced that resensitizes patients to their own insulin (insulin sensitizers), thereby reducing blood glucose and triglyceride levels, and thus abolishing, or at least reducing, the requirement for exogenous insulin. Troglitazone (Resulin.TM.) and rosiglitazone (Avandia.TM.) belong to the thiazolidinediones (TZD) class of chemicals, and are the first representatives of this class of chemicals approved for the treatment of type 2 diabetes in the United States and several other countries. These compounds, however, have side effects including rare but severe liver toxicities (i.e., troglitazone) and they can increase body weight in humans. Such side effects are of major concern for patients who might require treatment for a decade or longer. Therefore, new and better drugs for the treatment of type 2 diabetes and related disorders are needed. New heterocyclic derivatives that are useful, for example, to modulate metabolism (such as, for example, lipid metabolism and carbohydrate metabolism) or adipocyte differentiation, and especially to treat type 2 diabetes and other diseases are disclosed. The present invention relates to certain substituted heterocycles which are useful in the treatment of diseases related to lipid metabolism and adipocyte differentiation, such as type 2 diabetes; uncontrolled proliferation, such as lymphoma, Hodgkin's Disease, leukemia, breast cancer, prostate cancer, or cancers in general; and inflammation, such as osteoarthritis, rheumatoid arthritis, Crohn's Disease, or Inflammatory Bowel Disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Treatment of acute myeloid leukemia with indolinone compounds Inventor(s): O'Farrell, Anne-Marie; (Menlo Park, CA), Cherrington, Julie; (San Francisco, CA) Correspondence: FOLEY AND LARDNER; SUITE 500; 3000 K STREET NW; WASHINGTON; DC; 20007; US Patent Application Number: 20030130280 Date filed: October 28, 2002 Abstract: A method of treating acute myeloid leukemia in patient positive for FLT-3-ITD is described. The treatment is accomplished by administration of a compound of Formula I or II as defined herein. Excerpt(s): This application claims priority to U.S. Provisional Patent Application Serial No. 60/330,623, which is hereby incorporated in its entirety by reference. The invention relates to a method of treating acute myeloid leukemia by administering an indolinone compound. Acute myeloid leukemia (AML) is a disease in which cancerous cells develop in the blood and bone marrow. Untreated AML is a fatal disease with median survival time of 3 months. Patients with AML that are FLT-3-ITD (internal tandem duplication) positive typically exhibit poor response to traditional chemotherapy. The present invention is directed to treating AML patients and preferably patients positive
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for FLT-3-ITD but not restricted to FLT-3-ITD by administering indolinone compounds of Formula I or II. The present invention also is directed to a method of inhibiting phosphorylation of FLT-3. Acute myeloid leukemia, also called acute non-lymphocytic leukemia, is a form of cancer in which too many immature white blood cells are found in the blood and bone marrow. These immature cells, also called blasts, have failed to develop into mature infection-fighting cells. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Tumor-associated antigen RHAMM Inventor(s): Greiner, Jochen; (Ulm, DE), Schmitt, Michael; (Ulm, DE) Correspondence: WOLF GREENFIELD & SACKS, PC; FEDERAL RESERVE PLAZA; 600 ATLANTIC AVENUE; BOSTON; MA; 02210-2211; US Patent Application Number: 20030170755 Date filed: September 26, 2002 Abstract: The invention provides methods for diagnosing cancer including acute myeloid leukemia and chronic myeloid leukemia, based on the identification of certain cancer-associated polypeptides as antigens that elicit immune responses in cancer. The identified antigens can be utilized as markers for diagnosing cancer, and for following the course of treatment of cancer. Excerpt(s): This application claims priority under 35 U.S.C.sctn.119 from U.S. provisional application serial No. 60/324,989, filed Sep. 26, 2001. The invention relates to use of novel tumor-associated antigens in the diagnosis of cancer, including acute and chronic myeloid leukemia. The myeloid leukemias are members of a heterogeneous group of diseases characterized by infiltration of the blood, bone marrow, and other tissues by neoplastic cells of the hematopoietic system. There is a spectrum of symptoms of the mycloid leukemias, which range from to slowly progressive to rapidly fatal. (see; Harrison's Principles of Internal Medicine, 14/e, McGraw-Hill Companies, New York, 1998). Myeloid leukemias are categorized as either acute myeloid leukemia (AML) or chronic myeloid leukemia (CML) and they differ in their progression and prognosis. The onset of AML may be genetically based, or the result of exposure to radiation, chemicals, or drugs such as antineoplastic drugs used in cancer treatment. CML is also linked to chromosomal abnormalities and its progression is influenced by exposure to radiation and/or chemicals. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with leukemia, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “leukemia” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on leukemia.
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You can also use this procedure to view pending patent applications concerning leukemia. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON LEUKEMIA Overview This chapter provides bibliographic book references relating to leukemia. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on leukemia include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “leukemia” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on leukemia: ·
Communication Disorders in Childhood Cancer Source: London, United Kingdom: Whurr Publishers Ltd. 1999. 219 p. Contact: Available from Taylor and Francis, Inc. 7625 Empire Drive, Florence, KY 41042. (800) 634-7064. Fax (800) 248-4724. PRICE: $47.95 plus shipping and handling. ISBN: 1861561156. Summary: As the treatments become more effective, an increasing number of children displaying communication deficits as a consequence of treatment for childhood cancer have begun to appear in the caseloads of speech pathologists and other health professionals. This book offers an overview of the communication impairments that occur in association with the two most common forms of childhood cancer, namely leukemia and brain tumor. The treatments offered for these conditions, such as radiotherapy and chemotherapy, may have some long term adverse effects on brain structure and function leading to the development of a number of complications,
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including cognitive deficits as well as speech and language disorders. The book includes nine chapters, that cover the cancers themselves (leukemia and brain tumors), the effects of treatment for pediatric cancer on brain structure and function, language disorders in children treated for brain tumors, language recovery following treatment for pediatric brain tumors, variability in patterns of language impairment in children following treatment for posterior fossa tumor, language disorders in children treated for acute lymphoblastic leukemia, discourse abilities of children treated for neoplastic conditions, motor speech disorders in children treated for brain tumors, and the assessment and treatment of speech and language disorders occurring subsequent to cancer therapy in children. Each chapter includes extensive references and the textbook concludes with a subject index. ·
Young People and Chronic Illness: True Stories, Help and Hope Source: Minneapolis, MN: Free Spirit Publishing. 1998. 199 p. Contact: Available from Free Spirit Publishing. 400 First Avenue North, Suite 616, Minneapolis, MN 55401-1724. (612) 338-2068. Fax (612) 337-5050. E-mail:
[email protected]. Website: www.freespirit.com. PRICE: $14.95 plus shipping and handling. ISBN: 1575420414. Summary: This book offers information and advice about coping with a chronic illness during adolescence and young adulthood. Part one profiles 10 adolescents and young adults who are learning to balance their chronic illness and their active lives. Illnesses include diabetes, juvenile rheumatoid arthritis, asthma, leukemia, a congenital heart defect, epilepsy, hemophilia, lupus, and Crohn's disease. These young men and women share their stories and advice from discovery and diagnosis to management of day-today medical decisions, symptoms, family, friends, and school. Each story is followed by a question and answer section that provides more information about each illness, as well as a list of resources. Part two presents steps for managing the illness, ways to develop a good patient-doctor relationship, tips on telling friends and classmates about the illness, advice on communicating with family, strategies for coping with school, and suggestions on handling a fear of hospitals. It also provides information on support groups and national organizations.
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Integrating Traditional, Experimental & Complementary Therapies for Living Long & Living Well: First International Conference on Traditional & Complementary Therapies in the Prevention & Treat. of Contact: Institute for Learning Mastery, PO Box 314, Baltimore, MD, 21203, (410) 3667373. US Library of Congress, Congressional Research Service, 1st St & Independence Ave SE, Washington, DC, 20540, (202) 707-5700. Summary: This sound recording of proceedings from Changing the Odds; Living Long and Living Well, The First International Conference on Traditional and Complementary Therapies in the Prevention and Treatment of AIDS, held February 17-19, 1989, in Washington, D.C., features Dr. Charles Steinberg talking about progress in the treatment of Acquired immunodeficiency syndrome (AIDS), and combining traditional and alternative therapies into the most effective treatment. He opens his talk by saying that a survey showed that while 50 percent of the doctors responding would eat cookies prepared for them by a leukemia patient, only 23 percent would eat cookies prepared by a Person with AIDS (PWA). These attitudes, he said, are what need shifted. He says doctors and patients need to think of Human immunodeficiency virus (HIV) infection as a chronic, manageable disease, and that thinking needs to go beyond just survival and
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cure of a particular opportunistic infection; patients need to stop facing their dying, and start facing their living. Steinberg tells doctors and PWA's not to place too much faith in the results of tests. He then outlines available drug therapies, including azidothymidine (AZT), pentamidine, DDI, Compound Q, and acyclovir. He goes on to discuss other treatments, such as Chinese medicine, which includes acupuncture, nutrition, and herbal remedies. This treatment can often balance out the energy in the body and relieve symptoms like itching and headaches. Steinberg explains nutritional approaches to maximizing health and enhancing vitality and immunity. This creates a less favorable environment for some opportunistic infections. Steinberg moves on to talk about the vital role of physical exercise in mental, social, and physical health. His talk emphasizes the importance of support -- not just formal support groups, but also a network of people to talk to and call on. He discusses the importance of meditation and spiritual factors in soothing the mind. Steinberg tells several stories about patients from his own practice, and goes on to discuss society's attitudes toward PWA's. He gives advice on dealing with various symptoms and problems, such as insomnia and lack of appetite. Emphasizing empowerment, he says that taking control of one's own life and one's own tr.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in PrintÒ). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “leukemia” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “leukemia” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “leukemia” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): ·
100 Questions & Answers About Leukemia by Edward D. Ball, Gregory A. Lelek; ISBN: 0763720380; http://www.amazon.com/exec/obidos/ASIN/0763720380/icongroupinterna
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21st Century Complete Medical Guide to Leukemia - Authoritative Government Documents and Clinical References for Patients and Physicians with Practical Information on Diagnosis and Treatment Options by PM Medical Health News; ISBN: 1592480055; http://www.amazon.com/exec/obidos/ASIN/1592480055/icongroupinterna
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Acute childhood leukemia; ISBN: 3805520654; http://www.amazon.com/exec/obidos/ASIN/3805520654/icongroupinterna
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Acute Leukemia: Approach to Diagnosis by Harold R. Schumacher; ISBN: 0896401707; http://www.amazon.com/exec/obidos/ASIN/0896401707/icongroupinterna
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Acute Leukemia: Difficult, Controversial, Automated Analysiss by Harold R. Schumacher; ISBN: 0683305050; http://www.amazon.com/exec/obidos/ASIN/0683305050/icongroupinterna
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Acute Leukemias (1987); ISBN: 3540165568; http://www.amazon.com/exec/obidos/ASIN/3540165568/icongroupinterna
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Acute Leukemias (1992); ISBN: 3540539492; http://www.amazon.com/exec/obidos/ASIN/3540539492/icongroupinterna
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Acute Leukemias II (1990); ISBN: 3540509844; http://www.amazon.com/exec/obidos/ASIN/3540509844/icongroupinterna
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Acute leukemias IV : prognostic factors and treatment strategies; ISBN: 3540569510; http://www.amazon.com/exec/obidos/ASIN/3540569510/icongroupinterna
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Acute Leukemias IX by W. Hiddemann (Editor), et al; ISBN: 3540439714; http://www.amazon.com/exec/obidos/ASIN/3540439714/icongroupinterna
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Acute Leukemias V by Wormann (1996); ISBN: 0387578528; http://www.amazon.com/exec/obidos/ASIN/0387578528/icongroupinterna
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Acute Leukemias VIII: Prognostic Factors and Treatment Strategies (Hamatologie Und Bluttransfusion, 40.) by T. Buchner (Editor), et al (2001); ISBN: 3540411232; http://www.amazon.com/exec/obidos/ASIN/3540411232/icongroupinterna
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Acute Lymphoblastic Leukemia: Proceedings of a Wyeth-Ayerst-UCLA Western Workshop on Acute Lymphoblastic Leukemia Held at Tapatio Springs, Texas, nov by Robert Peter Gale (Editor), Dieter Hoelzer (Editor); ISBN: 0471567191; http://www.amazon.com/exec/obidos/ASIN/0471567191/icongroupinterna
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Acute Lymphocytic Leukemia - A Medical Dictionary, Bibliography, and Annotated Research Guide to Int by Health Publica Icon Health Publications (2003); ISBN: 0597835470; http://www.amazon.com/exec/obidos/ASIN/0597835470/icongroupinterna
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Acute Myelogenous Leukemia in Childhood; ISBN: 3540520708; http://www.amazon.com/exec/obidos/ASIN/3540520708/icongroupinterna
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Acute Myelogenous Leukemia in Childhood: Implications of Therapy Studies for Future Risk-Adapted Treatment Strategies by U. Creutzig, et al (1990); ISBN: 0387520708; http://www.amazon.com/exec/obidos/ASIN/0387520708/icongroupinterna
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Acute Myelogenous Leukemia: Progress and Controversies: Proceedings of a WyethAyerst-UCLA Symposia Western Workshop Held at Lake Lanier, Georgia, by Robert Peter Gale (Editor), University Of California; ISBN: 0471568724; http://www.amazon.com/exec/obidos/ASIN/0471568724/icongroupinterna
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Adult Leukemia: A Comprehensive Guide for Patients and Families by Barbara Lackritz; ISBN: 0596500017; http://www.amazon.com/exec/obidos/ASIN/0596500017/icongroupinterna
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Adult Leukemias 1 by C. D. Bloomfield (Editor) (1982); ISBN: 9024724783; http://www.amazon.com/exec/obidos/ASIN/9024724783/icongroupinterna
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Adult t Cell Leukemia and Related Diseases by Masao Hanaoka (Editor), et al; ISBN: 0306413353; http://www.amazon.com/exec/obidos/ASIN/0306413353/icongroupinterna
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Adult t Cell Leukemia and Related Diseases (Medical Intelligence Unit) by Takashi Uchiyama (Editor), Junji Yodoi (1995); ISBN: 1570591954; http://www.amazon.com/exec/obidos/ASIN/1570591954/icongroupinterna
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Adult T-Cell Leukemia (Oxford Medical Publications) by Kiyoshi Takatsuki (Editor) (1994); ISBN: 0192622846; http://www.amazon.com/exec/obidos/ASIN/0192622846/icongroupinterna
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Advances in acute leukemia; ISBN: 0444107657; http://www.amazon.com/exec/obidos/ASIN/0444107657/icongroupinterna
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Advances in Adult T-Cell Leukemia and Htlv-1 Research (Gann Monograph on Cancer Research, No 39) by Kiyoshi Takatsuki, et al; ISBN: 0849377463; http://www.amazon.com/exec/obidos/ASIN/0849377463/icongroupinterna
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Advances in Chronic Lymphocytic Leukemia by Aaron Polliack, Emilio Montserrat (Editor) (1991); ISBN: 3718652137; http://www.amazon.com/exec/obidos/ASIN/3718652137/icongroupinterna
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Advances in Comparative Leukemia Research 1981 (1982); ISBN: 0444003789; http://www.amazon.com/exec/obidos/ASIN/0444003789/icongroupinterna
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Advances in Comparative Leukemia Research 1981: Proceedings of the Xth International Symposium for Comparative Research on Leukemia and Related Diseases, Held at the University of California, Los by International Symposium for Comparative Research on Leukemia and Relat, et al (1982); ISBN: 0444007202; http://www.amazon.com/exec/obidos/ASIN/0444007202/icongroupinterna
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American Cancer Society Atlas of Clinical Oncology: Adult Leukemias (Book with CD-ROM) by Peter H., MD Wiernik, B C Decker Inc; ISBN: 1550091115; http://www.amazon.com/exec/obidos/ASIN/1550091115/icongroupinterna
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An Angel at My Side: Surviving Leukemia Through Love by Frances M. Schindler (2001); ISBN: 0595175996; http://www.amazon.com/exec/obidos/ASIN/0595175996/icongroupinterna
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Aspects of Leukemia Treatment With Special Reference to Drug Development by S. Roath; ISBN: 3718650770; http://www.amazon.com/exec/obidos/ASIN/3718650770/icongroupinterna
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At Least It's Not Contagious: A Personal Story of a Struggle With Leukemia by Samantha Miles; ISBN: 1863738150; http://www.amazon.com/exec/obidos/ASIN/1863738150/icongroupinterna
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Biologic Therapy of Leukemia (Contemporary Hematology Ser) by Matt Kalaycio (Editor), Maxwell K. Hearn (2003); ISBN: 1588290719; http://www.amazon.com/exec/obidos/ASIN/1588290719/icongroupinterna
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Biological Response Modifiers-Leukemias and Lymphomas (International Cancer Congress, Lectures and Symposia, Vol 10) by K. Lapis, S. Eckhardt (Editor) (1987); ISBN: 380554426X; http://www.amazon.com/exec/obidos/ASIN/380554426X/icongroupinterna
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Biology and Therapy of Acute Leukemia: Proceedings of the 17th Annual Detroit Cancer Symposium (Developments in Oncology) by Laurence Baker, et al (1985); ISBN: 0898387280; http://www.amazon.com/exec/obidos/ASIN/0898387280/icongroupinterna
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Borrowed Blood: Victory over Leukemia by Shawn Stephen Riley (1991); ISBN: 0936635061; http://www.amazon.com/exec/obidos/ASIN/0936635061/icongroupinterna
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Campath - 1 H: Emerging Frontline Therapy in Chronic Lymphocytic Leukemia by Kanti R. Rai, et al; ISBN: 1842140604; http://www.amazon.com/exec/obidos/ASIN/1842140604/icongroupinterna
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Cancer and leukemia : an alternative view by Jan De Vries; ISBN: 1851581359; http://www.amazon.com/exec/obidos/ASIN/1851581359/icongroupinterna
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Cancer in the First Year of Life: Leukemias, Neuroblastomas, Soft Tissue Sarcomas (Contributions to Oncology Beitrage Zur Onkologie, Vol. 41) by Germany)/ Lampert, F. Italo-German Workshop on Pediatric Oncology 1989 Braunfels (1991); ISBN: 3805552335; http://www.amazon.com/exec/obidos/ASIN/3805552335/icongroupinterna
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CD-ROM Atlas of Pathology, 3: Leukemias
by G. Flandrin (1998); ISBN: 3540146563; http://www.amazon.com/exec/obidos/ASIN/3540146563/icongroupinterna
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Central Nervous System Leukemia: Prevention and Treatment by R. Mastrangelo (Editor) (2002); ISBN: 0898385709; http://www.amazon.com/exec/obidos/ASIN/0898385709/icongroupinterna
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Childhood Leukemia: A Guide for Families, Friends and Caregivers (3rd Edition) by Nancy Keene; ISBN: 0596500157; http://www.amazon.com/exec/obidos/ASIN/0596500157/icongroupinterna
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Childhood Leukemia: Present Problems and Future Prospects by Tai Aker (Editor); ISBN: 0860084663; http://www.amazon.com/exec/obidos/ASIN/0860084663/icongroupinterna
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Childhood Leukemia: Present Problems and Future Prospects (Developments in Oncology, Vol 61) by Noboru Kobayashi, et al (1991); ISBN: 0792311388; http://www.amazon.com/exec/obidos/ASIN/0792311388/icongroupinterna
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Childhood Leukemia: The Facts (The Facts Series) by John S. Lilleyman (2000); ISBN: 019263142X; http://www.amazon.com/exec/obidos/ASIN/019263142X/icongroupinterna
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Childhood Leukemia: Why Not Cure All? (Advances in Regional Cancer Therapy, Vo. 35) by H. Riehm, K. Welte (Editor); ISBN: 3805550103; http://www.amazon.com/exec/obidos/ASIN/3805550103/icongroupinterna
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Childhood Leukemias by Ching-Hon Pui (Editor); ISBN: 0521581761; http://www.amazon.com/exec/obidos/ASIN/0521581761/icongroupinterna
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Childhood Lymphoblastic Leukemia (1985); ISBN: 0030717388; http://www.amazon.com/exec/obidos/ASIN/0030717388/icongroupinterna
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Childhood Lymphoblastic Leukemia by Carl Pochedly (Author); ISBN: 0275900487; http://www.amazon.com/exec/obidos/ASIN/0275900487/icongroupinterna
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Chromosomes and Genes in Acute Lymphoblastic Leukemia (Medical Intelligence Unit) by Lorna M. Secker-Walker (1997); ISBN: 0412107619; http://www.amazon.com/exec/obidos/ASIN/0412107619/icongroupinterna
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Chronic and Acute Leukemias in Adults (Cancer Treatment and Research) by Clara D. Bloomfield (Editor) (1985); ISBN: 0898387027; http://www.amazon.com/exec/obidos/ASIN/0898387027/icongroupinterna
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Chronic leukemia : approach to diagnosis by Harold R. Schumacher; ISBN: 4260142208; http://www.amazon.com/exec/obidos/ASIN/4260142208/icongroupinterna
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Chronic Leukemias and Lymphomas: Clinical Management by Gary J., MD Schiller (Editor); ISBN: 0896039072; http://www.amazon.com/exec/obidos/ASIN/0896039072/icongroupinterna
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Chronic Lymphocytic Leukemia by Robert Peter Gale; ISBN: 084512658X; http://www.amazon.com/exec/obidos/ASIN/084512658X/icongroupinterna
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Chronic Lymphocytic Leukemia by Aaron Polliack, Daniel Catovsky (Editor) (1988); ISBN: 3718648024; http://www.amazon.com/exec/obidos/ASIN/3718648024/icongroupinterna
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Chronic Lymphocytic Leukemia: Molecular Genetics, Biology, Diagnosis, and Management (Contemporary Hematology) by Guy B. Faguet (Editor) (2003); ISBN: 1588290999; http://www.amazon.com/exec/obidos/ASIN/1588290999/icongroupinterna
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Chronic Lymphocytic Leukemia: Recent Progress and Future Direction (UCLA Symposia on Molecular and Cellular Biology, New Series, Vol 59) by Robert Peter Gale, Kanti R. Rai (Editor); ISBN: 047160125X; http://www.amazon.com/exec/obidos/ASIN/047160125X/icongroupinterna
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Chronic Lymphocytic Leukemia: Scientific Advances and Clinical Developments (Basic and Clinical Oncology, Vol 1) by Bruce D. Cheson (Editor); ISBN: 0824787366; http://www.amazon.com/exec/obidos/ASIN/0824787366/icongroupinterna
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Chronic lymphocytic leukemia; clinical studies based on 189 cases followed for a long time by Mogens M²rk Hansen; ISBN: 8798023608; http://www.amazon.com/exec/obidos/ASIN/8798023608/icongroupinterna
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Chronic Lymphoid Leukemias (Bco Basic and Clinical Oncology) by Bruce D. Cheson (Editor) (2001); ISBN: 0824705432; http://www.amazon.com/exec/obidos/ASIN/0824705432/icongroupinterna
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Chronic Myelocytic Leukemia and Interferon: Pathophysiological Clinical, and Therapeutic Aspects by D. Huhn, et al (1988); ISBN: 0387190678; http://www.amazon.com/exec/obidos/ASIN/0387190678/icongroupinterna
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Chronic Myelocytic Leukemia and Interferon: Pathophysiological, Clinical and Therapeutical Aspects; ISBN: 3540190678; http://www.amazon.com/exec/obidos/ASIN/3540190678/icongroupinterna
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Chronic Myelogenous Leukemia: Molecular Approaches to Research and Therapy (Hematology Series, No 13) by Albert B. Deisseroth, Ralph B. Arlinghaus (Editor) (1991); ISBN: 0824783522; http://www.amazon.com/exec/obidos/ASIN/0824783522/icongroupinterna
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Chronic myeloid leukemia (CML) pipeline update [DOWNLOAD: PDF] by Datamonitor (Author); ISBN: B00008R40H; http://www.amazon.com/exec/obidos/ASIN/B00008R40H/icongroupinterna
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CHRONIC MYELOID LEUKEMIA 11#1 by SANTE TURA; ISBN: 3718654784; http://www.amazon.com/exec/obidos/ASIN/3718654784/icongroupinterna
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Chronic Myeloid Leukemia: biology and treatment by Angelo M. Carella (Editor), et al (2001); ISBN: 185317890X; http://www.amazon.com/exec/obidos/ASIN/185317890X/icongroupinterna
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Comparative leukemia research 1975; ISBN: 3805523165; http://www.amazon.com/exec/obidos/ASIN/3805523165/icongroupinterna
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Condemned by Leukemia by Alfred J Jr, Alfred J. Petit-Clair; ISBN: 0533079195; http://www.amazon.com/exec/obidos/ASIN/0533079195/icongroupinterna
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Coping With Leukemia (Coping) by Melanie Ann Apel; ISBN: 0823932001; http://www.amazon.com/exec/obidos/ASIN/0823932001/icongroupinterna
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Current concepts in the management of lymphoma and leukemia; ISBN: 0387053093; http://www.amazon.com/exec/obidos/ASIN/0387053093/icongroupinterna
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Diagnosis and Management of the Leukemias. Ed by Kenneth B. McCredie. Spons by the Univ of Texas System Cancer Ctr, M.D. Anderson Hospital & Tumor in by McCredie (1982); ISBN: 089004323X; http://www.amazon.com/exec/obidos/ASIN/089004323X/icongroupinterna
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Diagnosis and Therapy of Acute Leukemia in Adults (Advances in Blood Disorders) by J. M. Rowe; ISBN: 3718655594; http://www.amazon.com/exec/obidos/ASIN/3718655594/icongroupinterna
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Drug Resistance in Leukemia and Lymphoma II (Advances in Blood Disorders) by G. J. Kaspers (Editor), et al; ISBN: 3718659344; http://www.amazon.com/exec/obidos/ASIN/3718659344/icongroupinterna
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Drug Resistance in Leukemia and Lymphoma III (Advances in Experimental Medicine and Biology, 457) by G. J. L. Kaspers (Editor), et al (1999); ISBN: 0306460556; http://www.amazon.com/exec/obidos/ASIN/0306460556/icongroupinterna
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Drug Resistance in Leukemia and Lymphoma: The Clinical Value of Laboratory Studies by G. J. L. Kaspers (Editor), et al (1993); ISBN: 3718653877; http://www.amazon.com/exec/obidos/ASIN/3718653877/icongroupinterna
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Drugs of Tomorrow: Leukemia - Chemopotentiators Will Drive Growth in the Acute Leukemia Markets [DOWNLOAD: PDF] by Datamonitor (Author); ISBN: B00008R3X9; http://www.amazon.com/exec/obidos/ASIN/B00008R3X9/icongroupinterna
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Dynamic morphology of leukemia cells : a comparative study by scanning electron microscopy and microcinematography by Heidi Felix; ISBN: 0387084959; http://www.amazon.com/exec/obidos/ASIN/0387084959/icongroupinterna
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Effect of granulocyte chalone on acute and chronic granulocytic leukemia in man : report of seven cases; ISBN: 8716022513; http://www.amazon.com/exec/obidos/ASIN/8716022513/icongroupinterna
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Enzootic Bovine Leukosis and Bovine Leukemia Virus (Developments in Veterinary Virology) by A. Burny (Editor), M. Mammerickx (Editor) (1987); ISBN: 0898388465; http://www.amazon.com/exec/obidos/ASIN/0898388465/icongroupinterna
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Epidemiology of Childhood Leukemia by J. Michaelis (Editor) (1994); ISBN: 3437115251; http://www.amazon.com/exec/obidos/ASIN/3437115251/icongroupinterna
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Epidemiology of Leukemia and Lymphoma: Report of the Leukemia Research Fund International Workshop, Oxford, Uk, September 1984 by L.C. Chan (Editor), et al; ISBN: 0080320023; http://www.amazon.com/exec/obidos/ASIN/0080320023/icongroupinterna
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Everything You Need to Know About When Someone You Know Has Leukemia (Need to Know Library) by Heather Moehn; ISBN: 0823931218; http://www.amazon.com/exec/obidos/ASIN/0823931218/icongroupinterna
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Experimental Leukemia and Mammary Cancer: Induction, Prevention, Cure by Charles Brenton Huggins (1979); ISBN: 0226358607; http://www.amazon.com/exec/obidos/ASIN/0226358607/icongroupinterna
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Feline Leukemia by Richard G. Olsen; ISBN: 0849360706; http://www.amazon.com/exec/obidos/ASIN/0849360706/icongroupinterna
Books
351
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Feline Leukemia Virus: Proceedings of the Third International Feline Leukemia Virus Meeting, St. Thomas, United States Virgin Islands, May 5- by W. D. Hardy (Editor), et al; ISBN: 0444005692; http://www.amazon.com/exec/obidos/ASIN/0444005692/icongroupinterna
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GALE LEUKEMIA - RECENT ADVANCES IN BIOLOGY AND TREATMENT by RP GALE; ISBN: 0471629383; http://www.amazon.com/exec/obidos/ASIN/0471629383/icongroupinterna
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Gene Technology: Stem Cell and Leukemia Research (NATO Asi Series. Series H, Cell Biology, Vol 94) by A. R. Zander (Editor), et al (1996); ISBN: 3540607439; http://www.amazon.com/exec/obidos/ASIN/3540607439/icongroupinterna
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Glucocorticoid Receptors in Leukemia Cells (Molecular Biology Intelligence Unit) by B. Gametchu; ISBN: 3540592199; http://www.amazon.com/exec/obidos/ASIN/3540592199/icongroupinterna
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Graft Versus Leukemia in Man and Animal Models by James Okunewick, Ruby Meredith (1981); ISBN: 0849357454; http://www.amazon.com/exec/obidos/ASIN/0849357454/icongroupinterna
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Hairy Cell and Chronic Lymphocytic Leukemia: Thirty Years of Progress by Andrew T. Huang (Editor); ISBN: 0444012338; http://www.amazon.com/exec/obidos/ASIN/0444012338/icongroupinterna
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Hairy Cell Leukemia (Advances in Blood Disorders) by Martin S. Tallman (Editor), Aaron Polliack (Editor); ISBN: 9058230090; http://www.amazon.com/exec/obidos/ASIN/9058230090/icongroupinterna
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Hairy-cell leukemia; ISBN: 0387099204; http://www.amazon.com/exec/obidos/ASIN/0387099204/icongroupinterna
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Hairy-Cell Leukemia by J. Burthem, J. C. Cawley (1996); ISBN: 3540760288; http://www.amazon.com/exec/obidos/ASIN/3540760288/icongroupinterna
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Having Leukemia Isn't So Bad: Of Course It Wouldn't Be My First Choice by Cynthia Krumme (1993); ISBN: 0963555448; http://www.amazon.com/exec/obidos/ASIN/0963555448/icongroupinterna
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Human Cell Culture, Volume III: Cancer Cell Lines, Part 3: Leukemias and Lymphomas by John R. W. Masters (Editor), Bernhard O. Palsson (Editor); ISBN: 079236225X; http://www.amazon.com/exec/obidos/ASIN/079236225X/icongroupinterna
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Human Leukemias: Cytochemical and Ultrastructural Techniques in Diagnosis and Research by Aaron Polliack (Editor) (1984); ISBN: 0898385857; http://www.amazon.com/exec/obidos/ASIN/0898385857/icongroupinterna
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Human T-Cell Leukemia Lymphoma Virus by Robert C. Gallo (Editor); ISBN: 0879691700; http://www.amazon.com/exec/obidos/ASIN/0879691700/icongroupinterna
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Human T-Cell Leukemia Virus (1985); ISBN: 354013963X; http://www.amazon.com/exec/obidos/ASIN/354013963X/icongroupinterna
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Human T-Cell Leukemia Virus (Current Topics in Microbiology and Immunology, Vol 115) by Peter K. Vogt (Editor) (1985); ISBN: 038713963X; http://www.amazon.com/exec/obidos/ASIN/038713963X/icongroupinterna
352 Leukemia
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I'm Still Me, Coping With Leukemia (Dr. Wellbook, 7) by Tim Peters, Tim Peters and Company (1997); ISBN: 1879874547; http://www.amazon.com/exec/obidos/ASIN/1879874547/icongroupinterna
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Immunologic Approaches to the Classification and Management of Lymphomas and Leukemias (Cancer Treatment and Research) by John M. Bennett, Kenneth A. Foon (Editor) (1988); ISBN: 0898383552; http://www.amazon.com/exec/obidos/ASIN/0898383552/icongroupinterna
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Jeff's Denial: The Moving Story of a Teenage Son Who Fought Leukemia by Attacking Life by Ernest Zielasko; ISBN: 0967343607; http://www.amazon.com/exec/obidos/ASIN/0967343607/icongroupinterna
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Leukemia by Whittaker, Delamore (1987); ISBN: 0632013761; http://www.amazon.com/exec/obidos/ASIN/0632013761/icongroupinterna
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Leukemia by Edward S., MD Henderson (Editor), et al; ISBN: 0721690602; http://www.amazon.com/exec/obidos/ASIN/0721690602/icongroupinterna
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Leukemia by Judith Peacock, Barbara Asselin; ISBN: 0736802827; http://www.amazon.com/exec/obidos/ASIN/0736802827/icongroupinterna
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Leukemia by William Dameshek; ISBN: 0808915134; http://www.amazon.com/exec/obidos/ASIN/0808915134/icongroupinterna
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Leukemia; ISBN: 9290180617; http://www.amazon.com/exec/obidos/ASIN/9290180617/icongroupinterna
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Leukemia (Dahlem Workshop Report, No 30) by Dahlem Workshop Report (1985); ISBN: 3540134158; http://www.amazon.com/exec/obidos/ASIN/3540134158/icongroupinterna
·
Leukemia (Diseases and Disorders) by Melissa Abramovitz, Lucent Books (2002); ISBN: 1560068639; http://www.amazon.com/exec/obidos/ASIN/1560068639/icongroupinterna
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Leukemia (Diseases and People) by Alvin Silverstein, et al; ISBN: 0766013103; http://www.amazon.com/exec/obidos/ASIN/0766013103/icongroupinterna
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Leukemia (The Facts About Series) by Judy Monroe; ISBN: 0896865320; http://www.amazon.com/exec/obidos/ASIN/0896865320/icongroupinterna
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Leukemia (Understanding Illness (Mankato, Minn.).) by Sue Vander Hook, Sue Vander Hook; ISBN: 1583400273; http://www.amazon.com/exec/obidos/ASIN/1583400273/icongroupinterna
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Leukemia (Venture Book) by Dorothy Schainman Siegel, David E. Newton (1994); ISBN: 0531125092; http://www.amazon.com/exec/obidos/ASIN/0531125092/icongroupinterna
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Leukemia : recent advances in biology and treatment : proceedings of a UCLA Symposium held in Keystone, Colorado, January 27-February 2, 1985; ISBN: 084512627X; http://www.amazon.com/exec/obidos/ASIN/084512627X/icongroupinterna
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Leukemia and Lymphoma by J.M. Chessells, I.M. Hann; ISBN: 0702020753; http://www.amazon.com/exec/obidos/ASIN/0702020753/icongroupinterna
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Leukemia and lymphoma; ISBN: 0808908588; http://www.amazon.com/exec/obidos/ASIN/0808908588/icongroupinterna
Books
353
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Leukemia and Lymphoma by Emil J. Freireich; ISBN: 080891166X; http://www.amazon.com/exec/obidos/ASIN/080891166X/icongroupinterna
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Leukemia and Lymphoma Reviews 2 by A Polliack (Author); ISBN: 3718653745; http://www.amazon.com/exec/obidos/ASIN/3718653745/icongroupinterna
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Leukemia and Lymphoma Reviews 3 (Leukemia & Lymphoma Reviews Series) by Aaron Polliack; ISBN: 3718654903; http://www.amazon.com/exec/obidos/ASIN/3718654903/icongroupinterna
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Leukemia and Lymphoma Reviews 4 (Leukemia & Lymphoma Reviews Series) by Aaron Polliack (Editor); ISBN: 3718657600; http://www.amazon.com/exec/obidos/ASIN/3718657600/icongroupinterna
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Leukemia and Lymphoma Reviews, Vol. 1 by A. Polliack; ISBN: 371865251X; http://www.amazon.com/exec/obidos/ASIN/371865251X/icongroupinterna
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Leukemia and Lymphoma Supplement by Michael J. Keating; ISBN: 3718656647; http://www.amazon.com/exec/obidos/ASIN/3718656647/icongroupinterna
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Leukemia and Lymphoma: Detection of Minimal Residual Disease by Theodore F., Ph.D., Md. Zipf (Editor), et al (2002); ISBN: 0896039668; http://www.amazon.com/exec/obidos/ASIN/0896039668/icongroupinterna
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Leukemia and Non-Hodgkin Lymphoma by D. G. Crowther (1979); ISBN: 0080243908; http://www.amazon.com/exec/obidos/ASIN/0080243908/icongroupinterna
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Leukemia and Related Disorders by J. A. Whittaker (Editor), J. A. Holmes (Editor) (1999); ISBN: 0865426074; http://www.amazon.com/exec/obidos/ASIN/0865426074/icongroupinterna
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Leukemia cytochemistry : principles and practice; ISBN: 0745804160; http://www.amazon.com/exec/obidos/ASIN/0745804160/icongroupinterna
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Leukemia in Childhood by A. D. Lascari; ISBN: 0398028109; http://www.amazon.com/exec/obidos/ASIN/0398028109/icongroupinterna
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LEUKEMIA LYMPHONE SUPP 1 by POLLIACK; ISBN: 9057020769; http://www.amazon.com/exec/obidos/ASIN/9057020769/icongroupinterna
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Leukemia Markers by W. Knapp; ISBN: 0124167500; http://www.amazon.com/exec/obidos/ASIN/0124167500/icongroupinterna
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Leukemia Research: Advances in Cell Biology and Treatment by Sharon B. and Gilbert, John R. Murphy (Editor); ISBN: 0444007415; http://www.amazon.com/exec/obidos/ASIN/0444007415/icongroupinterna
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Leukemia Reviews International by Marvin a Rich (Editor) (1984); ISBN: 0824771575; http://www.amazon.com/exec/obidos/ASIN/0824771575/icongroupinterna
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Leukemia Reviews: International by Intl Symp for Comparative Research on Leukemia and Related Diseases (1983); ISBN: 0824770471; http://www.amazon.com/exec/obidos/ASIN/0824770471/icongroupinterna
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Leukemia Sourcebook: Basic Consumer Health Information About Adult and Childhood Leukemias (Health Reference Series) by Joyce Brennfleck Shannon (Editor) (2003); ISBN: 0780806271; http://www.amazon.com/exec/obidos/ASIN/0780806271/icongroupinterna
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Leukemia Therapy by Robert Peter Gale (Editor); ISBN: 0865420246; http://www.amazon.com/exec/obidos/ASIN/0865420246/icongroupinterna
354 Leukemia
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Leukemia Treatment by Gale; ISBN: 9999736378; http://www.amazon.com/exec/obidos/ASIN/9999736378/icongroupinterna
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Leukemia: A Research Report by Barry Leonard (Editor) (1993); ISBN: 0788171895; http://www.amazon.com/exec/obidos/ASIN/0788171895/icongroupinterna
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Leukemia: Advances in Research and Treatment (Cancer Treatment and Research, Ctar 64) by Emil J. Freireich, Hagop Kantarjian (Editor) (1993); ISBN: 0792319672; http://www.amazon.com/exec/obidos/ASIN/0792319672/icongroupinterna
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Leukemia: Cytology and Cytochemistry by Lawrence Kass; ISBN: 0397504632; http://www.amazon.com/exec/obidos/ASIN/0397504632/icongroupinterna
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Leukemia: Just a Shadow by Mary A. Croskey (1996); ISBN: 0965467805; http://www.amazon.com/exec/obidos/ASIN/0965467805/icongroupinterna
·
Leukemia: New Medical Therapies by Lisa Henderson; ISBN: 1930624166; http://www.amazon.com/exec/obidos/ASIN/1930624166/icongroupinterna
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Leukemia: Recent Advances in Biology and Treatment (UCLA Symposia on Molecular and Cellular Biology. New Series, Vol 28) by David W Golde, Robert Peter Gale (Editor); ISBN: 0471847585; http://www.amazon.com/exec/obidos/ASIN/0471847585/icongroupinterna
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Leukemia: Recent Developments in Diagnosis and Therapy (Recent Results in Cancer Research 93) by E. Thiel, S. Thierfelder (Editor); ISBN: 0387132899; http://www.amazon.com/exec/obidos/ASIN/0387132899/icongroupinterna
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Leukemia: Report of the Dahlem Workshop on Leukemia, Berlin 1983, November 1318 (Life Sciences Research Reports, No 30) by I.L. Weissman (Editor); ISBN: 0387134158; http://www.amazon.com/exec/obidos/ASIN/0387134158/icongroupinterna
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Leukemia: the past, the present, the future by Peter Jacobs; ISBN: 079920076X; http://www.amazon.com/exec/obidos/ASIN/079920076X/icongroupinterna
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Leukemia-lymphoma; a collection of papers; ISBN: 0815102070; http://www.amazon.com/exec/obidos/ASIN/0815102070/icongroupinterna
·
Leukemias by J. Fleischer (Editor); ISBN: 0387547827; http://www.amazon.com/exec/obidos/ASIN/0387547827/icongroupinterna
·
Leukemias by John M. Goldman (Editor), Harvey Priesler (Editor) (1984); ISBN: 0407023364; http://www.amazon.com/exec/obidos/ASIN/0407023364/icongroupinterna
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Leukemias and Lymphomas (Contemporary Issues in Clinical Oncology Vol 4) by Peter H. Wiernik (Editor); ISBN: 0443083452; http://www.amazon.com/exec/obidos/ASIN/0443083452/icongroupinterna
·
Leukemias, Lymphomas and Papillomas: Comparative Aspects. Ed by P.A. Bachmann Proc of Symp Held June, 1980 Org by Who Collab Ctr for Coll and Eval O by Munich Symposium on Microbiology (1980); ISBN: 0850662133; http://www.amazon.com/exec/obidos/ASIN/0850662133/icongroupinterna
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Living With Leukemia (Living With) by Patsy Westcott, Raintree Steck-Vaughn Publishers; ISBN: 0817257438; http://www.amazon.com/exec/obidos/ASIN/0817257438/icongroupinterna
Books
355
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Lymphocyte membrane markers in human leukemias and lymphomas by Maxime Seligmann; ISBN: 0950223026; http://www.amazon.com/exec/obidos/ASIN/0950223026/icongroupinterna
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Medical Management of Chronic Myelogenous Leukemia by Moshe Talpaz (Editor), et al; ISBN: 0824799011; http://www.amazon.com/exec/obidos/ASIN/0824799011/icongroupinterna
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Meningeal leukemia by Lawrence E. Broder; ISBN: 0306305941; http://www.amazon.com/exec/obidos/ASIN/0306305941/icongroupinterna
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Milestones in Leukemia Research and Therapy (The Johns Hopkins Series in Contemporary Medicine and Public Health) by Emil J. Freireich, Noreen A. Lemak; ISBN: 0801841305; http://www.amazon.com/exec/obidos/ASIN/0801841305/icongroupinterna
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Minimal Residual Disease in Acute Leukemia by B. Lowenberg (Editor) (2002); ISBN: 0898386306; http://www.amazon.com/exec/obidos/ASIN/0898386306/icongroupinterna
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Minimal Residual Disease in Acute Leukemia, 1986 (Developments in Oncology) by A. Hagenbeek (Editor) (1986); ISBN: 089838799X; http://www.amazon.com/exec/obidos/ASIN/089838799X/icongroupinterna
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Modern trends in human leukemia : biological, biochemical, and virological aspects; ISBN: 0808908529; http://www.amazon.com/exec/obidos/ASIN/0808908529/icongroupinterna
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Modern trends in human leukemia IV : latest results in clinical and biological research including pediatric oncology; ISBN: 0387106227; http://www.amazon.com/exec/obidos/ASIN/0387106227/icongroupinterna
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Modern Trends in Human Leukemia IX by Rolf Neth (1992); ISBN: 3540543600; http://www.amazon.com/exec/obidos/ASIN/3540543600/icongroupinterna
·
Modern Trends in Human Leukemia VII. New Results in Clinical and Biological Research Including Pedriatic Oncology: Wilsede Joint Meeting on Pedriatic Oncology IV. Hamburg, June 21, 1986 and Wilsede, June 22 - 25, 1986 by R. Neth (Editor), Et Al (Editor); ISBN: 354017754X; http://www.amazon.com/exec/obidos/ASIN/354017754X/icongroupinterna
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Modern trends in human leukemia VIII : new results in clinical and biological research including pediatric oncology; ISBN: 3540509674; http://www.amazon.com/exec/obidos/ASIN/3540509674/icongroupinterna
·
Molecular Biology of Hematopoiesis and Treatment of Leukemias and Lymphomas: 10th Symposium, Hamburg, July 1997, Proceedings (Acta Heamatologica , Vol 99, No 3) by Abraham N.G. (Editor), et al (1998); ISBN: 3805566816; http://www.amazon.com/exec/obidos/ASIN/3805566816/icongroupinterna
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Molecular Genetics and Therapy of Leukemia (Cancer Treatment and Research, V. 84) by Emil J. Freireich (Editor), Hagop Kantarjian (Editor) (1996); ISBN: 0792339126; http://www.amazon.com/exec/obidos/ASIN/0792339126/icongroupinterna
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Monocytes, monocytosis, and monocytic leukemia by Lawrence Kass; ISBN: 0398028834; http://www.amazon.com/exec/obidos/ASIN/0398028834/icongroupinterna
356 Leukemia
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My favourite poem : an anthology of verse chosen by the famous in aid of the Sharon Allen Leukemia Trust; ISBN: 0552127132; http://www.amazon.com/exec/obidos/ASIN/0552127132/icongroupinterna
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Myelodysplastic Syndromes & Secondary Acute Myelogenus Leukemia: Directions for the New Millennium by Azra Raza (Editor), Suneel D., Ph.D. Mundle (Editor); ISBN: 0792373960; http://www.amazon.com/exec/obidos/ASIN/0792373960/icongroupinterna
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New Approaches to the Treatment of Leukemia (Eso Monographs) by E. J. Freireich (Editor); ISBN: 0387522611; http://www.amazon.com/exec/obidos/ASIN/0387522611/icongroupinterna
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New Findings on Aclarubicin in the Treatment of Acute Myeloid Leukemia by W. Hiddemann, R. Mertelsmann (Editor) (1990); ISBN: 0387526137; http://www.amazon.com/exec/obidos/ASIN/0387526137/icongroupinterna
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New Findings on Aclarubicin in the Treatment of Acute Myeloid Leukemia (1990); ISBN: 3540526137; http://www.amazon.com/exec/obidos/ASIN/3540526137/icongroupinterna
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No Safe Place: Toxic Waste, Leukemia, and Community Action by Phil Brown, Edwin J. Mikkelsen (Contributor); ISBN: 0520070348; http://www.amazon.com/exec/obidos/ASIN/0520070348/icongroupinterna
·
Nomenclature, methodology and results of clinical trials in acute leukemias; ISBN: 038706401X; http://www.amazon.com/exec/obidos/ASIN/038706401X/icongroupinterna
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Non-Lymphoid Leukemias in Children (1985); ISBN: 0030720613; http://www.amazon.com/exec/obidos/ASIN/0030720613/icongroupinterna
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Non-Lymphoid Leukemias in Children by Carl Pochedly (Editor) (1985); ISBN: 0275900096; http://www.amazon.com/exec/obidos/ASIN/0275900096/icongroupinterna
·
Oncogenes in the Development of Leukemia (Cancer Survey Series, Vol 15) by Owen N. Witte (1992); ISBN: 0879694068; http://www.amazon.com/exec/obidos/ASIN/0879694068/icongroupinterna
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One Day at a Time: Children Living With Leukemia (Don't Turn Away) by Thomas Bergman (Photographer); ISBN: 1555329136; http://www.amazon.com/exec/obidos/ASIN/1555329136/icongroupinterna
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Pathogenesis of Leukemias & Lymphomas: Environmental Influences by Ian T. Magrath (Editor) (1984); ISBN: 0608004022; http://www.amazon.com/exec/obidos/ASIN/0608004022/icongroupinterna
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Pathogenesis of Leukemias and Lymphomas Environmental Influences by Ian T. Magrath (Editor); ISBN: 0890049017; http://www.amazon.com/exec/obidos/ASIN/0890049017/icongroupinterna
·
Pediatric Cancer Sourcebook: Basic Consumer Health Information About Leukemias, Brain Tumors, Sarcomas (Health Reference Series) by Edward J. Prucha (Editor), Ed Prucha (Editor); ISBN: 0780802454; http://www.amazon.com/exec/obidos/ASIN/0780802454/icongroupinterna
·
Perinatal Risk Factors for Childhood Leukemia (Comprehensive Summaries of Uppsala Dissertations from the Faculty of mediciNe, 1111) by Estelle Naumberg
Books
357
(2002); ISBN: 9155452051; http://www.amazon.com/exec/obidos/ASIN/9155452051/icongroupinterna ·
Programmed Instruction: Leukemia by Melissa Ern; ISBN: 089352221X; http://www.amazon.com/exec/obidos/ASIN/089352221X/icongroupinterna
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Radiation Toxicology: Bone Marrow and Leukemia by J. H. Hendry (Editor), Brian I. Lord (Editor) (1995); ISBN: 0748403388; http://www.amazon.com/exec/obidos/ASIN/0748403388/icongroupinterna
·
Radiology of Childhood Leukemia and Its Therapy by Nancy S. Rosenfield (1982); ISBN: 0875271731; http://www.amazon.com/exec/obidos/ASIN/0875271731/icongroupinterna
·
Recent Advances in Cell Biology of Acute Leukemia (1993); ISBN: 3540564179; http://www.amazon.com/exec/obidos/ASIN/3540564179/icongroupinterna
·
Recent Advances in Cell Biology of Acute Leukemia: Impact on Clinical Diagnosis and Therapy (Recent Results in Cancer Research, Vol 131) by W.-D. Ludwig, E. Thiel (Editor); ISBN: 0387564179; http://www.amazon.com/exec/obidos/ASIN/0387564179/icongroupinterna
·
Recent Advances in Leukemia and Lymphoma (UCLA Symposia on Molecular and Cellular Biology, New Ser, Vol 61) by Robert Peter Gale (Editor), David W. Golde (Editor); ISBN: 0471602566; http://www.amazon.com/exec/obidos/ASIN/0471602566/icongroupinterna
·
Roentgenology of the Lymphomas and Leukemias: A Seminars in Roentgenology Reprint, July and October 1980 by Benjamin Felson; ISBN: 0808913336; http://www.amazon.com/exec/obidos/ASIN/0808913336/icongroupinterna
·
Shannon: A Book for Parents of Children With Leukemia by Frank Leonard, Johnson; ISBN: 0801567769; http://www.amazon.com/exec/obidos/ASIN/0801567769/icongroupinterna
·
Slide Atlas of Acute and Chronic Leukemias (Slide Atlas of Diagnostic Oncology) by Arthur T. Skarin MD; ISBN: 1563750414; http://www.amazon.com/exec/obidos/ASIN/1563750414/icongroupinterna
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Slide Atlas of Solid Tumors, Leukemias, and Lymphomas of Childhood by Steven Sallan MD; ISBN: 1563750449; http://www.amazon.com/exec/obidos/ASIN/1563750449/icongroupinterna
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Supportive Therapy in Leukemia Patients: Clinical Handbook with Checklist (Supportive Measures in Oncology) by Volker Heinemann, Ulrich Jehn; ISBN: 3137955017; http://www.amazon.com/exec/obidos/ASIN/3137955017/icongroupinterna
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Surviving Leukemia: A Practical Guide by Robert Dr Patenaude, E. Donnall Thomas (Preface) (1999); ISBN: 1552093549; http://www.amazon.com/exec/obidos/ASIN/1552093549/icongroupinterna
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Terminal Transfer Erase in Immunobiology and Leukemia (Advances in Experimental Medicine and Biology, 145) by Umberto Bertazzoni; ISBN: 0306409895; http://www.amazon.com/exec/obidos/ASIN/0306409895/icongroupinterna
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The Acute Leukemias by Thomas F. Necheles; ISBN: 0913258571; http://www.amazon.com/exec/obidos/ASIN/0913258571/icongroupinterna
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The Acute Leukemias: Biologic, Diagnostic, and Therapeutic Determinants (Hematology Series, No 6) by Sanford A. Stass (Editor); ISBN: 0824777662; http://www.amazon.com/exec/obidos/ASIN/0824777662/icongroupinterna
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The Alternative vs. Orthodox Treatment Of Leukemia by Lana Corrine Cantrell; ISBN: 0962074918; http://www.amazon.com/exec/obidos/ASIN/0962074918/icongroupinterna
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The Biology of Human Leukemia (Johns Hopkins Series in Contemporary Medicine and Public Health) by Alvin M. Mauer (Editor); ISBN: 0801839076; http://www.amazon.com/exec/obidos/ASIN/0801839076/icongroupinterna
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The Breuss Cancer Cure: Advice for the Prevention and Natural Treatment of Cancer, Leukemia and Other Seemingly Incurable Diseases by Rudolf Breuss (1998); ISBN: 0920470564; http://www.amazon.com/exec/obidos/ASIN/0920470564/icongroupinterna
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The Child With Leukemia. by Carl. Pochedly; ISBN: 0398027358; http://www.amazon.com/exec/obidos/ASIN/0398027358/icongroupinterna
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The Chromosomes in Human Cancer and Leukemia by Avery A. Sandberg (Editor); ISBN: 0838510922; http://www.amazon.com/exec/obidos/ASIN/0838510922/icongroupinterna
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The chronic leukemias; chemistry, pathophysiology, and treatment by John R. Durant; ISBN: 0398022755; http://www.amazon.com/exec/obidos/ASIN/0398022755/icongroupinterna
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The Cure of Childhood Leukemia: Into the Age of Miracles by John Laszlo (1996); ISBN: 0813523850; http://www.amazon.com/exec/obidos/ASIN/0813523850/icongroupinterna
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The Geographical Epidemiology of Childhood Leukemia and Non-Hodgkin Lymphomas in Great Britain, 1966-83 (Studies on Medical and Population Subjects) by Gerald Draper (1991); ISBN: 0116913576; http://www.amazon.com/exec/obidos/ASIN/0116913576/icongroupinterna
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The Journey Back: A Survivors Guide to Leukemia by Jack L. Smedley, Iva Smedley (1996); ISBN: 1880451190; http://www.amazon.com/exec/obidos/ASIN/1880451190/icongroupinterna
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The Leukemia cell; ISBN: 0849350093; http://www.amazon.com/exec/obidos/ASIN/0849350093/icongroupinterna
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The leukemia patient as a partner in therapy : a guidebook for patients, relatives, nurses, and physicians by Marcel U. Heim; ISBN: 086577515X; http://www.amazon.com/exec/obidos/ASIN/086577515X/icongroupinterna
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The Leukemia Patient As Partner in Therapy: A Guidebook for Patients, Relatives, Nurses and Physicians (Supportive Measures in Oncology/Import) by Marcel U. Heim, Ulla Vehling-Kaiser; ISBN: 3131271019; http://www.amazon.com/exec/obidos/ASIN/3131271019/icongroupinterna
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The Leukemia-Lymphoma Cell Line Factsbook (Factsbook Series) by Hans G. Drexler (2000); ISBN: 0122219708; http://www.amazon.com/exec/obidos/ASIN/0122219708/icongroupinterna
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The Leukemias: Epidemiologic Aspects (Monographs in Epidemiology and Biostatistics, Vol. 6) by Martha S. Linet; ISBN: 0195034481; http://www.amazon.com/exec/obidos/ASIN/0195034481/icongroupinterna
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The Official Parent's Sourcebook on Childhood Acute Lymphoblastic Leukemia: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2002); ISBN: 0597833451; http://www.amazon.com/exec/obidos/ASIN/0597833451/icongroupinterna
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The Official Parent's Sourcebook on Childhood Acute Myeloid Leukemia by James N., Md. Parker (Editor), et al (2002); ISBN: 0597834520; http://www.amazon.com/exec/obidos/ASIN/0597834520/icongroupinterna
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The Official Patient's Sourcebook on Adult Acute Myeloid Leukemia by James N., Md. Parker (Editor), et al (2002); ISBN: 0597834547; http://www.amazon.com/exec/obidos/ASIN/0597834547/icongroupinterna
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The Official Patient's Sourcebook on Chronic Lymphocytic Leukemia: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2002); ISBN: 0597834601; http://www.amazon.com/exec/obidos/ASIN/0597834601/icongroupinterna
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The Official Patient's Sourcebook on Hairy Cell Leukemia by James N., Md. Parker, et al (2002); ISBN: 0597834628; http://www.amazon.com/exec/obidos/ASIN/0597834628/icongroupinterna
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The Role of Stat1 in Retinoic Acid-Induced Myelomonocytic Differentiation of Human Leukemia Cells (Comprehensive Summaries of Uppsala Dissertations from the Faculty of mediciNe, 1117) by Anna Dimberg (2002); ISBN: 9155452248; http://www.amazon.com/exec/obidos/ASIN/9155452248/icongroupinterna
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This Day Is Mine: Living With Leukemia (Crisis (Mankato, Minn.).) by Jane Claypool Miner, et al; ISBN: 0896861732; http://www.amazon.com/exec/obidos/ASIN/0896861732/icongroupinterna
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Treatment of Acute Leukemias: New Directions for Clinical Research by Ching-Hon Pui (Editor), Chinghon Pui; ISBN: 0896038343; http://www.amazon.com/exec/obidos/ASIN/0896038343/icongroupinterna
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Treatment of acute lymphocytic leukemia by Donald Pinkel; ISBN: 0950223034; http://www.amazon.com/exec/obidos/ASIN/0950223034/icongroupinterna
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Two Decades of Adult T-Cell Leukemia and Htlv-I Research: Gann Monograph on Cancer Research (Gann Mongraph on Cancer Research) by Monograph Committee Japanese Cancer Association (Editor) (2003); ISBN: 3805575432; http://www.amazon.com/exec/obidos/ASIN/3805575432/icongroupinterna
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Understanding Leukemia; ISBN: 0317474626; http://www.amazon.com/exec/obidos/ASIN/0317474626/icongroupinterna
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Understanding Leukemia by Cynthia P. Margolies, Kenneth, M.D. McCredie; ISBN: 0684179784; http://www.amazon.com/exec/obidos/ASIN/0684179784/icongroupinterna
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Understanding Leukemia: What It Is, How to Treat It and How to Cope With It by Cynthia P. Margolies, et al; ISBN: 0684187256; http://www.amazon.com/exec/obidos/ASIN/0684187256/icongroupinterna
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Unifying concepts of leukemia; ISBN: 3805513836; http://www.amazon.com/exec/obidos/ASIN/3805513836/icongroupinterna
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Vaccine Intervention Against Virus-Induced Tumors (Leukemia and Lymphoma Research) by John M. Goldman (Editor) (1986); ISBN: 0943818931; http://www.amazon.com/exec/obidos/ASIN/0943818931/icongroupinterna
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William Dameshek and Frederick Gunz's Leukemia by William Dameshek; ISBN: 080890843X; http://www.amazon.com/exec/obidos/ASIN/080890843X/icongroupinterna
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Workshop on Prognostic Factors in Human Acute Leukemia by G. Raspe, Raspé ISBN: 0080196217; http://www.amazon.com/exec/obidos/ASIN/0080196217/icongroupinterna
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You and Leukemia: A Day at a Time by Lynn S., Md. Baker, et al (2002); ISBN: 072169067X; http://www.amazon.com/exec/obidos/ASIN/072169067X/icongroupinterna
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “leukemia” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 ·
"Purinethol" 6-mercaptopurine, "Myleran" busulfan, "Leukeran" chlorambucil; "B. W. & Co." products for the treatment of leukemia. Author: Burroughs Wellcome and Company.; Year: 1964; [Tuckahoe, N. Y.] 1963
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Atypical leukemia. Author: Blair, Thomas Richard,; Year: 1966; [Minneapolis] 1965
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Effects of concurrent infections and their toxins on the course of leukemia [by] Louis Pelner, George A. Fowler, and Helen C. Nauts. Author: Pelner, Louis,; Year: 1958; Stockholm, 1958
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Leukemia in animals and man; proceedings, edited by H. J. Bendixen. Author: Bendixen, H. J. (Hans Jørgen); Year: 1965; Basel, New York, Karger, 1968
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Methodological approaches to the study of leukemias; a symposium held at the Wistar Institute of Anatomy and Biology, April 5 and 6, 1965. Author: Defendi, Vittorio,; Year: 1966; Philadelphia, Wistar Institute Press, 1965
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Pathology of leukemia. Author: Amromin, George D.,; Year: 1965; New York, London, Hoeber [c1968]
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Perspectives in leukemia. A presentation of the Leukemia Society of America, Inc., New Orleans, Louisiana, December, 1966. Edited by William Dameshek and Ray M. Dutcher. Author: Dameshek, William,; Year: 1965; New York, Grune; Stratton, 1968
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Symposium on changing concepts in Hodgkin's disease, lymphomas, and leukemias. Philip Rubin, Malcolm A. Bagshaw, guest editors. Author: Rubin, Philip,; Year: 1965; Philadelphia, London, Saunders [c1968]
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In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
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The adrenothymic constitution and susceptibility to leukemia in mice; a study of the AKR Author: Arnesen, Kristen.; Year: 1956; Oslo, 1956
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The leukemias; etiology, pathophysiology, and treatment; ed. by John W. Rebuck [et al.]. Author: Rebuck, John Walter,; Year: 1963; New York, Academic Press, 1957
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The Philadelphia chromosome in leukemia research; a bibliography. Author: Stemple, Ruth M.; Year: 1963; Oak Ridge, Tenn. Oak Ridge National Laboratory, 1968
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Two decades of adult T-cell leukemia and HTLV-I research Author: Sugamura, Kazuo.; Year: 2003; Tokyo: Japan Scientific Societies Press; Basel; New York: Karger, 2003; ISBN: 4762230030
Chapters on Leukemia In order to find chapters that specifically relate to leukemia, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and leukemia using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “leukemia” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on leukemia: ·
Neoplasms of the Immune System: Lymphomas, Leukemias, and Langerhans Cell Histiocytoses Source: in Marx, R.E.; Stern, D. Oral and Maxillofacial Pathology: A Rationale for Diagnosis and Treatment. Chicago, IL: Quintessence Publishing Co, Inc. 2003. p.829-875. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail: [email protected]. Website: www.quintpub.com. PRICE: $ 399.00 plus shipping and handling. ISBN: 0867153903. Summary: This chapter on neoplasms of the immune system is from a clinically oriented guide for oral and maxillofacial surgeons and other advanced dental and medical specialists who deal with pathologies in the oral cavity, midface, and neck. The chapter covers lymphomas, leukemia, and Langerhans cell histiocytosis. An introductory section discusses cancer cell development, proliferation, and behavior; and an overview and classification of lymphomas (Hodgkin and non-Hodgkin), leukemias, and Langerhans cell histiocytosis. The authors then discuss specific conditions of each of these categories. For each condition, the authors discuss clinical presentation and pathogenesis, differential diagnosis, diagnostic work-up, histopathology, treatment, and prognosis. Full-color photographs illustrate the chapter. 46 figures. 6 tables.
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CHAPTER 8. MULTIMEDIA ON LEUKEMIA Overview In this chapter, we show you how to keep current on multimedia sources of information on leukemia. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on leukemia is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “leukemia” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “leukemia” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on leukemia: ·
Living and Dying With AIDS Contact: Films for the Humanities and Sciences, PO Box 2053, Princeton, NJ, 08543, (800) 257-5126. Summary: The centerpiece of this video is the film documentary of the final days of "Purlie" a gay man dying of AIDS in Tennessee. He is shown at home receiving care from his partner and friends, one of whom is a registered nurse. Intertwined around this central story are the stories of many others who are affected by HIV/AIDS. Purlie's social worker is shown helping an African man infected in his native country; and a mother with HIV and cancer, whose husband was fired because of her condition and whose infant daughter carries HIV antibodies. The mother of an eleven-year old boy who became infected through transfused blood used during his treatment for leukemia, talks about the discrimination against her son. Tennessee HIV educators are shown in the streets distributing information, condoms and bleach. A former drug abuser and male prostitute is shown working in a homeless shelter where homosexuality and drug use are considered sins. The urgent need for good HIV education in the schools and the
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dramatic increase in HIV/AIDS seen in health clinics is addressed. The thoughts that are expressed, throughout the video, focus on the lack of compassion for people living with AIDS in the United States; the sense that these individuals, regardless of how they contracted the disease, should be allowed to suffer because they brought it upon themselves by their behavior or sexual orientation.
Audio Recordings The Combined Health Information Database contains abstracts on audio productions. To search CHID, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find audio productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Sound Recordings.” Type “leukemia” (or synonyms) into the “For these words:” box. The following is a typical result when searching for sound recordings on leukemia: ·
The Cauldron Journey for Healing Contact: Nicki Scully, PO Box 5025, Eugene, OR, 97405, (541) 484-1099. Summary: This sound recording is a guided meditation with music, which is advocated as a cure for those who have Acquired immunodeficiency syndrome (AIDS), Human immunodeficiency virus (HIV) infection, or leukemia. The meditative journey takes the listener to Kuan Yin, the Chinese Bodhisattva, or goddess of Compassion.
Bibliography: Multimedia on Leukemia The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in leukemia (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on leukemia: ·
Acute leukemia: the nursing approach [slide] Source: Roswell Park Memorial Institute, in cooperation with the Lakes Area Regional Medical Program; Year: 1975; Format: Slide; [Buffalo]: Communications in Learning, 1975
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Acute leukemia [slide] Source: [American Society of Hematology]; Year: 1974; Format: Slide; [Seattle: The Society: for sale by University of Washington Health Sciences Center for Educational Resources, 1974]
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Adults with acute leukemia [videorecording] Source: University of Texas System Cancer Center; Year: 1976; Format: Videorecording; Houston: The Center, 1976
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Bone marrow transplantation for treatment of leukemia [videorecording] Source: a production of the UCLA Public Information Office, in association with UCLA Media Center; Year: 1976; Format: Videorecording; Berkeley, Calif.: Regents of the University of California, c1976
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Care of the individual having leukemia [sound recording] Source: Roswell Park Memorial Institute; Year: 1977; Format: Sound recording; Buffalo: Communications in Learning, [1977]
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Care of the patient with leukemia [filmstrip] Source: Trainex Corporation; Year: 1970; Format: Filmstrip; Garden Grove, Calif.: Trainex, c1970
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Chronic lymphatic leukemia [videorecording] Source: [Henry E.] Wilson; produced by Ohio State University, Medical Audiovisual and Television Center; Year: 1971; Format: Videorecording; [Columbus, Ohio]: The Center, c1971
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Chronic lymphocytic leukemia [videorecording] Source: author, Charles Koller; faculty consultant, Roland Hiss; Biomedical Media Production Unit, the University of Michigan Medical Center, Office of Educational Resources & Research; Year: 1981; Format: Videorecording; Ann Arbor, Mich.: University of Michigan, c1981
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Classification and management of the leukemias [slide] Source: John M. Bennett, Claude Sultan; Year: 9999; Format: Slide; [New York]: Medcom, c1982-
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Cytochemistry of acute leukemias and hairy cell leukemia [videorecording] Source: American Society of Clinical Pathologists; Year: 1979; Format: Videorecording; Chicago: The Society, c1979
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Extramedullary disease-leukemia [videorecording] Source: University of Texas System Cancer Center M. D. Anderson Hospital and Tumor Institute; Year: 1975; Format: Videorecording; Houston: The Institute, 1975
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Growth regulation of leukemia in normal hemopoietic tissue [videorecording] Source: University of Texas System Cancer Center M. D. Anderson Hospital and Tumor Institute; Year: 1976; Format: Videorecording; Houston: The Institute, 1976
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Leukemia: a bird's eye view [slide]: food for thought Source: Health Sciences McMaster University; produced by Audio Visual Services, McMaster University; Year: 1972; Format: Slide; [Hamilton, Ont.]: Health Sciences McMaster Univ., 1972
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Leukemia [videorecording] Source: University of Texas System Cancer Center M. D. Anderson Hospital and Tumor Institute; Year: 1975; Format: Videorecording; Houston: The Institute, 1975
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Leukemia in children [filmstrip] Source: Medical Electronic Educational Services; produced by School of Nursing University of Missouri-Columbia; Year: 1973; Format: Filmstrip; Columbia: The University, c1973
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Management of acute leukemia [videorecording] Source: University of Texas System Cancer Center M. D. Anderson Hospital and Tumor Institute; Year: 1976; Format: Videorecording; Houston: The Institute, 1976
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Oral manifestations and management of leukemia in children [slide]: a selfinstructional program Source: Frank H. Farrington, in cooperation with the Office of Educational Services, Medical University of South Carolina; Year: 1979; Format: Slide; Chapel Hill, N. C.: Health Sciences Consortium, c1979
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Teaching a child about leukemia [filmstrip] Source: Madeline Petrillo; Year: 1975; Format: Filmstrip; Scarsdale, N. Y.: Steve Campus Productions: [for sale by Campus Film Distributors], c1975
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The Leukemias [slide] Source: James W. Linman; Year: 1971; Format: Slide; New York: Medcom, c1971
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The Management of acute leukemia [videorecording] Source: University of Texas System Cancer Center M. D. Anderson Hospital and tumor Institute; [produced by] MDA-TV; Year: 1977; Format: Videorecording; Houston: The Center, 1977
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Treatment of acute leukemia [slide] Source: Roswell Park Memorial Institute, in cooperation with the Lakes Area Regional Medical Program; Year: 1975; Format: Slide; [Buffalo]: Communications in Learning, 1975
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X-ray findings associated with leukemia and multiple myeloma [videorecording] Source: M. I. Goldstein; produced by Ohio State University, Medical Audiovisual and Television Center; Year: 1972; Format: Videorecording; [Columbus, Ohio]: The Center, c1972
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CHAPTER 9. PERIODICALS AND NEWS ON LEUKEMIA Overview In this chapter, we suggest a number of news sources and present various periodicals that cover leukemia.
News Services and Press Releases One of the simplest ways of tracking press releases on leukemia is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing.
PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “leukemia” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance.
Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to leukemia. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “leukemia” (or synonyms). The following was recently listed in this archive for leukemia: ·
Leukemia risk higher among heavy babies Source: Reuters Health eLine Date: November 04, 2003
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High birth weight is a risk factor for childhood leukemia Source: Reuters Medical News Date: November 04, 2003
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Elevated CD86 levels predict poor survival with leukemia Source: Reuters Medical News Date: October 24, 2003
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Ilex files for U.S. FDA approval of leukemia drug Source: Reuters Industry Breifing Date: October 22, 2003
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DNA vaccine improves survival in animal model of leukemia Source: Reuters Industry Breifing Date: October 20, 2003
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Oncogene activation to blame for leukemia with SCID-X1 gene therapy Source: Reuters Medical News Date: October 16, 2003
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Racial disparity in leukemia outcomes can be overcome with intensive therapy Source: Reuters Medical News Date: October 14, 2003
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Intensive therapy beats racial leukemia gap Source: Reuters Health eLine Date: October 14, 2003
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Single microarray subclassifies pediatric lymphoblastic leukemia Source: Reuters Medical News Date: October 13, 2003
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Ilex gets fast track for pediatric leukemia drug Source: Reuters Industry Breifing Date: September 09, 2003
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Acute lymphoblastic leukemia curable, normal survival achievable Source: Reuters Medical News Date: August 13, 2003
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New drug eliminates leukemia in some patients Source: Reuters Health eLine Date: July 15, 2003
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JJ says Zarnestra eliminated signs of leukemia in some elderly patients Source: Reuters Medical News Date: July 15, 2003
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JJ says leukemia drug eliminated signs of cancer Source: Reuters Industry Breifing Date: July 15, 2003
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Teva gets North American rights to leukemia drug Source: Reuters Industry Breifing Date: July 01, 2003
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E.U. panel backs survival claim for ILEX, Schering leukemia therapy Source: Reuters Industry Breifing Date: June 25, 2003
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Vitamin D2 analog active against leukemia, myeloma, and colon cancer Source: Reuters Medical News Date: June 23, 2003
Periodicals and News
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Use of aspirin, but not other NSAIDs, linked to reduced risk of leukemia Source: Reuters Industry Breifing Date: June 17, 2003
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Encouraging response seen with FLT3 inhibitor in acute myelogenous leukemia Source: Reuters Industry Breifing Date: June 05, 2003
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Possible cause of common childhood leukemia found Source: Reuters Health eLine Date: May 22, 2003
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Gleevec wins pediatric leukemia indication Source: Reuters Medical News Date: May 21, 2003
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Gleevec wins pediatric leukemia approval Source: Reuters Health eLine Date: May 21, 2003
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Novartis' Gleevec wins pediatric leukemia indication Source: Reuters Industry Breifing Date: May 20, 2003
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In mice, estrogen receptors play role in leukemia Source: Reuters Health eLine Date: May 05, 2003
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Protein may be marker for leukemia prognosis Source: Reuters Health eLine Date: May 01, 2003
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Pentostatin/cyclophosphamide promising for pretreated chronic lymphocytic leukemia Source: Reuters Industry Breifing Date: April 25, 2003
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Leukemia cells show treatment-specific changes in gene expression Source: Reuters Medical News Date: April 25, 2003
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Troxacitabine-based chemotherapy effective in refractory myeloid leukemias Source: Reuters Industry Breifing Date: April 10, 2003
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New strategy preserves graft-versus-leukemia response without lethal GVHD Source: Reuters Medical News Date: April 09, 2003
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WT1 gene expression reflects success of stem cell transplants in leukemia Source: Reuters Medical News Date: April 07, 2003
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Vion tests Triapine as combination therapy for leukemia Source: Reuters Industry Breifing Date: March 31, 2003
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PDl licenses failed phase III leukemia drug to Actinium Source: Reuters Industry Breifing Date: March 18, 2003
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Gleevec cannot control CNS leukemia in mouse model Source: Reuters Medical News Date: March 10, 2003
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Adverse skin reactions common with imatinib leukemia treatment Source: Reuters Industry Breifing Date: February 24, 2003
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Early blast clearance predicts better outcome in acute myeloid leukemia Source: Reuters Medical News Date: February 10, 2003
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Schering's Fludara approved in Europe as first-line leukemia treatment Source: Reuters Industry Breifing Date: February 06, 2003
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Rapamycin shows promise for chronic lymphocytic leukemia Source: Reuters Medical News Date: January 27, 2003
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Phosphodiesterase inhibitors show activity against leukemia cells Source: Reuters Industry Breifing Date: January 24, 2003
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Agent Orange increases leukemia risk Source: Reuters Medical News Date: January 24, 2003
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IL-11 treatment reduces bacteremia during chemotherapy for leukemia Source: Reuters Industry Breifing Date: January 23, 2003
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Agent Orange can cause leukemia, experts say Source: Reuters Health eLine Date: January 23, 2003
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All-trans retinoic acid provides long-term survival benefit in acute promyelocytic leukemia Source: Reuters Industry Breifing Date: January 14, 2003
The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine.
Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name.
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Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “leukemia” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests.
Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “leukemia” (or synonyms). If you know the name of a company that is relevant to leukemia, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/.
BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “leukemia” (or synonyms).
Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “leukemia” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on leukemia: ·
Mouth Is a Mirror of the Body Source: Closing the Gap. p. 13. July 1999. Contact: Available from Office of Minority Health Resource Center. P.O. Box 37337, Washington, DC 20013-7337. (800) 444-6472. Summary: Dental care providers have changed their identity and have taken on the responsibility of primary care providers. This brief newsletter article describes how signs and symptoms that show up in the mouth can be indicators for general systemic health and disease and notes that dentists may be the first health care providers to recognize these signs and symptoms. The author briefly reports on symptoms of
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immune deficiency, viral diseases, cancer, leukemia, diabetes, and heart disease, as well as medications (drug effects). The author stresses that although signs in the mouth may represent a serious condition or systemic disease, they can also be completely harmless. Clinical signs alone are not diagnostic of systemic diseases; they must be supplemented with laboratory procedures such as biopsies or blood tests to confirm the presence of disease. ·
Warning Signs in the Mouth Source: Closing the Gap. p. 13. July 1999. Contact: Available from Office of Minority Health Resource Center. P.O. Box 37337, Washington, DC 20013-7337. (800) 444-6472. Summary: This brief newsletter article describes the warning signs and symptoms that may show up in the mouth with systemic diseases such as kidney disease, anemia, hemophilia and other bleeding disorders, adrenal gland disorders, and inflammatory bowel diseases. Chronic renal (kidney) disease has several early oral signs, including a metallic taste in the mouth, dry mouth, swelling glands, and frequent infection of the soft tissues. In the early stages of anemia, patients often complain about their tongue becoming smooth and glistening and feeling like it is burning. Unprovoked bleeding of the gums is a warning sign of bleeding disorders such as hemophilia, von Willebrand's disease, leukemia, and lymphomas. Brown or black splotches on the inner lining of the cheeks and lips are seen in the early stages of Addison's disease and other adrenal gland disorders. A cobblestone appearance of the soft tissue of the mouth and a generalized swelling of the linings of the cheeks and lips are early signs of inflamed bowels and Crohn's disease. Patients with ulcers often have a history of oral cold sores because mouth and intestinal tissues are closely related.
Academic Periodicals covering Leukemia Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to leukemia. In addition to these sources, you can search for articles covering leukemia that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for leukemia. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DIÒ Advice for the PatientÒ can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with leukemia. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to leukemia: Alemtuzumab ·
Systemic - U.S. Brands: Campath http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500303.html
Allopurinol ·
Systemic - U.S. Brands: Aloprim; Zyloprim http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202021.html
Arsenic Trioxide ·
Systemic - U.S. Brands: Trisenox http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500241.html
Asparaginase ·
Systemic - U.S. Brands: Elspar http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202072.html
Busulfan ·
Systemic - U.S. Brands: Busulfex; Myleran http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202101.html
Chlorambucil ·
Systemic - U.S. Brands: Leukeran http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202124.html
Cladribine ·
Systemic - U.S. Brands: Leustatin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202699.html
Corticosteroids ·
Dental - U.S. Brands: Kenalog in Orabase; Orabase-HCA; Oracort; Oralone http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202010.html
·
Inhalation - U.S. Brands: AeroBid; AeroBid-M; Azmacort; Beclovent; Decadron Respihaler; Pulmicort Respules; Pulmicort Turbuhaler; Vanceril; Vanceril 84 mcg Double Strength http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202011.html
·
Nasal - U.S. Brands: Beconase; Beconase AQ; Dexacort Turbinaire; Flonase; Nasacort; Nasacort AQ; Nasalide; Nasarel; Nasonex; Rhinocort; Vancenase; Vancenase AQ 84 mcg; Vancenase pockethaler http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202012.html
·
Ophthalmic - U.S. Brands: AK-Dex; AK-Pred; AK-Tate; Baldex; Decadron; Dexair; Dexotic; Econopred; Econopred Plus; Eflone; Flarex; Fluor-Op; FML Forte; FML Liquifilm; FML S.O.P.; HMS Liquifilm; Inflamase Forte; Inflamase Mild; I-Pred; Lite Pred; Maxidex; Ocu-Dex; Ocu-Pred; Ocu-Pr http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202013.html
·
Otic - U.S. Brands: Decadron http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202014.html
Researching Medications
·
Rectal - U.S. Brands: Anucort-HC; Anu-Med HC; Anuprep HC; Anusol-HC; Anutone-HC; Anuzone-HC; Cort-Dome; Cortenema; Cortifoam; Hemorrhoidal HC; Hemril-HC Uniserts; Proctocort; Proctosol-HC; Rectosol-HC http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203366.html
Cyclophosphamide ·
Systemic - U.S. Brands: Cytoxan; Neosar http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202174.html
Cytarabine ·
Systemic - U.S. Brands: Cytosar-U http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202177.html
Daunorubicin ·
Systemic - U.S. Brands: Cerubidine http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202183.html
Doxorubicin ·
Systemic - U.S. Brands: Rubex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202209.html
Fludarabine ·
Systemic - U.S. Brands: Fludara http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202630.html
Gemtuzumab Ozogamicin ·
Systemic - U.S. Brands: Mylotarg http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500153.html
Heparin ·
Systemic - U.S. Brands: Calciparine; Liquaemin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202280.html
Hydroxyurea ·
Systemic - U.S. Brands: Droxia; Hydrea http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202291.html
Idarubicin ·
Systemic - U.S. Brands: Idamycin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202611.html
Ifosfamide ·
Systemic - U.S. Brands: IFEX http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202293.html
Imatinib ·
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Systemic - U.S. Brands: Gleevec http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500297.html
376 Leukemia
Interferons, Alpha ·
Systemic - U.S. Brands: Alferon N; Intron A; Roferon-A http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202299.html
Mercaptopurine ·
Systemic - U.S. Brands: Purinethol http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202350.html
Mitoxantrone ·
Systemic - U.S. Brands: Novantrone http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202378.html
Pentostatin ·
Systemic - U.S. Brands: Nipent http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202650.html
Teniposide ·
Systemic - U.S. Brands: Vumon http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203661.html
Thioguanine ·
Systemic - U.S. Brands: http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202650.html
Topotecan ·
Systemic - U.S. Brands: Hycamtin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203049.html
Tretinoin ·
Systemic - U.S. Brands: Vesanoid http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203663.html
Vincristine ·
Systemic - U.S. Brands: Oncovin; Vincrex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202594.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug ConsultÔ Mosby’s Drug ConsultÔ database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing
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377
information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.
PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html.
Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.
Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to leukemia by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “leukemia” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for leukemia: ·
Gemtuzumab Zogamicin http://www.rarediseases.org/nord/search/nodd_full?code=1004
·
Histamine (trade name: Maxamine) http://www.rarediseases.org/nord/search/nodd_full?code=1009
378 Leukemia
·
Phenlbutyrate http://www.rarediseases.org/nord/search/nodd_full?code=1016
·
Tazofurin (2-Beta-D-ribofuranosy1-4-thiazolecarbox http://www.rarediseases.org/nord/search/nodd_full?code=1081
·
Tiazofurin (2-Beta-D-ribofuranosy1-4-thiazolecarbo http://www.rarediseases.org/nord/search/nodd_full?code=1091
·
Imatinib (trade name: Glivec) http://www.rarediseases.org/nord/search/nodd_full?code=1095
·
Imatinib (trade name: Gleevec) http://www.rarediseases.org/nord/search/nodd_full?code=1115
·
Tretinoin (trade name: Vesanoid) http://www.rarediseases.org/nord/search/nodd_full?code=112
·
Pegaspargase (trade name: Oncaspar) http://www.rarediseases.org/nord/search/nodd_full?code=342
·
clofarabine (trade name: Clofarex) http://www.rarediseases.org/nord/search/nodd_full?code=1239
·
clofarabine (trade name: Clofarex) http://www.rarediseases.org/nord/search/nodd_full?code=1240
·
homoharringtonine (trade name: NONE Assigned) http://www.rarediseases.org/nord/search/nodd_full?code=1242
·
arsenic (trade name: Trisenox) http://www.rarediseases.org/nord/search/nodd_full?code=1145
·
arsenic trioxide (trade name: trisenox) http://www.rarediseases.org/nord/search/nodd_full?code=1146
·
augmerosen (trade name: Genasense) http://www.rarediseases.org/nord/search/nodd_full?code=1147
·
Mitoxantrone HCL (trade name: Novantrone) http://www.rarediseases.org/nord/search/nodd_full?code=115
·
Tretinoin (trade name: Atragen) http://www.rarediseases.org/nord/search/nodd_full?code=117
·
Imatinib (trade name: Gleevec) http://www.rarediseases.org/nord/search/nodd_full?code=1170
·
Arsenic (trade name: Trisenox) http://www.rarediseases.org/nord/search/nodd_full?code=1211
·
Arenic Trioxide (trade name: Trisenox) http://www.rarediseases.org/nord/search/nodd_full?code=1212
Researching Medications
·
379
clofarabine (trade name: Clofarex) http://www.rarediseases.org/nord/search/nodd_full?code=1264
·
clofarabine (trade name: Clofarex) http://www.rarediseases.org/nord/search/nodd_full?code=1265
·
homoharringtonine http://www.rarediseases.org/nord/search/nodd_full?code=1270
·
Lintuzumab (trade name: Zamyl) http://www.rarediseases.org/nord/search/nodd_full?code=1305
·
Monoclonal antibody PM-81 http://www.rarediseases.org/nord/search/nodd_full?code=137
·
Iodine I 131 murine monoclonal antibody IgG2a to B (trade name: Immurait, L1-2-I131) http://www.rarediseases.org/nord/search/nodd_full?code=146
·
2-chlorodeoxyadenosine http://www.rarediseases.org/nord/search/nodd_full?code=2
·
5-aza-2'-deoxycytidine http://www.rarediseases.org/nord/search/nodd_full?code=502
·
9-cis retinoic acid (trade name: Panretin) http://www.rarediseases.org/nord/search/nodd_full?code=508
·
Roquinimex (trade name: Linomide) http://www.rarediseases.org/nord/search/nodd_full?code=25
·
ST1-RTA immunotoxin (SR 44163) http://www.rarediseases.org/nord/search/nodd_full?code=29
·
Technetium Tc-99m murine monoclonal antibody (IgG2 (trade name: LymphoScan) http://www.rarediseases.org/nord/search/nodd_full?code=311
·
Teniposide (trade name: Vumon for injection) http://www.rarediseases.org/nord/search/nodd_full?code=334
·
Sargramostim (trade name: Leukine) http://www.rarediseases.org/nord/search/nodd_full?code=35
·
Pentostatin http://www.rarediseases.org/nord/search/nodd_full?code=360
·
Pentostatin for injection (trade name: Nipent) http://www.rarediseases.org/nord/search/nodd_full?code=361
·
Erwinia L-asparaginase (trade name: Erwinase) http://www.rarediseases.org/nord/search/nodd_full?code=428
380 Leukemia
·
Ricin (blocked) conjugated murine MCA (anti-my9) http://www.rarediseases.org/nord/search/nodd_full?code=455
·
Ricin (blocked) conjugated murine MCA (anti-my9) http://www.rarediseases.org/nord/search/nodd_full?code=461
·
Ricin (blocked) conjugated murine MCA (anti-my9) http://www.rarediseases.org/nord/search/nodd_full?code=465
·
Anagrelide (trade name: Agrelin) http://www.rarediseases.org/nord/search/nodd_full?code=553
·
Allopurinol sodium (trade name: Zyloprim for Injection) http://www.rarediseases.org/nord/search/nodd_full?code=520
·
Ricin (blocked) conjugated murine mca (anti b-4) http://www.rarediseases.org/nord/search/nodd_full?code=6
·
Cladribine (trade name: Leustatin Injection) http://www.rarediseases.org/nord/search/nodd_full?code=645
·
Cladribine (trade name: Leustatin Injection) http://www.rarediseases.org/nord/search/nodd_full?code=646
·
Buffered intrathecal electrolyte/dextrose injectio (trade name: Elliotts B Solution) http://www.rarediseases.org/nord/search/nodd_full?code=805
·
Ricin (blocked) conjugated murine monoclonal antib http://www.rarediseases.org/nord/search/nodd_full?code=7
·
Fludarabine phosphate (trade name: Fludara) http://www.rarediseases.org/nord/search/nodd_full?code=704
·
Interferon alfa-2a (trade name: Roferon A) http://www.rarediseases.org/nord/search/nodd_full?code=77
·
Idarubicin (trade name: Idamycin) http://www.rarediseases.org/nord/search/nodd_full?code=774
·
Idarubicin HC1 for injection (trade name: Idamycin) http://www.rarediseases.org/nord/search/nodd_full?code=775
·
Iodine I 131 murine monoclonal antibody IgG2a to B (trade name: Immurait, L1-2-I131) http://www.rarediseases.org/nord/search/nodd_full?code=782
·
2'-deoxycytidine http://www.rarediseases.org/nord/search/nodd_full?code=790
·
Filgrastim (trade name: Neupogen) http://www.rarediseases.org/nord/search/nodd_full?code=800
Researching Medications
·
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CAMPATH-1H http://www.rarediseases.org/nord/search/nodd_full?code=852
·
Cladribine (trade name: Laustatin) http://www.rarediseases.org/nord/search/nodd_full?code=881
·
Ricin (blocked) conjugated murine MCA (anti-my9) http://www.rarediseases.org/nord/search/nodd_full?code=895
·
Aldesleukin (trade name: Proleukin) http://www.rarediseases.org/nord/search/nodd_full?code=928
·
506U78 http://www.rarediseases.org/nord/search/nodd_full?code=990
·
Peginteron alfa-2a (trade name: PEGASYS) http://www.rarediseases.org/nord/search/nodd_full?code=994
If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
385
APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: ·
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
·
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
·
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
·
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
·
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
·
National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
·
National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
·
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
12
These publications are typically written by one or more of the various NIH Institutes.
386 Leukemia
·
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
·
National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
·
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
·
National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
·
National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
·
National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
·
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
·
National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
·
National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
·
National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
·
National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
·
National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
·
National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
·
Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
·
National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
·
National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
·
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
·
Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 ·
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
·
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
·
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
·
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
·
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
·
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
·
Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
·
Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
·
Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
·
Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
·
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
13
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.
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Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
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Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database
A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “leukemia” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “leukemia” (or synonyms) into the “For these words:” box. The following is a sample result: ·
Adult T-Cell Leukemia Associated With Human T-Lymphotropic Virus Type I (HTLV-I) Infection - North Carolina Source: Morbidity and Mortality Weekly Report; Vol. 36, no. 49. Contact: US Government Printing Office, PO Box 371954, Pittsburgh, PA, 15250-7954, (202) 512-1800, http://www.access.gpo.gov. Massachusetts Medical Society, Medical Publishing Group, CSPO Box 9121, Waltham, MA, 02254, (800) 843-6356. Summary: This report contains epidemiologic notes and reports related to adult T-Cell Leukemia/Lymphoma associated with Human T-cell lymphotropic virus type I (HTLV I) infection in North Carolina. The article focuses on a patient who developed jaundice in December 1986 after several weeks of anorexia, fatigue, and fever. The patient's history throughout hospitalization is then reported.
The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “leukemia” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category.
15 16
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH).
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Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 174071 1457 1346 425 4 177303
HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “leukemia” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
17
Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html.
18
The HSTAT URL is http://hstat.nlm.nih.gov/.
19
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 20 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 21
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story.
22
After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: ·
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
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Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
The Genome Project and Leukemia In the following section, we will discuss databases and references which relate to the Genome Project and leukemia.
Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).23 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “leukemia” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for leukemia: ·
Abelson Murine Leukemia Viral Oncogene Homolog 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?189980
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Acute Myelogenous Leukemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602439
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Acute Myelogenous Leukemia, Familial Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601626
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Acute Promyelocytic Leukemia, Inducer of Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?102578
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B-cell Leukemia/lymphoma 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?109560
Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
23
Physician Resources
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Brain and Acute Leukemia Gene, Cytoplasmic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606602
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Chronic Lymphocytic Leukemia Deletion Region Gene 6 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607866
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Deleted in Lymphocytic Leukemia, 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605765
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Deleted in Lymphocytic Leukemia, 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605766
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Dohle Bodies and Leukemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?223350
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Eleven Nineteen Lysine-rich Leukemia Gene Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600284
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Erythroleukemia, Familial Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?133180
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Friend Leukemia Virus Integration 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?193067
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Friend Murine Leukemia Virus Integration Site 1, Mouse, Homolog of Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?136750
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Friend Murine Leukemia Virus Integration Site 3, Mouse, Homolog of Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?136770
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Hepatic Leukemia Factor Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?142385
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Human T-cell Leukemia Virus Enhancer Factor Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?143089
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Human T-cell Leukemia Virus Receptor Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?143090
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Juvenile Myelomonocytic Leukemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607785
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Leukemia Inhibitory Factor Receptor Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?151443
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Leukemia Viral Bmi-1 Oncogene, Mouse, Homolog of Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?164831
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Leukemia, Acute Monocytic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?151380
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Leukemia, Acute Myelocytic, with Polyposis Coli and Colon Cancer Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?246470
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Leukemia, Acute T-cell Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?151390
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Leukemia, Acute, ?x-linked Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?308960
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Leukemia, Chronic Lymphatic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?151400
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Leukemia, Lymphoid, 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?151440
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Leukemia/lymphoma, Chronic B-cell, 5 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?151441
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Leukemia-associated Protein with a Cxxc Domain Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607790
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Leukemia-inhibitory Factor Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?159540
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Lymphoblastic Leukemia, Acute, with Lymphomatous Features Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?247640
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Megakaryoblastic Leukemia 1 Gene Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606078
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Mixed Lineage Leukemia, Translocated To, 6 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600328
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Moloney Leukemia Virus Integration Site 2, Mouse, Homolog of Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?157960
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Monocytic Leukemia Zinc Finger Protein-related Factor Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605880
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Myelocytic Leukemia-like Syndrome, Familial, Chronic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600080
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Myeloid Cell Leukemia 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?159552
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Myeloid Leukemia Factor 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601402
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Myeloid Leukemia Factor 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601401
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Myeloid Leukemia-related Gene Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601308
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Myeloid/lymphoid or Mixed Lineage Leukemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?159555
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Myeloid/lymphoid or Mixed Lineage Leukemia 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602113
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Myeloid/lymphoid or Mixed Lineage Leukemia, Translocated To, 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?159556
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Myeloid/lymphoid or Mixed Lineage Leukemia, Translocated To, 10 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602409
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Myeloid/lymphoid or Mixed Lineage Leukemia, Translocated To, 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?159557
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Myeloid/lymphoid or Mixed Lineage Leukemia, Translocated To, 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?159558
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Myeloid/lymphoid or Mixed Lineage Leukemia, Translocated To, 4 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?159559
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Myeloid/lymphoid or Mixed Lineage Leukemia, Translocated To, 7 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?300033
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Myeloid/lymphoid or Mixed-lineage Leukemia 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606833
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Myeloid/lymphoid or Mixed-lineage Leukemia 4 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606834
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Myeloproliferative Leukemia Virus Oncogene Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?159530
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Pre-b-cell Leukemia Transcription Factor 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?176310
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Pre-b-cell Leukemia Transcription Factor 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?176311
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Pre-b-cell Leukemia Transcription Factor 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?176312
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Pre-b-cell Leukemia Transcription Factor 4 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?608127
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Set Translocation, Myeloid Leukemia-associated Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600960
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Simian Sarcoma-associated Virus-1/gibbon Ape Leukemia Virus Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?182090
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Six-twelve Leukemia Gene Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602532
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T-cell Acute Lymphoblastic Leukemia 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?186855
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T-cell Acute Lymphocytic Leukemia 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?187040
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T-cell Leukemia Homeo Box 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604640
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T-cell Leukemia Translocation-associated Gene Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600690
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T-cell Leukemia/lymphoma 1a Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?186960
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T-cell Leukemia/lymphoma 4 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?186860
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T-cell Leukemia/lymphoma 6 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604412
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T-cell Lymphoma/leukemia 1b Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603769
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V-abl Abelson Murine Leukemia Viral Oncogene Homolog 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?164690
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V-erb-b2 Avian Erythroblastic Leukemia Viral Oncogene Homolog 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?164870
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V-erb-b2 Avian Erythroblastic Leukemia Viral Oncogene Homolog 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?190151
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V-erb-b2 Avian Erythroblastic Leukemia Viral Oncogene Homolog 4 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600543
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V-raf-1 Murine Leukemia Viral Oncogene Homolog 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?164760
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V-ral Simian Leukemia Viral Oncogene Homolog a Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?179550
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V-ral Simian Leukemia Viral Oncogene Homolog B Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?179551
Genes and Disease (NCBI - Map) The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: ·
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
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Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
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Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
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Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
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Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease,
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Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html ·
Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html
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Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html
Entrez Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: ·
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
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To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “leukemia” (or synonyms) into the search box and click “Go.”
Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database24 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database25 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “leukemia” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 25 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission. 24
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on leukemia can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to leukemia. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly.
The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below.
Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to leukemia. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “leukemia”:
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Other guides Hodgkin's Disease http://www.nlm.nih.gov/medlineplus/hodgkinsdisease.html Multiple Myeloma http://www.nlm.nih.gov/medlineplus/multiplemyeloma.html
Within the health topic page dedicated to leukemia, the following was listed: ·
General/Overview Leukemia http://www.nlm.nih.gov/medlineplus/tutorials/leukemialoader.html Leukemia Source: Nemours Foundation http://kidshealth.org/parent/medical/cancer/cancer_leukemia.html
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Diagnosis/Symptoms How is Childhood Leukemia Diagnosed? Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_4_3x_how_is_leukemia_diagno sed_24.asp How is Childhood Leukemia Staged? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_3x_How_is_Childhood_L eukemia_Staged.asp Platelet Count Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/platelet/test.html Understanding Blood Counts Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9452 White Blood Cell Count Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/wbc/test.html
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Treatment Blood and Marrow Stem Cell Transplantation Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=2443 Blood Transfusion Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=17813 Childhood Acute Lymphoblastic Leukemia (PDQ): Treatment Source: National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/childALL/patient/
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Childhood Acute Myeloid Leukemia / Other Myeloid Malignancies (PDQ): Treatment Source: National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/childAML/patient/ FDA Approves Gleevec for Pediatric Leukemia Treatment Source: Food and Drug Administration http://www.fda.gov/bbs/topics/NEWS/2003/NEW00909.html Immunotherapy Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9889 Long Term and Late Effects of Treatment for Blood-Related Cancers Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9965 New Approaches to Treatment Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_page?item_id=4702 Understanding Drug Therapy and Managing Side Effects Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=4826 What Happens after Treatment for Childhood Leukemia? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_2_6X_What_happens_after_t reatment_for_childhood_leukemia_24.asp?sitearea= ·
Alternative Therapy Complementary & Alternative Therapies for Leukemia, Lymphoma, Hodgkin's Disease, & Myeloma Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9882
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Nutrition Nutrition for Children with Cancer Source: American Cancer Society http://www.cancer.org/docroot/MBC/MBC_6_1_nutrition_for_children_with_can cer.asp
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Coping Emotional Aspects of Childhood Leukemia Source: Leukemia & Lymphoma Society http://www.leukemialymphoma.org/all_mat_detail.adp?item_id=28602&sort_order=5&cat_id=
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Specific Conditions/Aspects Acute Lymphoblastic Leukemia in Children Source: National Cancer Institute http://www.cancer.gov/newscenter/all3 Acute Myelogenous Leukemia (AML) Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_page?item_id=8459 Choosing a Treatment Facility Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9877 Choosing and Communicating with a Cancer Specialist Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9872 Chronic Myelomonocytic Leukemias(CMML) Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=69974 Classification of Childhood Leukemias Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_2_3X_Classification_of_chil dhood_leukemias_24.asp?sitearea= Facts and Statistics Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_page?item_id=12486 Insurance Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_page?item_id=8763 Patient Financial Aid Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_page?item_id=4603 What Are the Differences between Cancers in Adults and in Children? Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_4_1x_what_are_the_differences _between_cancers_in_adults_and_in_children_31.asp What Should You Ask Your Doctor about Childhood Leukemia? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_5X_What_should_you_as k_your_physician_about_leukemia_24.asp When Your Child Goes Back to School Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_6x_When_Your_Child_Goes _Back_to_School.asp?sitearea= Young People with Cancer: A Handbook for Parents Source: National Cancer Institute http://www.cancer.gov/cancerinfo/youngpeople
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From the National Institutes of Health Questions and Answers About Care for Children and Adolescents with Cancer Source: National Cancer Institute http://cis.nci.nih.gov/fact/1_21.htm What You Need to Know about Leukemia Source: National Cancer Institute http://www.cancer.gov/cancerinfo/wyntk/leukemia
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Latest News DNA Drug Offers Leukemia Hope Source: 10/21/2003, United Press International http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14366 .html Gene Therapy Did Cause Cancer in Boys, Study Shows Source: 10/16/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14312 .html Intensive Therapy Beats Racial Leukemia Gap Source: 10/14/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14280 .html Study Finds Equal Cure Rates among Black, White Children with Leukemia Source: 10/22/2003, American Cancer Society http://www.cancer.org/docroot/NWS/content/NWS_1_1x_Study_Finds_Equal_C ure_Rates_Among_Black_White_Children_with_Leukemia.asp
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Organizations American Cancer Society http://www.cancer.org/ Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/hm_lls National Cancer Institute http://www.cancer.gov/ National Marrow Donor Program http://www.marrow.org/
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Prevention/Screening What Are the Risk Factors for Leukemia? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_2X_What_are_the_risk_fa ctors_for_leukemia_24.asp
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Research Brain Radiation Not Needed for Most Children with Leukemia Source: American Cancer Society http://www.cancer.org/docroot/NWS/content/NWS_1_1x_Study_Brain_Radiatio n_Not_Needed_For_Most_Children_With_Leukemia.asp National Cancer Institute Research on Childhood Cancers Source: National Cancer Institute http://cis.nci.nih.gov/fact/6_40.htm Research Updates: Latest News Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_news_brief?news_type=4&source_id=4 Study Finds Equal Cure Rates among Black, White Children with Leukemia Source: American Cancer Society http://www.cancer.org/docroot/NWS/content/NWS_1_1x_Study_Finds_Equal_C ure_Rates_Among_Black_White_Children_with_Leukemia.asp What's New in Leukemia Research and Treatment? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_6X_Whats_new_in_leuke mia_research_and_treatment_24.asp
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Statistics What Are the Key Statistics about Childhood Leukemia? Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_4_1x_what_are_the_key_statist ics_for_leukemia_24.asp
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on leukemia. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: ·
Ataxia-Telangiectasia: A Guide for Teachers Source: Harpenden, Herts, United Kingdom: Ataxia-Telangiectasia Society. 199x. [2 p.].
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Contact: Available from A-T Project. 3002 Enfield Road, Austin, TX 78703. (512) 3235161. E-mail: [email protected]. Website: www.atproject.org. PRICE: Single copy free. Summary: Ataxia-telangiectasia (A-T) is a rare genetic progressive disorder that first shows itself in children between the ages of one and five. The condition has two obvious clinical features: ataxia, the loss of balance and coordination; and telangiectasia, weblike prominent blood vessels most commonly found in the whites of the eyes (making them look bloodshot). A-T can also affect a child's immune system and can increase the child's risk of leukemia and some cancers. This brochure describes A-T and offers suggestions for educators who may be working with children who have this disorder. Children with A-T suffer from a high level of fatigue, as it takes great physical effort on their part to move about, walk, and talk. Speech may be slowed and slurred; eye coordination and tracking difficulties may make reading and following moving objects difficult or painful. The brochure notes that there is no specific learning disorder associated with this condition. The brochure concludes with information about the Ataxia-Telangiectasia Society, a parent-organized association established in the United Kingdom to provide information, research, support, and a specialist clinic. ·
Arthritis in Children Source: Healthology, Inc. 2003. 4 p. Contact: Available from Healthology, Inc. Website: http://healingwell.healthology.com. Summary: This fact sheet provides information about the causes, diagnosis, and treatment of arthritis in children. Arthritis is an inflammatory disease of the joints. Inflammation is caused by fluid accumulating inside the joint or lining of the joint. Common symptoms of arthritis in children include joint pain, joint swelling, limping, holding an affected joint in one position, inability to move the joint, heat over the joint, and stiffness. Symptoms in infants include irritability and crying on handling. Fever rash, mouth sores, or red and watering eyes may also accompany joint symptoms. In children, acute arthritis may be caused by trauma; infection-related arthritis including Lyme disease, septic arthritis, viral arthritis; or by immune-- related arthritis including rheumatic fever, serum sickness, or Kawasaki disease. Causes of chronic arthritis include juvenile rheumatoid arthritis, systemic lupus erythematosus, and psoriasis. Some conditions that mimic arthritis include acute leukemia, neuroblastoma, hypothyroidism, Perthe's Disease, hypermobility of joints, and slipped capital femoral epiphysis. Arthralgia (joint pain without inflammation) may be caused by many different conditions including growing pains, excess physical activity, bone diseases, viral diseases, neurological diseases, leukemia, psychosocial problems, or depression. Diagnosis for arthritis must be based upon a medical history, careful physical examination, and laboratory tests and imaging studies. Treatment depends upon the cause of the arthritis.
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Kids on the Block Source: Columbia, MD: Kids on the Block. 199x. 6 p. Contact: Available from Kids on the Block, Inc. 9385-C Gerwig, Columbia, MD 21046. (410) 290-9095; (800) 368-KIDS; Fax (410) 290-9358. PRICE: Single copy free. Summary: This full-color brochure describes the educational program, 'The Kids on the Block'. Through the use of puppets and scripted presentations, this program teaches audiences of all ages what it's like to be a person who has a disability or a health
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difference. The puppets are available for purchase through the workshop, which includes training materials to help teachers and presenters. Over 35 programs are available on a variety of disabilities, social concerns, and medical differences; each is researched thoroughly with the national organizations representing the issue. Disabilities covered include autism, blindness, cerebral palsy, deafness, mental retardation, and spina bifida; medical issues covered include AIDS, arthritis, asthma, diabetes, epilepsy, leukemia, pediatric hospice, and severe burns.
The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “leukemia” (or synonyms). The following was recently posted: ·
An evidence-based analysis of the effect of busulfan, hydroxyurea, interferon, and allogeneic bone marrow transplantation in treating the chronic phase of chronic myeloid leukemia Source: American Society of Hematology - Medical Specialty Society; 1999 September 1; 20 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2363&nbr=1589&a mp;string=leukemia
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Drug therapy for chronic myeloid leukemia Source: Practice Guidelines Initiative - State/Local Government Agency [Non-U.S.]; 1998 August 24 (updated online 2000 Jul); Various pagings http://www.guideline.gov/summary/summary.aspx?doc_id=3005&nbr=2231&a mp;string=leukemia
Healthfinder™ Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: ·
DreamLine: Free Travel for Children Coping With Serious Illness Summary: This is the web site of an organization that provides free vacation travel for children currently undergoing treatment for (or recovering from) a brain tumor, cancer, or leukemia. Source: Commercial Entity--Follow the Resource URL for More Information http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4763
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How is Fanconi Anemia Related to Leukemia and Other Cancers Summary: This document discusses Fanconi anemia patients' risks of developing leukemia and other related cancers. Source: Fanconi Anemia Research Fund, Inc. http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4636
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Leukemia, Lymphomas, and Myeloma: About the Diseases Summary: Browse this site for patient information about leukemia, lymphomas, and myeloma. Source: Leukemia & Lymphoma Society http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2292
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What You Need To Know About™ Leukemia Summary: This National Cancer Institute (NCI) booklet describes the symptoms of leukemia and explains how this disease is diagnosed and treated. Source: Cancer Information Service, National Cancer Institute http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7133 The NIH Search Utility
The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to leukemia. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html.
Additional Web Sources
A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: ·
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDÒHealth: http://my.webmd.com/health_topics
Associations and Leukemia The following is a list of associations that provide information on and resources relating to leukemia: ·
Hairy Cell Leukemia Research Foundation Telephone: (847) 843-1975 Toll-free: (800) 693-6173 Fax: (815) 425-6734 Email: [email protected] (all lower case) Web Site: HAIRYCELLLEUKEMIA.ORG Background: The Hairy Cell Leukemia Research Foundation is an organization created and run by HCL patients, with the goal of providing support and information to individuals and families, as well as raising funds for research. It is an all volunteer, nonprofit organization. Hairy cell leukemia is a rare blood disorder that affects mostly males in middle age. However, it has been identified in both sexes and among younger adults. It is a chronic leukemia and does not develop into acute leukemia.
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Leukemia and Lymphoma Society Telephone: (914) 949-5213 Toll-free: (800) 955-4572 Fax: (914) 949-6691 Email: [email protected] Web Site: http://www.leukemia-lymphoma.org Background: The Leukemia and Lymphoma Society is a national voluntary health agency dedicated to curing leukemia, lymphoma, Hodgkin's disease and myeloma, and to improving the quality of life of patients and their families. The Society was established in 1949 as the de Villiers Foundation. In 2000, the Society changed its name from The Leukemia Society of America to The Leukemia and Lymphoma Society to emphasize its commitment to fighting all blood-related cancers. Today, the Society supports the following major programs: research, patient services, public and professional education, advocacy and community services. With headquarters in White Plains, NY, the Society has chapter offices across the United States and is a single corporation doing business under New York State not-for-profit corporate laws. Relevant area(s) of interest: Leukemia
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National Leukemia Research Association, Inc Telephone: (516) 222-1944 Toll-free: TTY: Fax: (516) 222-0457 Background: The National Leukemia Research Association, Inc. (NLRA) was founded in 1965 as a not-for-profit voluntary organization dedicated to raising funds to support research efforts into the causes and cure of leukemia and to provide patient aid to those families in need while meeting the expense incurred in leukemia treatment. Leukemia is any of several types of cancer in which there is usually an abnormal accumulation of
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white blood cells within the bone marrow often resulting in decreased production of red blood cells, platelets, and normal white blood cells. Other organs such as the liver, lymph nodes, and brain may fail to function properly as they are infiltrated by leukemia cells. As part of its Patient Aid Services Program, NLRA requests families seeking aid submit an application to the Patient Aid director. All claims are investigated by the Patient Aid committee and money is allocated to the affected families covering drugs, lab fees, and other valid claims after review by committee; unusual and extraordinary expenses will also be considered based upon need and availability of funds. As part of its Scientific Investigation Program, a Medical Advisory Committee consisting of prominent internationally known and respected specialists in the field of blood disorders (hematologists) reviews research grants submitted yearly for consideration of funding. The objectives of this committee are to direct the funds of the NLRA into the most promising projects and where funding would not duplicate other funding sources. The objectives of NLRA are to find the causes and cure for leukemia. Relevant area(s) of interest: Leukemia
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to leukemia. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with leukemia.
The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about leukemia. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797.
Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “leukemia” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received
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your search results, click on the name of the organization for its description and contact information.
The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “leukemia”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “leukemia” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “leukemia” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.26
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
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Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)27: ·
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
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Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
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Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
Finding Medical Libraries
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: ·
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
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Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
·
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on leukemia: ·
Basic Guidelines for Leukemia All Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000541.htm Cll Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000532.htm Leukemia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001299.htm Leukemia - resources Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002151.htm
·
Signs & Symptoms for Leukemia Bruising Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003235.htm
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Fatigue Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Fever Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003090.htm Gingival swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003066.htm Hepatosplenomegaly Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003275.htm Leukemia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001299.htm Pallor Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003244.htm Petechiae Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003235.htm Purpura Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003232.htm Splenomegaly Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003276.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm ·
Diagnostics and Tests for Leukemia CT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003330.htm Differential Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003657.htm LDH Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003471.htm Uric acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003476.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm
·
Surgery and Procedures for Leukemia Bone marrow transplant Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003009.htm
Online Glossaries 417
·
Background Topics for Leukemia Chemotherapy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002324.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Leukemia Resources Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002151.htm Proliferation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002276.htm Resources Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002150.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: ·
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
·
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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LEUKEMIA DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 9-cis retinoic acid: A drug being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Abortion: 1. The premature expulsion from the uterus of the products of conception - of the embryo, or of a nonviable fetus. The four classic symptoms, usually present in each type of abortion, are uterine contractions, uterine haemorrhage, softening and dilatation of the cervix, and presentation or expulsion of all or part of the products of conception. 2. Premature stoppage of a natural or a pathological process. [EU] Acantholysis: Separation of the prickle cells of the stratum spinosum of the epidermis, resulting in atrophy of the prickle cell layer. It is seen in diseases such as pemphigus vulgaris (see pemphigus) and keratosis follicularis. [NIH] Accelerated phase: Refers to chronic myelogenous leukemia that is progressing. The number of immature, abnormal white blood cells in the bone marrow and blood is higher than in the chronic phase, but not as high as in the blast phase. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] ACE: Angiotensin-coverting enzyme. A drug used to decrease pressure inside blood vessels. [NIH]
Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Acne Vulgaris: A chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular nodules. The cause is unknown, but heredity and age are predisposing factors. [NIH] Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and
420 Leukemia
increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acute leukemia: A rapidly progressing cancer of the blood-forming tissue (bone marrow). [NIH]
Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH] Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphoblastic leukemia. [NIH] Acute myelogenous leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myeloid leukemia or acute nonlymphocytic leukemia. [NIH] Acute myeloid leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myelogenous leukemia or acute nonlymphocytic leukemia. [NIH] Acute nonlymphocytic leukemia: A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myeloid leukemia or acute myelogenous leukemia. [NIH] Acyclovir: Functional analog of the nucleoside guanosine. It acts as an antimetabolite, especially in viruses. It is used as an antiviral agent, especially in herpes infections. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adduct: Complex formed when a carcinogen combines with DNA or a protein. [NIH] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenosine Deaminase: An enzyme that catalyzes the hydrolysis of adenosine to inosine with the elimination of ammonia. Since there are wide tissue and species variations in the enzyme, it has been used as a tool in the study of human and animal genetics and in medical diagnosis. EC 3.5.4.4. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adjuvant Therapy: Treatment given after the primary treatment to increase the chances of a cure. Adjuvant therapy may include chemotherapy, radiation therapy, or hormone therapy. [NIH]
Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of
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solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]
Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Ageing: A physiological or morphological change in the life of an organism or its parts, generally irreversible and typically associated with a decline in growth and reproductive vigor. [NIH] Aggressiveness: The quality of being aggressive (= characterized by aggression; militant; enterprising; spreading with vigour; chemically active; variable and adaptable). [EU] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU]
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Alkaline Phosphatase: An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1. [NIH] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [NIH]
Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allo: A female hormone. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allogeneic bone marrow transplantation: A procedure in which a person receives stem cells, the cells from which all blood cells develop, from a compatible, though not genetically identical, donor. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alternative Splicing: A process whereby multiple protein isoforms are generated from a single gene. Alternative splicing involves the splicing together of nonconsecutive exons during the processing of some, but not all, transcripts of the gene. Thus a particular exon may be connected to any one of several alternative exons to form messenger RNA. The alternative forms produce proteins in which one part is common while the other part is different. [NIH] Amikacin: A broad-spectrum antibiotic derived from kanamycin. It is reno- and ototoxic like the other aminoglycoside antibiotics. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation
Dictionary 423
of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Motifs: Commonly observed structural components of proteins formed by simple combinations of adjacent secondary structures. A commonly observed structure may be composed of a conserved sequence which can be represented by a consensus sequence. [NIH]
Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Amsacrine: N-(4-(9-Acridinylamino)-3-methoxyphenyl)methanesulfonamide. Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects. [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anabolic Steroids: Chemical derivatives of testosterone that are used for anabolic promotion of growth and repair of body tissues and the development of male sexual characteristics. [NIH] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaplastic: A term used to describe cancer cells that divide rapidly and bear little or no resemblance to normal cells. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anchorage: In dentistry, points of retention of fillings and artificial restorations and
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appliances. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Aneuploidy: The chromosomal constitution of cells which deviate from the normal by the addition or subtraction of chromosomes or chromosome pairs. In a normally diploid cell the loss of a chromosome pair is termed nullisomy (symbol: 2N-2), the loss of a single chromosome is monosomy (symbol: 2N-1), the addition of a chromosome pair is tetrasomy (symbol: 2N+2), the addition of a single chromosome is trisomy (symbol: 2N+1). [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angioplasty: Endovascular reconstruction of an artery, which may include the removal of atheromatous plaque and/or the endothelial lining as well as simple dilatation. These are procedures performed by catheterization. When reconstruction of an artery is performed surgically, it is called endarterectomy. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Antecedent: Existing or occurring before in time or order often with consequential effects. [EU]
Anterior chamber: The space in front of the iris and behind the cornea. [NIH] Anthracycline: A member of a family of anticancer drugs that are also antibiotics. [NIH] Antiangiogenic: Having to do with reducing the growth of new blood vessels. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody therapy: Treatment with an antibody, a substance that can directly kill specific tumor cells or stimulate the immune system to kill tumor cells. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood
Dictionary 425
thinner. [NIH] Antidote: A remedy for counteracting a poison. [EU] Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]
Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antiproliferative: Counteracting a process of proliferation. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Antiviral Agents: Agents used in the prophylaxis or therapy of virus diseases. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. [NIH] Anuria: Inability to form or excrete urine. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Aorta: The main trunk of the systemic arteries. [NIH]
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Aphakia: Absence of crystalline lens totally or partially from field of vision, from any cause except after cataract extraction. Aphakia is mainly congenital or as result of lens dislocation and subluxation. [NIH] Aplasia: Lack of development of an organ or tissue, or of the cellular products from an organ or tissue. [EU] Aplastic anemia: A condition in which the bone marrow is unable to produce blood cells. [NIH]
Apnea: A transient absence of spontaneous respiration. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Appendicitis: Acute inflammation of the vermiform appendix. [NIH] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Approximate: Approximal [EU] Aqueous: Having to do with water. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arenavirus: The only genus in the family Arenaviridae. It contains two groups LCM-Lassa complex viruses and Tacaribe complex viruses, which are distinguished by antigenic relationships and geographic distribution. [NIH] Aromatic: Having a spicy odour. [EU] Arsenic trioxide: An anticancer drug that induces programmed cell death (apoptosis) in certain cancer cells. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Arthralgia: Pain in the joint. [NIH] Articular: Of or pertaining to a joint. [EU] Asbestos: Fibrous incombustible mineral composed of magnesium and calcium silicates with or without other elements. It is relatively inert chemically and used in thermal insulation and fireproofing. Inhalation of dust causes asbestosis and later lung and gastrointestinal neoplasms. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Asparaginase: A hydrolase enzyme that converts L-asparagine and water to L-aspartate and NH3. EC 3.5.1.1. [NIH]
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Aspartate: A synthetic amino acid. [NIH] Aspergillosis: Infections with fungi of the genus Aspergillus. [NIH] Aspirate: Fluid withdrawn from a lump, often a cyst, or a nipple. [NIH] Aspiration: The act of inhaling. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astatine: Astatine. A radioactive halogen with the atomic symbol At, atomic number 85, and atomic weight 210. Its isotopes range in mass number from 200 to 219 and all have an extremely short half-life. Astatine may be of use in the treatment of hyperthyroidism. [NIH] Astringent: Causing contraction, usually locally after topical application. [EU] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Astrocytoma: A tumor that begins in the brain or spinal cord in small, star-shaped cells called astrocytes. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Augmerosen: A drug that may kill cancer cells by blocking the production of a protein that makes cancer cells live longer. Also called bcl-2 antisense oligodeoxynucleotide G3139. [NIH] Aural: Pertaining to or perceived by the ear, as an aural stimulus. [EU] Auricular: Pertaining to an auricle or to the ear, and, formerly, to an atrium of the heart. [EU] Autacoids: A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities. [NIH]
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Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Autologous bone marrow transplantation: A procedure in which bone marrow is removed from a person, stored, and then given back to the person after intensive treatment. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Azacitidine: A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent. [NIH] Bacteremia: The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as sedatives and anesthetics, and they have been used to treat the convulsions associated with epilepsy. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of
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donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Basophil: A type of white blood cell. Basophils are granulocytes. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bifida: A defect in development of the vertebral column in which there is a central deficiency of the vertebral lamina. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioassay: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and
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protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bispecific antibodies: Antibodies developed in the laboratory to recognize more than one protein on the surface of different cells. Examples include bispecific antibodies 2B1, 520C9xH22, mDX-H210, and MDX447. [NIH] Bladder: The organ that stores urine. [NIH] Blast Crisis: Rapid increase in the proportion of blast cells in the blood and bone marrow. [NIH]
Blast phase: The phase of chronic myelogenous leukemia in which the number of immature, abnormal white blood cells in the bone marrow and blood is extremely high. Also called blast crisis. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Blasts: Immature blood cells. [NIH] Blister: Visible accumulations of fluid within or beneath the epidermis. [NIH] Blood Cell Count: A count of the number of leukocytes and erythrocytes per unit volume in a sample of venous blood. A complete blood count (CBC) also includes measurement of the hemoglobin, hematocrit, and erythrocyte indices. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood Groups: The classification systems (or schemes) of the different antigens located on erythrocytes.The antigens are the phenotypic expression of the genetic differences characteristic of specific blood groups. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood Preservation: The process by which blood or its components are kept viable outside of the organism from which they are derived (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism). [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH]
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Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone marrow aspiration: The removal of a small sample of bone marrow (usually from the hip) through a needle for examination under a microscope. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Bone marrow metastases: Cancer that has spread from the original (primary) tumor to the bone marrow. [NIH] Bone Marrow Transplantation: The transference of bone marrow from one human or animal to another. [NIH] Bone Morphogenetic Proteins: Bone-growth regulatory factors that are members of the transforming growth factor-beta superfamily of proteins. They are synthesized as large precursor molecules which are cleaved by proteolytic enzymes. The active form can consist of a dimer of two identical proteins or a heterodimer of two related bone morphogenetic proteins. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH] Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Bronchial: Pertaining to one or more bronchi. [EU] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Buffers: A chemical system that functions to control the levels of specific ions in solution. When the level of hydrogen ion in solution is controlled the system is called a pH buffer. [NIH]
Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge
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of electricity. [NIH] Busulfan: An anticancer drug that belongs to the family of drugs called alkylating agents. [NIH]
Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Cachexia: General ill health, malnutrition, and weight loss, usually associated with chronic disease. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Camptothecin: An alkaloid isolated from the stem wood of the Chinese tree, Camptotheca acuminata. This compound selectively inhibits the nuclear enzyme DNA topoisomerase. Several semisynthetic analogs of camptothecin have demonstrated antitumor activity. [NIH] Candidiasis: Infection with a fungus of the genus Candida. It is usually a superficial infection of the moist cutaneous areas of the body, and is generally caused by C. albicans; it most commonly involves the skin (dermatocandidiasis), oral mucous membranes (thrush, def. 1), respiratory tract (bronchocandidiasis), and vagina (vaginitis). Rarely there is a systemic infection or endocarditis. Called also moniliasis, candidosis, oidiomycosis, and formerly blastodendriosis. [EU] Candidosis: An infection caused by an opportunistic yeasts that tends to proliferate and become pathologic when the environment is favorable and the host resistance is weakened. [NIH]
Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capillary Fragility: The lack of resistance, or susceptibility, of capillaries to damage or disruption under conditions of increased stress. [NIH] Capsaicin: Cytotoxic alkaloid from various species of Capsicum (pepper, paprika), of the Solanaceae. [NIH] Capsid: The outer protein protective shell of a virus, which protects the viral nucleic acid. [NIH]
Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carboplatin: An organoplatinum compound that possesses antineoplastic activity. [NIH] Carboxy: Cannabinoid. [NIH] Carboxy-terminal: The end of any polypeptide or protein that bears a free carboxyl group. [NIH]
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Carcinogen: Any substance that causes cancer. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoid: A type of tumor usually found in the gastrointestinal system (most often in the appendix), and sometimes in the lungs or other sites. Carcinoid tumors are usually benign. [NIH]
Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardiotoxic: Having a poisonous or deleterious effect upon the heart. [EU] Cardiotoxicity: Toxicity that affects the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Castor Oil: Oil obtained from seeds of Ricinus communis that is used as a cathartic and as a plasticizer. [NIH] Cataract: An opacity, partial or complete, of one or both eyes, on or in the lens or capsule, especially an opacity impairing vision or causing blindness. The many kinds of cataract are classified by their morphology (size, shape, location) or etiology (cause and time of occurrence). [EU] Catechin: Extracted from Uncaria gambier, Acacia catechu and other plants; it stabilizes collagen and is therefore used in tanning and dyeing; it prevents capillary fragility and abnormal permeability, but was formerly used as an antidiarrheal. [NIH] Catechol: A chemical originally isolated from a type of mimosa tree. Catechol is used as an astringent, an antiseptic, and in photography, electroplating, and making other chemicals. It can also be man-made. [NIH] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in
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obstructions. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] CDC2: It is crucial for entry into mitosis of eukaryotic cells. [NIH] Ceftazidime: Semisynthetic, broad-spectrum antibacterial derived from cephaloridine and used especially for Pseudomonas and other gram-negative infections in debilitated patients. [NIH]
Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell Lineage: The developmental history of cells as traced from the first division of the original cell or cells in the embryo. [NIH] Cell motility: The ability of a cell to move. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Cellulitis: An acute, diffuse, and suppurative inflammation of loose connective tissue, particularly the deep subcutaneous tissues, and sometimes muscle, which is most commonly seen as a result of infection of a wound, ulcer, or other skin lesions. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Centrosome: The cell center, consisting of a pair of centrioles surrounded by a cloud of amorphous material called the pericentriolar region. During interphase, the centrosome
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nucleates microtubule outgrowth. The centrosome duplicates and, during mitosis, separates to form the two poles of the mitotic spindle (mitotic spindle apparatus). [NIH] Cephaloridine: A cephalosporin antibiotic. [NIH] Ceramide: A type of fat produced in the body. It may cause some types of cells to die, and is being studied in cancer treatment. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebellum: Part of the metencephalon that lies in the posterior cranial fossa behind the brain stem. It is concerned with the coordination of movement. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [NIH] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebral Palsy: Refers to a motor disability caused by a brain dysfunction. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemoprevention: The use of drugs, vitamins, or other agents to try to reduce the risk of, or delay the development or recurrence of, cancer. [NIH] Chemopreventive: Natural or synthetic compound used to intervene in the early precancerous stages of carcinogenesis. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotherapeutic agent: A drug used to treat cancer. [NIH] Chemotherapeutics: Noun plural but singular or plural in constructions : chemotherapy.
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[EU]
Chemotherapy: Treatment with anticancer drugs. [NIH] Chimera: An individual that contains cell populations derived from different zygotes. [NIH] Chimeric Proteins: Proteins in individuals that are derived from genetically different zygotes. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] Chlorambucil: An anticancer drug that belongs to the family of drugs called alkylating agents. [NIH] Chlorhexidine: Disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque. [NIH] Chlorine: A greenish-yellow, diatomic gas that is a member of the halogen family of elements. It has the atomic symbol Cl, atomic number 17, and atomic weight 70.906. It is a powerful irritant that can cause fatal pulmonary edema. Chlorine is used in manufacturing, as a reagent in synthetic chemistry, for water purification, and in the production of chlorinated lime, which is used in fabric bleaching. [NIH] Chloroform: A commonly used laboratory solvent. It was previously used as an anesthetic, but was banned from use in the U.S. due to its suspected carcinogenecity. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chondrocytes: Polymorphic cells that form cartilage. [NIH] Choriocarcinoma: A malignant tumor of trophoblastic epithelium characterized by secretion of large amounts of chorionic gonadotropin. It usually originates from chorionic products of conception (i.e., hydatidiform mole, normal pregnancy, or following abortion), but can originate in a teratoma of the testis, mediastinum, or pineal gland. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chromosome Aberrations: Deviations from the normal number or structure of chromosomes, not necessarily associated with disease. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic granulocytic leukemia: A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myelogenous leukemia or chronic myeloid leukemia. [NIH] Chronic leukemia: A slowly progressing cancer of the blood-forming tissues. [NIH]
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Chronic lymphocytic leukemia: A slowly progressing disease in which too many white blood cells (called lymphocytes) are found in the body. [NIH] Chronic myelogenous leukemia: CML. A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myeloid leukemia or chronic granulocytic leukemia. [NIH] Chronic phase: Refers to the early stages of chronic myelogenous leukemia or chronic lymphocytic leukemia. The number of mature and immature abnormal white blood cells in the bone marrow and blood is higher than normal, but lower than in the accelerated or blast phase. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciliary Body: A ring of tissue extending from the scleral spur to the ora serrata of the retina. It consists of the uveal portion and the epithelial portion. The ciliary muscle is in the uveal portion and the ciliary processes are in the epithelial portion. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Cisplatin: An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle. [NIH] C-kit receptor: A protein on the surface of some cells that binds to stem cell factor (a substance that causes certain types of cells to grow). Altered forms of this receptor may be associated with some types of cancer. [NIH] Cladribine: An antineoplastic agent used in the treatment of lymphoproliferative diseases including hairy-cell leukemia. [NIH] Clavulanic Acid: Clavulanic acid (C8H9O5N) and its salts and esters. The acid is a suicide inhibitor of bacterial beta-lactamase enzymes from Streptomyces clavuligerus. Administered alone, it has only weak antibacterial activity against most organisms, but given in combination with beta-lactam antibiotics prevents antibiotic inactivation by microbial lactamase. [NIH] Cleave: A double-stranded cut in DNA with a restriction endonuclease. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical Protocols: Precise and detailed plans for the study of a medical or biomedical problem and/or plans for a regimen of therapy. [NIH] Clinical resistance: The failure of a cancer to shrink after treatment. [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA
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molecules. [NIH] Cluster Analysis: A set of statistical methods used to group variables or observations into strongly inter-related subgroups. In epidemiology, it may be used to analyze a closely grouped series of events or cases of disease or other health-related phenomenon with welldefined distribution patterns in relation to time or place or both. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Codon: A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (codon, terminator). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, transfer) complementary to all codons. These codons are referred to as unassigned codons (codons, nonsense). [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Colchicine: A major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (periodic disease). [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colon Polyps: Small, fleshy, mushroom-shaped growths in the colon. [NIH] Colony-Stimulating Factors: Glycoproteins found in a subfraction of normal mammalian plasma and urine. They stimulate the proliferation of bone marrow cells in agar cultures and the formation of colonies of granulocytes and/or macrophages. The factors include interleukin-3 (IL-3), granulocyte colony-stimulating factor (G-CSF), macrophage colonystimulating factor (M-CSF), and granulocyte-macrophage colony-stimulating factor (GM-
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CSF). [NIH] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Combination chemotherapy: Treatment using more than one anticancer drug. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Communis: Common tendon of the rectus group of muscles that surrounds the optic foramen and a portion of the superior orbital fissure, to the anterior margin of which it is attached at the spina recti lateralis. [NIH] Compassionate: A process for providing experimental drugs to very sick patients who have no treatment options. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementation: The production of a wild-type phenotype when two different mutations are combined in a diploid or a heterokaryon and tested in trans-configuration. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete
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response. [NIH] Complete response: The disappearance of all signs of cancer in response to treatment. This does not always mean the cancer has been cured. [NIH] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Condoms: A sheath that is worn over the penis during sexual behavior in order to prevent pregnancy or spread of sexually transmitted disease. [NIH] Cones: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide sharp central vision and color vision. [NIH] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Consensus Sequence: A theoretical representative nucleotide or amino acid sequence in which each nucleotide or amino acid is the one which occurs most frequently at that site in the different sequences which occur in nature. The phrase also refers to an actual sequence which approximates the theoretical consensus. A known conserved sequence set is represented by a consensus sequence. Commonly observed supersecondary protein structures (amino acid motifs) are often formed by conserved sequences. [NIH] Conserved Sequence: A sequence of amino acids in a polypeptide or of nucleotides in DNA or RNA that is similar across multiple species. A known set of conserved sequences is represented by a consensus sequence. Amino acid motifs are often composed of conserved sequences. [NIH] Constitutional: 1. Affecting the whole constitution of the body; not local. 2. Pertaining to the constitution. [EU] Consumption: Pulmonary tuberculosis. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Continuous infusion: The administration of a fluid into a blood vessel, usually over a prolonged period of time. [NIH] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contralateral: Having to do with the opposite side of the body. [NIH]
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Contrast Sensitivity: The ability to detect sharp boundaries (stimuli) and to detect slight changes in luminance at regions without distinct contours. Psychophysical measurements of this visual function are used to evaluate visual acuity and to detect eye disease. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]
Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Cooperative group: A group of physicians, hospitals, or both formed to treat a large number of persons in the same way so that new treatment can be evaluated quickly. Clinical trials of new cancer treatments often require many more people than a single physician or hospital can care for. [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Artery Bypass: Surgical therapy of ischemic coronary artery disease achieved by grafting a section of saphenous vein, internal mammary artery, or other substitute between the aorta and the obstructed coronary artery distal to the obstructive lesion. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH]
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Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Croton Oil: Viscous, nauseating oil obtained from the shrub Croton tiglium (Euphorbaceae). It is a vesicant and skin irritant used as pharmacologic standard for skin inflammation and allergy and causes skin cancer. It was formerly used as an emetic and cathartic with frequent mortality. [NIH] Cryostat: A batchwise operating apparatus in which a cryogenic liquid or solid is used to maintain by evaporation a cryotemperature which needs not be constant but may vary in a predetermined fashion. [NIH] Culture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as agar or gelatin. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclin: Molecule that regulates the cell cycle. [NIH] Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [NIH] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cyst: A sac or capsule filled with fluid. [NIH] Cytarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Cytidine: A pyrimidine nucleoside that is composed of the base cytosine linked to the fivecarbon sugar D-ribose. [NIH] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups
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and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytochrome b: Cytochromes (electron-transporting proteins) with protoheme or a related heme as the prosthetic group. The prosthetic group is not covalently bound to the protein moiety. [NIH] Cytogenetic Analysis: Examination of chromosomes to diagnose, classify, screen for, or manage genetic diseases and abnormalities. Following preparation of the sample, karyotyping is performed and/or the specific chromosomes are analyzed. [NIH] Cytogenetics: A branch of genetics which deals with the cytological and molecular behavior of genes and chromosomes during cell division. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] Cytopenia: A reduction in the number of blood cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytosine: A pyrimidine base that is a fundamental unit of nucleic acids. [NIH] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Daunorubicin: Very toxic anthracycline aminoglycoside antibiotic isolated from Streptomyces peucetius and others, used in treatment of leukemias and other neoplasms. [NIH]
De novo: In cancer, the first occurrence of cancer in the body. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Decitabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of
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sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Care: The total of dental diagnostic, preventive, and restorative services provided to meet the needs of a patient (from Illustrated Dictionary of Dentistry, 1982). [NIH] Dentists: Individuals licensed to practice dentistry. [NIH] Deoxycytidine: A drug that protects healthy tissues from the toxic effects of anticancer drugs. [NIH] Deoxyribonucleic: A polymer of subunits called deoxyribonucleotides which is the primary genetic material of a cell, the material equivalent to genetic information. [NIH] Deoxyribonucleic acid: A polymer of subunits called deoxyribonucleotides which is the primary genetic material of a cell, the material equivalent to genetic information. [NIH] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Depsipeptide: Anticancer drugs obtained from microorganisms. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Dermatosis: Any skin disease, especially one not characterized by inflammation. [EU] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Developing Countries: Countries in the process of change directed toward economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diastolic: Of or pertaining to the diastole. [EU]
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Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dihydroxyacetone: A ketotriose compound. Its addition to blood preservation solutions results in better maintenance of 2,3-diphosphoglycerate levels during storage. It is readily phosphorylated to dihydroxyacetone phosphate by triokinase in erythrocytes. In combination with naphthoquinones it acts as a sunscreening agent. [NIH] Dihydroxyacetone Phosphate: An important intermediate in lipid biosynthesis and in glycolysis. [NIH] Dilatation: The act of dilating. [NIH] Dilution: A diluted or attenuated medicine; in homeopathy, the diffusion of a given quantity of a medicinal agent in ten or one hundred times the same quantity of water. [NIH] Dimerization: The process by which two molecules of the same chemical composition form a condensation product or polymer. [NIH] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Dimethyl Sulfoxide: A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during cryopreservation. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation. [NIH] Diphtheria: A localized infection of mucous membranes or skin caused by toxigenic strains of Corynebacterium diphtheriae. It is characterized by the presence of a pseudomembrane at the site of infection. Diphtheria toxin, produced by C. diphtheriae, can cause myocarditis, polyneuritis, and other systemic toxic effects. [NIH] Diphtheria Toxin: A 60 kD single chain protein elaborated by Corynebacterium diphtheriae that causes the sign and symptoms of diphtheria; it can be broken into two unequal fragments, the smaller (A fragment) inhibits protein synthesis and is the lethal moiety that needs the larger (B fragment) for entry into cells. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Discrimination: The act of qualitative and/or quantitative differentiation between two or more stimuli. [NIH] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disease-Free Survival: Period after successful treatment in which there is no appearance of the symptoms or effects of the disease. [NIH] Disparity: Failure of the two retinal images of an object to fall on corresponding retinal
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points. [NIH] Disposition: A tendency either physical or mental toward certain diseases. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dose-dependent: Refers to the effects of treatment with a drug. If the effects change when the dose of the drug is changed, the effects are said to be dose dependent. [NIH] Dosimetry: All the methods either of measuring directly, or of measuring indirectly and computing, absorbed dose, absorbed dose rate, exposure, exposure rate, dose equivalent, and the science associated with these methods. [NIH] Doxorubicin: Antineoplastic antibiotic obtained from Streptomyces peucetics. It is a hydroxy derivative of daunorubicin and is used in treatment of both leukemia and solid tumors. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Combinations: Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture. It is differentiated from combination drug therapy in which two or more drugs are administered separately for a combined effect. [NIH] Drug Design: The molecular designing of drugs for specific purposes (such as DNAbinding, enzyme inhibition, anti-cancer efficacy, etc.) based on knowledge of molecular properties such as activity of functional groups, molecular geometry, and electronic structure, and also on information cataloged on analogous molecules. Drug design is generally computer-assisted molecular modeling and does not include pharmacokinetics, dosage analysis, or drug administration analysis. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended
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effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duodenum: The first part of the small intestine. [NIH] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dynein: A transport protein that normally binds proteins to the microtubule. [NIH] Dysmenorrhea: Painful menstruation. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Ectopic: Pertaining to or characterized by ectopia. [EU] Eczema: A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed). [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electroplating: Coating with a metal or alloy by electrolysis. [NIH] Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryogenesis: The process of embryo or embryoid formation, whether by sexual (zygotic) or asexual means. In asexual embryogenesis embryoids arise directly from the explant or on intermediary callus tissue. In some cases they arise from individual cells (somatic cell embryoge). [NIH] Emetic: An agent that causes vomiting. [EU] Empirical: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion
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medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Endarterectomy: Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called atherectomy. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endoderm: The inner of the three germ layers of the embryo. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endotoxic: Of, relating to, or acting as an endotoxin (= a heat-stable toxin, associated with the outer membranes of certain gram-negative bacteria. Endotoxins are not secreted and are released only when the cells are disrupted). [EU] Endotoxin: Toxin from cell walls of bacteria. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Enterocolitis: Inflammation of the intestinal mucosa of the small and large bowel. [NIH] Enterohepatic: Of or involving the intestine and liver. [EU] Enterohepatic Circulation: Recycling through liver by excretion in bile, reabsorption from intestines into portal circulation, passage back into liver, and re-excretion in bile. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Induction: An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis. [NIH] Enzyme Repression: The interference in synthesis of an enzyme due to the elevated level of an effector substance, usually a metabolite, whose presence would cause depression of the gene responsible for enzyme synthesis. [NIH] Eosinophil: A polymorphonuclear leucocyte with large eosinophilic granules in its
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cytoplasm, which plays a role in hypersensitivity reactions. [NIH] Eosinophilia: Abnormal increase in eosinophils in the blood, tissues or organs. [NIH] Eosinophilic: A condition found primarily in grinding workers caused by a reaction of the pulmonary tissue, in particular the eosinophilic cells, to dust that has entered the lung. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epidural: The space between the wall of the spinal canal and the covering of the spinal cord. An epidural injection is given into this space. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epirubicin: An anthracycline antibiotic which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA. Clinical studies indicate activity in breast cancer, non-Hodgkin's lymphomas, ovarian cancer, soft-tissue sarcomas, pancreatic cancer, gastric cancer, small-cell lung cancer and acute leukemia. It is equal in activity to doxorubicin but exhibits less acute toxicities and less cardiotoxicity. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythrocyte Indices: Quantification of size and cell hemoglobin content or concentration of the erythrocyte, usually derived from erythrocyte count, blood hemoglobin concentration, and hematocrit. Includes the mean cell volume (MCV), mean cell hemoglobin (MCH), and mean cell hemoglobin concentration (MCHC). Use also for cell diameter and thickness. [NIH] Erythrocyte Membrane: The semipermeable outer portion of the red corpuscle. It is known
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as a 'ghost' after hemolysis. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythroid Progenitor Cells: Committed, erythroid stem cells derived from myeloid stem cells. The progenitor cells develop in two phases: erythroid burst-forming units (BFU-E) followed by erythroid colony-forming units (CFU-E). BFU-E differentiate into CFU-E on stimulation by erythropoietin, and then further differentiate into erythroblasts when stimulated by other factors. [NIH] Erythroleukemia: Cancer of the blood-forming tissues in which large numbers of immature, abnormal red blood cells are found in the blood and bone marrow. [NIH] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Estrogen: One of the two female sex hormones. [NIH] Estrogen receptor: ER. Protein found on some cancer cells to which estrogen will attach. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Ethmoid: An unpaired cranial bone which helps form the medial walls of the orbits and contains the themoidal air cells which drain into the nose. [NIH] Ethylmaleimide: A sulfhydryl reagent that is widely used in experimental biochemical studies. [NIH] Etodolac: A nonsteroidal anti-inflammatory agent with potent analgesic and antiarthritic properties. It has been shown to be effective in the treatment of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and in the alleviation of postoperative pain. [NIH] Etoposide: A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evaluable patients: Patients whose response to a treatment can be measured because enough information has been collected. [NIH] Exatecan mesylate: An anticancer drug that belongs to the family of drugs called topoisomerase inhibitors. Also called DX-8951f. [NIH] Excisional: The surgical procedure of removing a tumor by cutting it out. The biopsy is then examined under a microscope. [NIH] Excisional biopsy: A surgical procedure in which an entire lump or suspicious area is
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removed for diagnosis. The tissue is then examined under a microscope. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excrete: To get rid of waste from the body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Expiration: The act of breathing out, or expelling air from the lungs. [EU] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Facial: Of or pertaining to the face. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue
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development. [NIH] Femoral: Pertaining to the femur, or to the thigh. [EU] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fenretinide: A synthetic retinoid that is used orally as a chemopreventive against prostate cancer and in women at risk of developing contralateral breast cancer. It is also effective as an antineoplastic agent. [NIH] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [NIH] Ferritin: An iron-containing protein complex that is formed by a combination of ferric iron with the protein apoferritin. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosarcoma: A type of soft tissue sarcoma that begins in fibrous tissue, which holds bones, muscles, and other organs in place. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Filgrastim: A colony-stimulating factor that stimulates the production of neutrophils (a type of white blood cell). It is a cytokine that belongs to the family of drugs called hematopoietic (blood-forming) agents. Also called granulocyte colony-stimulating factor (G-CSF). [NIH] Filtration: The passage of a liquid through a filter, accomplished by gravity, pressure, or vacuum (suction). [EU] Finasteride: An orally active testosterone 5-alpha-reductase inhibitor. It is used as a surgical alternative for treatment of benign prostatic hyperplasia. [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [EU]
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Flaccid: Weak, lax and soft. [EU] Flavopiridol: Belongs to the family of anticancer drugs called flavinols. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fluconazole: Triazole antifungal agent that is used to treat oropharyngeal candidiasis and cryptococcal meningitis in AIDS. [NIH] Fludarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Fluorouracil: A pyrimidine analog that acts as an antineoplastic antimetabolite and also has immunosuppressant. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. [NIH] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Follicles: Shafts through which hair grows. [NIH] Fossa: A cavity, depression, or pit. [NIH] Fovea: The central part of the macula that provides the sharpest vision. [NIH] Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Frozen Sections: Thinly cut sections of frozen tissue specimens prepared with a cryostat or freezing microtome. [NIH]
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Fungemia: The presence of fungi circulating in the blood. Opportunistic fungal sepsis is seen most often in immunosuppressed patients with severe neutropenia or in postoperative patients with intravenous catheters and usually follows prolonged antibiotic therapy. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Gait: Manner or style of walking. [NIH] Gallate: Antioxidant present in tea. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gamma Rays: Very powerful and penetrating, high-energy electromagnetic radiation of shorter wavelength than that of x-rays. They are emitted by a decaying nucleus, usually between 0.01 and 10 MeV. They are also called nuclear x-rays. [NIH] Gamma-Glutamyl Hydrolase: Catalyzes the hydrolysis of pteroylpolyglutamic acids in gamma linkage to pterolylmonoglutamic acid and free glutamic acid. EC 3.4.19.9. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria. [NIH]
Gastric Mucosa: Surface epithelium in the stomach that invaginates into the lamina propria, forming gastric pits. Tubular glands, characteristic of each region of the stomach (cardiac, gastric, and pyloric), empty into the gastric pits. The gastric mucosa is made up of several different kinds of cells. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as
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a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gemcitabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Fusion: Fusion of structural genes to analyze protein behavior or fusion of regulatory sequences with structural genes to determine mechanisms of regulation. [NIH] Gene Rearrangement: The ordered rearrangement of gene regions by DNA recombination such as that which occurs normally during development. [NIH] Gene Targeting: The integration of exogenous DNA into the genome of an organism at sites where its expression can be suitably controlled. This integration occurs as a result of homologous recombination. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] Gene-modified: Cells that have been altered to contain different genetic material than they originally contained. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Germ Layers: The three layers of cells comprising the early embryo. [NIH] Germline mutation: A gene change in the body's reproductive cells (egg or sperm) that becomes incorporated into the DNA of every cell in the body of offspring; germline mutations are passed on from parents to offspring. Also called hereditary mutation. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of
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fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Gestational trophoblastic disease: A rare cancer in women of child-bearing age in which cancer cells grow in the tissues that are formed in the uterus after conception. Also called gestational trophoblastic tumor, gestational trophoblastic neoplasia, molar pregnancy, or choriocarcinoma. [NIH] Gestational trophoblastic neoplasia: A rare cancer in women of child-bearing age in which cancer cells grow in the tissues that are formed in the uterus after conception. Also called gestational trophoblastic disease, gestational trophoblastic tumor, molar pregnancy, or choriocarcinoma. [NIH] Gestational trophoblastic tumor: A rare cancer in women of child-bearing age in which cancer cells grow in the tissues that are formed in the uterus after conception. Also called gestational trophoblastic disease, gestational trophoblastic neoplasia, molar pregnancy, or choriocarcinoma. [NIH] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] Gingival Hyperplasia: A pathological increase in the depth of the gingival crevice surrounding a tooth at the gum margin. [NIH] Ginseng: An araliaceous genus of plants that contains a number of pharmacologically active agents used as stimulants, sedatives, and tonics, especially in traditional medicine. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glioblastoma: A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides
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in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glucuronides: Glycosides of glucuronic acid formed by the reaction of uridine diphosphate glucuronic acid with certain endogenous and exogenous substances. Their formation is important for the detoxification of drugs, steroid excretion and bilirubin metabolism to a more water-soluble compound that can be eliminated in the urine and bile. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycolysis: The pathway by which glucose is catabolized into two molecules of pyruvic acid with the generation of ATP. [NIH] Glycophorin: The major sialoglycoprotein of the human erythrocyte membrane. It consists of at least two sialoglycopeptides and is composed of 60% carbohydrate including sialic acid and 40% protein. It is involved in a number of different biological activities including the binding of MN blood groups, influenza viruses, kidney bean phytohemagglutinin, and wheat germ agglutinin. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosaminoglycans: Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or Nacetylgalactosamine. [NIH] Glycosidic: Formed by elimination of water between the anomeric hydroxyl of one sugar and a hydroxyl of another sugar molecule. [NIH] Gonad: A sex organ, such as an ovary or a testicle, which produces the gametes in most multicellular animals. [NIH] Gonadal: Pertaining to a gonad. [EU] Gonadotropin: The water-soluble follicle stimulating substance, by some believed to originate in chorionic tissue, obtained from the serum of pregnant mares. It is used to supplement the action of estrogens. [NIH] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH]
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Graft-versus-host disease: GVHD. A reaction of donated bone marrow or peripheral stem cells against a person's tissue. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Granule: A small pill made from sucrose. [EU] Granulocyte: A type of white blood cell that fights bacterial infection. Neutrophils, eosinophils, and basophils are granulocytes. [NIH] Granulocyte-Macrophage Colony-Stimulating Factor: An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages. [NIH] Granulomatous Disease, Chronic: A recessive X-linked defect of leukocyte function in which phagocytic cells ingest but fail to digest bacteria, resulting in recurring bacterial infections with granuloma formation. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanine: One of the four DNA bases. [NIH] Guinea Pigs: A common name used for the family Caviidae. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research. [NIH]
Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Hairy cell leukemia: A type of chronic leukemia in which the abnormal white blood cells appear to be covered with tiny hairs when viewed under a microscope. [NIH] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Helix-loop-helix: Regulatory protein of cell cycle. [NIH] Hematocrit: Measurement of the volume of packed red cells in a blood specimen by centrifugation. The procedure is performed using a tube with graduated markings or with automated blood cell counters. It is used as an indicator of erythrocyte status in disease. For example, anemia shows a low hematocrit, polycythemia, high values. [NIH]
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Hematologic malignancies: Cancers of the blood or bone marrow, including leukemia and lymphoma. Also called hematologic cancers. [NIH] Hematology: A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues. [NIH] Hematopoiesis: The development and formation of various types of blood cells. [NIH] Hematopoietic growth factors: A group of proteins that cause blood cells to grow and mature. [NIH] Hematopoietic Stem Cell Transplantation: The transference of stem cells from one animal or human to another (allogeneic), or within the same individual (autologous). The source for the stem cells may be the bone marrow or peripheral blood. Stem cell transplantation has been used as an alternative to autologous bone marrow transplantation in the treatment of a variety of neoplasms. [NIH] Hematopoietic Stem Cells: Progenitor cells from which all blood cells derive. [NIH] Hematopoietic tissue: Tissue in which new blood cells are formed. [NIH] Hematuria: Presence of blood in the urine. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemolysis: The destruction of erythrocytes by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity. [NIH] Hemophilia: Refers to a group of hereditary disorders in which affected individuals fail to make enough of certain proteins needed to form blood clots. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Heparan Sulfate Proteoglycan: A substance released by astrocytes, which is critical in stopping nervous fibers in their tracks. [NIH] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatitis A: Hepatitis caused by hepatovirus. It can be transmitted through fecal contamination of food or water. [NIH] Hepatocyte: A liver cell. [NIH]
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Hepatocyte Growth Factor: Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is proto-oncogene protein C-met. [NIH] Hepatoma: A liver tumor. [NIH] Hepato-splenomegaly: Enlargement of the liver and spleen. [NIH] Hepatovirus: A genus of Picornaviridae causing infectious hepatitis naturally in humans and experimentally in other primates. It is transmitted through fecal contamination of food or water. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Hereditary mutation: A gene change in the body's reproductive cells (egg or sperm) that becomes incorporated into the DNA of every cell in the body of offspring; hereditary mutations are passed on from parents to offspring. Also called germline mutation. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes simplex or to herpes zoster. [EU] Heterodimer: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Hidradenitis: The inflammation of a sweat gland (usually of the apocrine type). The condition can be idiopathic or occur as a result of or in association with another underlying condition. Neutrophilic eccrine hidradenitis is a relatively rare variant that has been reported in patients undergoing chemotherapy, usually for non-Hodgkin lymphomas or leukemic conditions. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histamine Release: The secretion of histamine from mast cell and basophil granules by exocytosis. This can be initiated by a number of factors, all of which involve binding of IgE, cross-linked by antigen, to the mast cell or basophil's Fc receptors. Once released, histamine binds to a number of different target cell receptors and exerts a wide variety of effects. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histiocytosis: General term for the abnormal appearance of histiocytes in the blood. Based on the pathological features of the cells involved rather than on clinical findings, the histiocytic diseases are subdivided into three groups: Langerhans cell histiocytosis, nonLangerhans cell histiocytosis, and malignant histiocytic disorders. [NIH] Histocompatibility: The degree of antigenic similarity between the tissues of different individuals, which determines the acceptance or rejection of allografts. [NIH] Histocompatibility Antigens: A group of antigens that includes both the major and minor histocompatibility antigens. The former are genetically determined by the major histocompatibility complex. They determine tissue type for transplantation and cause allograft rejections. The latter are systems of allelic alloantigens that can cause weak transplant rejection. [NIH]
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Histone Deacetylase: Hydrolyzes N-acetyl groups on histones. [NIH] Homeobox: Distinctive sequence of DNA bases. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] Homoharringtonine: An anticancer drug that belongs to the plant alkaloid family of drugs. [NIH]
Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Homosexuality: Sexual attraction or relationship between members of the same sex. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hormone therapy: Treatment of cancer by removing, blocking, or adding hormones. Also called endocrine therapy. [NIH] Hospice: Institution dedicated to caring for the terminally ill. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydatidiform Mole: A trophoblastic disease characterized by hydrops of the mesenchymal portion of the villus. Its karyotype is paternal and usually homozygotic. The tumor is indistinguishable from chorioadenoma destruens or invasive mole ( = hydatidiform mole, invasive) except by karyotype. There is no apparent relation by karyotype to choriocarcinoma. Hydatidiform refers to the presence of the hydropic state of some or all of the villi (Greek hydatis, a drop of water). [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH]
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Hydroxamic Acids: A class of weak acids with the general formula R-conhoh. [NIH] Hydroxylamine: A colorless inorganic compound (HONH2) used in organic synthesis and as a reducing agent, due to its ability to donate nitric oxide. [NIH] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hydroxyurea: An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase. [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypercalcemia: Abnormally high level of calcium in the blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthermia: A type of treatment in which body tissue is exposed to high temperatures to damage and kill cancer cells or to make cancer cells more sensitive to the effects of radiation and certain anticancer drugs. [NIH] Hyperthyroidism: Excessive functional activity of the thyroid gland. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] Hypochlorous Acid: HClO. An oxyacid of chlorine containing monovalent chlorine that acts as an oxidizing or reducing agent. [NIH] Hypogammaglobulinemia: The most common primary immunodeficiency in which antibody production is deficient. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypothyroidism: Deficiency of thyroid activity. In adults, it is most common in women and is characterized by decrease in basal metabolic rate, tiredness and lethargy, sensitivity to cold, and menstrual disturbances. If untreated, it progresses to full-blown myxoedema. In infants, severe hypothyroidism leads to cretinism. In juveniles, the manifestations are intermediate, with less severe mental and developmental retardation and only mild symptoms of the adult form. When due to pituitary deficiency of thyrotropin secretion it is called secondary hypothyroidism. [EU] Ibuprofen: A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis. [NIH]
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Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idarubicin: An orally administered anthracycline antibiotic. The compound has shown activity against breast cancer, lymphomas and leukemias, together with potential for reduced cardiac toxicity. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Idiotype: The unique antigenic determinant in the variable region. [NIH] Ileitis: Inflammation of the ileum. [EU] Ileum: The lower end of the small intestine. [NIH] Immune adjuvant: A drug that stimulates the immune system to respond to disease. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoconjugates: Combinations of diagnostic or therapeutic substances linked with specific immune substances such as immunoglobulins, monoclonal antibodies or antigens. Often the diagnostic or therapeutic substance is a radionuclide. These conjugates are useful tools for specific targeting of drugs and radioisotopes in the chemotherapy and radioimmunotherapy of certain cancers. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodeficiency syndrome: The inability of the body to produce an immune response. [NIH]
Immunofluorescence: A technique for identifying molecules present on the surfaces of cells or in tissues using a highly fluorescent substance coupled to a specific antibody. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunophenotyping: Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort Tlymphocytes into subsets based on CD antigens by the technique of flow cytometry. [NIH] Immunophilins: Members of a family of highly conserved proteins which are all cis-trans peptidyl-prolyl isomerases (peptidylprolyl isomerase). They bind the immunosuppressant drugs cyclosporine; tacrolimus and sirolimus. They possess rotomase activity, which is inhibited by the immunosuppressant drugs that bind to them. EC 5.2.1.- [NIH]
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Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Immunotoxin: An antibody linked to a toxic substance. Some immmunotoxins can bind to cancer cells and kill them. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indolent: A type of cancer that grows slowly. [NIH] Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Induction therapy: Treatment designed to be used as a first step toward shrinking the cancer and in evaluating response to drugs and other agents. Induction therapy is followed by additional therapy to eliminate whatever cancer remains. [NIH] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus,
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or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Informed Consent: Voluntary authorization, given to the physician by the patient, with full comprehension of the risks involved, for diagnostic or investigative procedures and medical and surgical treatment. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inlay: In dentistry, a filling first made to correspond with the form of a dental cavity and then cemented into the cavity. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insertional: A technique in which foreign DNA is cloned into a restriction site which occupies a position within the coding sequence of a gene in the cloning vector molecule. Insertion interrupts the gene's sequence such that its original function is no longer expressed. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insomnia: Difficulty in going to sleep or getting enough sleep. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood
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glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Intercalating Agents: Agents that are capable of inserting themselves between the successive bases in DNA, thus kinking, uncoiling or otherwise deforming it and therefore preventing its proper functioning. They are used in the study of DNA. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-10: Factor that is a coregulator of mast cell growth. It is produced by T-cells and B-cells and shows extensive homology with the Epstein-Barr virus BCRFI gene. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-3: A multilineage cell growth factor secreted by lymphocytes, epithelial cells, and astrocytes which stimulates clonal proliferation and differentiation of various types of blood and tissue cells. Also called multi-CSF, it is considered one of the hematopoietic colony stimulating factors. [NIH] Interleukin-5: Factor promoting eosinophil differentiation and activation in hematopoiesis. It also triggers activated B-cells for a terminal differentiation into Ig-secreting cells. [NIH] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus. IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [NIH] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH]
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Interphase: The interval between two successive cell divisions during which the chromosomes are not individually distinguishable and DNA replication occurs. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestinal Mucosa: The surface lining of the intestines where the cells absorb nutrients. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Intrahepatic: Within the liver. [NIH] Intraperitoneal: IP. Within the peritoneal cavity (the area that contains the abdominal organs). [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irinotecan: An anticancer drug that belongs to a family of anticancer drugs called topoisomerase inhibitors. It is a camptothecin analogue. Also called CPT 11. [NIH] Iris: The most anterior portion of the uveal layer, separating the anterior chamber from the posterior. It consists of two layers - the stroma and the pigmented epithelium. Color of the iris depends on the amount of melanin in the stroma on reflection from the pigmented epithelium. [NIH] Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU]
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Islet: Cell producing insulin in pancreas. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]
Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Kanamycin: Antibiotic complex produced by Streptomyces kanamyceticus from Japanese soil. Comprises 3 components: kanamycin A, the major component, and kanamycins B and C, the minor components. [NIH] Karyotype: The characteristic chromosome complement of an individual, race, or species as defined by their number, size, shape, etc. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratin: A class of fibrous proteins or scleroproteins important both as structural proteins and as keys to the study of protein conformation. The family represents the principal constituent of epidermis, hair, nails, horny tissues, and the organic matrix of tooth enamel. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms an alpha-helix, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Keratitis: Inflammation of the cornea. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH] Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [NIH] Killer Cells: Lymphocyte-like effector cells which mediate antibody-dependent cell cytotoxicity. They kill antibody-coated target cells which they bind with their Fc receptors. [NIH]
Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2.
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Chemically unstable. [EU] Lactate Dehydrogenase: A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of lactate and pyruvate. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist. [NIH] Lactation: The period of the secretion of milk. [EU] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Language Disorders: Conditions characterized by deficiencies of comprehension or expression of written and spoken forms of language. These include acquired and developmental disorders. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Latency: The period of apparent inactivity between the time when a stimulus is presented and the moment a response occurs. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Leiomyosarcoma: A tumor of the muscles in the uterus, abdomen, or pelvis. [NIH] Leishmaniasis: A disease caused by any of a number of species of protozoa in the genus Leishmania. There are four major clinical types of this infection: cutaneous (Old and New World), diffuse cutaneous, mucocutaneous, and visceral leishmaniasis. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Lethal: Deadly, fatal. [EU] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leucovorin: The active metabolite of folic acid. Leucovorin is used principally as its calcium salt as an antidote to folic acid antagonists which block the conversion of folic acid to folinic acid. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukoencephalopathy: A condition with spongy holes in the brain's white matter. [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood
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is reduced. [NIH] Leukoplakia: A white patch that may develop on mucous membranes such as the cheek, gums, or tongue and may become cancerous. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [NIH] Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties. [NIH] Lipopolysaccharides: Substance consisting of polysaccaride and lipid. [NIH] Liposomal: A drug preparation that contains the active drug in very tiny fat particles. This fat-encapsulated drug is absorbed better, and its distribution to the tumor site is improved. [NIH]
Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver cancer: A disease in which malignant (cancer) cells are found in the tissues of the liver. [NIH]
Liver Neoplasms: Tumors or cancer of the liver. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Loss of Heterozygosity: The loss of one allele at a specific locus, caused by a deletion mutation; or loss of a chromosome from a chromosome pair. It is detected when heterozygous markers for a locus appear monomorphic because one of the alleles was deleted. When this occurs at a tumor suppressor gene locus where one of the alleles is already abnormal, it can result in neoplastic transformation. [NIH] Lucida: An instrument, invented by Wollaton, consisting essentially of a prism or a mirror through which an object can be viewed so as to appear on a plane surface seen in direct view and on which the outline of the object may be traced. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU]
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Lumbar puncture: A procedure in which a needle is put into the lower part of the spinal column to collect cerebrospinal fluid or to give anticancer drugs intrathecally. Also called a spinal tap. [NIH] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lutein Cells: The cells of the corpus luteum which are derived from the granulosa cells and the theca cells of the Graafian follicle. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphadenopathy: Disease or swelling of the lymph nodes. [NIH] Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphoblastic: One of the most aggressive types of non-Hodgkin lymphoma. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphocyte Subsets: A classification of lymphocytes based on structurally or functionally different populations of cells. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphocytic Choriomeningitis Virus: The type species of arenavirus, part of the LCMLassa complex viruses, producing an inapparent infection in house and laboratory mice. In humans, infection with LCMV can be inapparent, or can present with an influenza-like illness, a benign aseptic meningitis, or a severe meningoencephalomyelitis. The virus can also infect monkeys, dogs, field mice, guinea pigs, and hamsters, the latter an epidemiologically important host. [NIH] Lymphocytosis: Excess of normal lymphocytes in the blood or in any effusion. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lymphosarcoma: An obsolete term for a malignant tumor of lymphatic tissue. [NIH] Lymphotoxin: Soluble substance released by lymphocytes activated by antigens or T-cell mitogens, that is cytotoxic to other cells. It is involved in allergies and chronic inflammatory diseases. Lymphotoxin is antigenically distinct from tumor necrosis factor-alpha (tumor
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necrosis factor), though they both share a common receptor, biological activities, and significant amino acid sequences. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Macrophage Colony-Stimulating Factor: A mononuclear phagocyte colony-stimulating factor synthesized by mesenchymal cells. The compound stimulates the survival, proliferation, and differentiation of hematopoietic cells of the monocyte-macrophage series. M-CSF is a disulfide-bonded glycoprotein dimer with a MW of 70 kDa. It binds to a specific high affinity receptor (receptor, macrophage colony-stimulating factor). [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Maintenance therapy: Treatment that is given to help a primary (original) treatment keep working. Maintenance therapy is often given to help keep cancer in remission. [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant fibrous histiocytoma: A sarcoma that usually begins in soft tissue. It usually appears as an enlarging, painful mass that can cause fracture due to destruction of the bone by a spreading tumor. [NIH] Malignant mesothelioma: A rare type of cancer in which malignant cells are found in the sac lining the chest or abdomen. Exposure to airborne asbestos particles increases one's risk of developing malignant mesothelioma. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammary: Pertaining to the mamma, or breast. [EU] Man-made: Ionizing radiation emitted by artificial or concentrated natural, radioactive material or resulting from the operation of high voltage apparatus, such as X-ray apparatus or particle accelerators, of nuclear reactors, or from nuclear explosions. [NIH] Mannans: Polysaccharides consisting of mannose units. [NIH] Mastication: The act and process of chewing and grinding food in the mouth. [NIH] Masticatory: 1. subserving or pertaining to mastication; affecting the muscles of mastication. 2. a remedy to be chewed but not swallowed. [EU] Matched-Pair Analysis: A type of analysis in which subjects in a study group and a comparison group are made comparable with respect to extraneous factors by individually pairing study subjects with the comparison group subjects (e.g., age-matched controls). [NIH]
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Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Maxillary: Pertaining to the maxilla : the irregularly shaped bone that with its fellow forms the upper jaw. [EU] Median survival time: The point in time from either diagnosis or treatment at which half of the patients with a given disease are found to be, or expected to be, still alive. In a clinical trial, median survival time is one way to measure how effective a treatment is. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Oncology: A subspecialty of internal medicine concerned with the study of neoplasms. [NIH] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] Mefenamic Acid: A non-steroidal anti-inflammatory agent with analgesic, antiinflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase. [NIH] Megakaryocytes: Very large bone marrow cells which release mature blood platelets. [NIH] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - melphalan, the racemic mixture - merphalan, and the dextro isomer medphalan; toxic to bone marrow, but little vesicant action; potential carcinogen. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Menarche: The establishment or beginning of the menstrual function. [EU]
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Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningioma: A type of tumor that occurs in the meninges, the membranes that cover and protect the brain and spinal cord. Meningiomas usually grow slowly. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Menopause: Permanent cessation of menstruation. [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mental Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH]
Mercaptopurine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesoderm: The middle germ layer of the embryo. [NIH] Mesonephros: The excretory organ of the embryo, collective Wolffian tubules, which forms the urogenital fold from which the reproductive organs develop. The mesonephros is the permanent kidney in fish and amphibians, but atrophies in reptiles, birds, and mammals. [NIH]
Mesothelioma: A benign (noncancerous) or malignant (cancerous) tumor affecting the lining of the chest or abdomen. Exposure to asbestos particles in the air increases the risk of developing malignant mesothelioma. [NIH] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metaphase: The second phase of cell division, in which the chromosomes line up across the equatorial plane of the spindle prior to separation. [NIH] Metaplasia: A condition in which there is a change of one adult cell type to another similar adult cell type. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from
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cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Methanol: A colorless, flammable liquid used in the manufacture of formaldehyde and acetic acid, in chemical synthesis, antifreeze, and as a solvent. Ingestion of methanol is toxic and may cause blindness. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Methotrexate: An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of dihydrofolate reductase and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA. [NIH] Methylprednisolone: (6 alpha,11 beta)-11,17,21-Trihydroxy-6-methylpregna-1,4-diene-3,2dione. A prednisolone derivative which has pharmacological actions similar to prednisolone. [NIH] Methyltransferase: A drug-metabolizing enzyme. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Minor Histocompatibility Antigens: Allelic alloantigens often responsible for weak graft rejection in cases when (major) histocompatibility has been established by standard tests. In the mouse they are coded by more than 500 genes at up to 30 minor histocompatibility loci. The most well-known minor histocompatibility antigen in mammals is the H-Y antigen. [NIH]
Minor Histocompatibility Loci: Genetic loci responsible for the encoding of histocompatibility antigens other than those encoded by the major histocompatibility complex. The antigens encoded by these genes are often responsible for graft rejection in cases where histocompatibility has been established by standard tests. The location of some of these loci on the X and Y chromosomes explains why grafts from males to females may be rejected while grafts from females to males are accepted. In the mouse roughly 30 minor histocompatibility loci have been recognized, comprising more than 500 genes. [NIH] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH]
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Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mitotic: Cell resulting from mitosis. [NIH] Mitotic Spindle Apparatus: An organelle consisting of three components: (1) the astral microtubules, which form around each centrosome and extend to the periphery; (2) the polar microtubules which extend from one spindle pole to the equator; and (3) the kinetochore microtubules, which connect the centromeres of the various chromosomes to either centrosome. [NIH] Mitoxantrone: An anthracenedione-derived antineoplastic agent. [NIH] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]
Molar pregnancy: A rare cancer in women of child-bearing age in which cancer cells grow in the tissues that are formed in the uterus after conception. Also called gestational trophoblastic disease, gestational trophoblastic neoplasia, gestational trophoblastic tumor, or choriocarcinoma. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular mass: The sum of the atomic masses of all atoms in a molecule, based on a scale in which the atomic masses of hydrogen, carbon, nitrogen, and oxygen are 1, 12, 14, and 16, respectively. For example, the molecular mass of water, which has two atoms of hydrogen and one atom of oxygen, is 18 (i.e., 2 + 16). [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Monophosphate: So called second messenger for neurotransmitters and hormones. [NIH] Monosomy: The condition in which one chromosome of a pair is missing. In a normally diploid cell it is represented symbolically as 2N-1. [NIH] Monotherapy: A therapy which uses only one drug. [EU] Morphological: Relating to the configuration or the structure of live organs. [NIH]
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Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Morula: The early embryo at the developmental stage in which the blastomeres, resulting from repeated mitotic divisions of the fertilized ovum, form a compact mass. [NIH] Motility: The ability to move spontaneously. [EU] Mucocutaneous: Pertaining to or affecting the mucous membrane and the skin. [EU] Mucor: A genus of zygomycetous fungi of the family Mucoraceae, order Mucorales. It is primarily saprophytic, but may cause mucormycosis in man from spores germinating in the lungs. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucositis: A complication of some cancer therapies in which the lining of the digestive system becomes inflamed. Often seen as sores in the mouth. [NIH] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multidrug resistance: Adaptation of tumor cells to anticancer drugs in ways that make the drugs less effective. [NIH] Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multivalent: Pertaining to a group of 5 or more homologous or partly homologous chromosomes during the zygotene stage of prophase to first metaphasis in meiosis. [NIH] Muscular Diseases: Acquired, familial, and congenital disorders of skeletal muscle and smooth muscle. [NIH] Mustard Gas: Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed). [NIH] Mutagen: Any agent, such as X-rays, gamma rays, mustard gas, TCDD, that can cause abnormal mutation in living cells; having the power to cause mutations. [NIH] Mutagenic: Inducing genetic mutation. [EU] Mycosis: Any disease caused by a fungus. [EU] Mycosis Fungoides: A chronic malignant T-cell lymphoma of the skin. In the late stages the lymph nodes and viscera are affected. [NIH] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelitis: Inflammation of the spinal cord. Relatively common etiologies include infections; autoimmune diseases; spinal cord; and ischemia (see also spinal cord vascular diseases). Clinical features generally include weakness, sensory loss, localized pain, incontinence, and other signs of autonomic dysfunction. [NIH] Myelodysplasia: Abnormal bone marrow cells that may lead to myelogenous leukemia.
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[NIH]
Myelodysplastic syndrome: Disease in which the bone marrow does not function normally. Also called preleukemia or smoldering leukemia. [NIH] Myelofibrosis: A disorder in which the bone marrow is replaced by fibrous tissue. [NIH] Myelogenous: Produced by, or originating in, the bone marrow. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myeloid Progenitor Cells: One of the two stem cells derived from hematopoietic stem cells the other being the lymphoid progenitor cell. Derived from these myeloid progenitor cells are the erythroid progenitor cells and the myeloid cells (monocytes and granulocytes). [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [NIH] Myeloproliferative Disorders: Disorders in which one or more stimuli cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential. [NIH] Myelosuppression: A condition in which bone marrow activity is decreased, resulting in fewer red blood cells, white blood cells, and platelets. Myelosuppression is a side effect of some cancer treatments. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocarditis: Inflammation of the myocardium; inflammation of the muscular walls of the heart. [EU] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myopia: That error of refraction in which rays of light entering the eye parallel to the optic axis are brought to a focus in front of the retina, as a result of the eyeball being too long from front to back (axial m.) or of an increased strength in refractive power of the media of the eye (index m.). Called also nearsightedness, because the near point is less distant than it is in emmetropia with an equal amplitude of accommodation. [EU] Myristate: Pharmacological activator of protein kinase C. [NIH] Naive: Used to describe an individual who has never taken a certain drug or class of drugs (e. g., AZT-naive, antiretroviral-naive), or to refer to an undifferentiated immune system cell. [NIH] Naphthoquinones: Naphthalene rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups. [NIH] Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout. [NIH] Nasal Cavity: The proximal portion of the respiratory passages on either side of the nasal septum, lined with ciliated mucosa, extending from the nares to the pharynx. [NIH] Natural killer cells: NK cells. A type of white blood cell that contains granules with enzymes that can kill tumor cells or microbial cells. Also called large granular lymphocytes (LGL). [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH]
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Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephropathy: Disease of the kidneys. [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nerve Growth Factor: Nerve growth factor is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neuritis: A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include pain; paresthesias; paresis; or hypesthesia. [NIH] Neuroblastoma: Cancer that arises in immature nerve cells and affects mostly infants and children. [NIH] Neurodegenerative Diseases: Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH] Neurology: A medical specialty concerned with the study of the structures, functions, and diseases of the nervous system. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neurosurgery: A surgical specialty concerned with the treatment of diseases and disorders of the brain, spinal cord, and peripheral and sympathetic nervous system. [NIH] Neurotoxicity: The tendency of some treatments to cause damage to the nervous system. [NIH]
Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins,
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endorphins, and serotonin. [EU] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutrophil: A type of white blood cell. [NIH] Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Node-positive: Cancer that has spread to the lymph nodes. [NIH] Non-small cell lung cancer: A group of lung cancers that includes squamous cell carcinoma, adenocarcinoma, and large cell carcinoma. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclear Matrix: The fibrogranular network of residual structural elements within which are immersed both chromatin and ribonucleoproteins. It extends throughout the nuclear interior from the nucleolus to the nuclear pore complexes along the nuclear periphery. [NIH] Nuclear Pore: An opening through the nuclear envelope formed by the nuclear pore complex which transports nuclear proteins or RNA into or out of the cell nucleus and which, under some conditions, acts as an ion channel. [NIH] Nucleates: Bacteria-inducing ice nucleation at warm temperatures (between zero and minus ten degrees C.). [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleic Acid Probes: Nucleic acid which complements a specific mRNA or DNA molecule, or fragment thereof; used for hybridization studies in order to identify microorganisms and for genetic studies. [NIH] Nucleocapsid: A protein-nucleic acid complex which forms part or all of a virion. It consists of a capsid plus enclosed nucleic acid. Depending on the virus, the nucleocapsid may correspond to a naked core or be surrounded by a membranous envelope. [NIH] Nucleolus: A small dense body (sub organelle) within the nucleus of eukaryotic cells, visible by phase contrast and interference microscopy in live cells throughout interphase. Contains RNA and protein and is the site of synthesis of ribosomal RNA. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nursing Care: Care given to patients by nursing service personnel. [NIH] Nystatin: Macrolide antifungal antibiotic complex produced by Streptomyces noursei, S.
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aureus, and other Streptomyces species. The biologically active components of the complex are nystatin A1, A2, and A3. [NIH] Occupational Exposure: The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation. [NIH] Odour: A volatile emanation that is perceived by the sense of smell. [EU] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH] Omeprazole: A highly effective inhibitor of gastric acid secretion used in the therapy of gastric ulcers and Zollinger-Ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in a pH-dependent manner. This ATPase is considered the proton pump in the secretory membrane of the parietal cell. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Oncology: The study of cancer. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Ophthalmology: A surgical specialty concerned with the structure and function of the eye and the medical and surgical treatment of its defects and diseases. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]
Optic disc: The circular area (disc) where the optic nerve connects to the retina. [NIH] Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Optic Neuritis: Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as multiple sclerosis, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis). [NIH]
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Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] Oral Hygiene: The practice of personal hygiene of the mouth. It includes the maintenance of oral cleanliness, tissue tone, and general preservation of oral health. [NIH] Oral Manifestations: Disorders of the mouth attendant upon non-oral disease or injury. [NIH]
Orbit: One of the two cavities in the skull which contains an eyeball. Each eye is located in a bony socket or orbit. [NIH] Orbital: Pertaining to the orbit (= the bony cavity that contains the eyeball). [EU] Orderly: A male hospital attendant. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteogenic sarcoma: A malignant tumor of the bone. Also called osteosarcoma. [NIH] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Osteosarcoma: A cancer of the bone that affects primarily children and adolescents. Also called osteogenic sarcoma. [NIH] Ototoxic: Having a deleterious effect upon the eighth nerve, or upon the organs of hearing and balance. [EU] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overall survival: The percentage of subjects in a study who have survived for a defined period of time. Usually reported as time since diagnosis or treatment. Often called the survival rate. [NIH] Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH]
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Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] P53 gene: A tumor suppressor gene that normally inhibits the growth of tumors. This gene is altered in many types of cancer. [NIH] Paclitaxel: Antineoplastic agent isolated from the bark of the Pacific yew tree, Taxus brevifolia. Paclitaxel stabilizes microtubules in their polymerized form and thus mimics the action of the proto-oncogene proteins c-mos. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Palsy: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancytopenia: Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets. [NIH] Papilloma: A benign epithelial neoplasm which may arise from the skin, mucous membranes or glandular ducts. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Paranasal Sinuses: Air-filled extensions of the respiratory part of the nasal cavity into the frontal, ethmoid, sphenoid, and maxillary cranial bones. They vary in size and form in different individuals and are lined by the ciliated mucous membranes of the nasal cavity. [NIH]
Paraparesis: Mild to moderate loss of bilateral lower extremity motor function, which may be a manifestation of spinal cord diseases; peripheral nervous system diseases; muscular diseases; intracranial hypertension; parasagittal brain lesions; and other conditions. [NIH] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. [NIH] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Parturition: The act or process of given birth to a child. [EU] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH]
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Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathologist: A doctor who identifies diseases by studying cells and tissues under a microscope. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
PDQ: Physician Data Query. PDQ is an online database developed and maintained by the National Cancer Institute. Designed to make the most current, credible, and accurate cancer information available to health professionals and the public, PDQ contains peer-reviewed summaries on cancer treatment, screening, prevention, genetics, and supportive care; a registry of cancer clinical trials from around the world; and directories of physicians, professionals who provide genetics services, and organizations that provide cancer care. Most of this information is available on the CancerNet Web site, and more specific information about PDQ can be found at http://cancernet.nci.nih.gov/pdq.html. [NIH] Pediatric Dentistry: The practice of dentistry concerned with the dental problems of children, proper maintenance, and treatment. The dental care may include the services provided by dental specialists. [NIH] Pedigree: A record of one's ancestors, offspring, siblings, and their offspring that may be used to determine the pattern of certain genes or disease inheritance within a family. [NIH] Pelvic: Pertaining to the pelvis. [EU] Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Pemphigus: Group of chronic blistering diseases characterized histologically by acantholysis and blister formation within the epidermis. [NIH] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Pentamidine: Antiprotozoal agent effective in trypanosomiasis, leishmaniasis, and some fungal infections; used in treatment of Pneumocystis carinii pneumonia in HIV-infected patients. It may cause diabetes mellitus, central nervous system damage, and other toxic effects. [NIH] Pentostatin: A potent inhibitor of adenosine deaminase. The drug is effective in the treatment of many lymphoproliferative malignancies, particularly hairy-cell leukemia. It is also synergistic with some other antineoplastic agents and has immunosuppressive activity. [NIH]
Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Pepsin A: Formed from pig pepsinogen by cleavage of one peptide bond. The enzyme is a single polypeptide chain and is inhibited by methyl 2-diaazoacetamidohexanoate. It cleaves peptides preferentially at the carbonyl linkages of phenylalanine or leucine and acts as the principal digestive enzyme of gastric juice. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: Ulcer that occurs in those portions of the alimentary tract which come into contact with gastric juice containing pepsin and acid. It occurs when the amount of acid and pepsin is sufficient to overcome the gastric mucosal barrier. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH]
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Peptide Elongation Factors: Protein factors uniquely required during the elongation phase of protein synthesis. [NIH] Perennial: Lasting through the year of for several years. [EU] Pericarditis: Inflammation of the pericardium. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Nervous System Diseases: Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves. [NIH] Peripheral stem cell transplantation: A method of replacing blood-forming cells destroyed by cancer treatment. Immature blood cells (stem cells) in the circulating blood that are similar to those in the bone marrow are given after treatment to help the bone marrow recover and continue producing healthy blood cells. Transplantation may be autologous (an individual's own blood cells saved earlier), allogeneic (blood cells donated by someone else), or syngeneic (blood cells donated by an identical twin). Also called peripheral stem cell support. [NIH] Peripheral stem cells: Immature cells found circulating in the bloodstream. New blood cells develop from peripheral stem cells. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phallic: Pertaining to the phallus, or penis. [EU] Pharmacodynamics: The study of the biochemical and physiological effects of drugs and the mechanisms of their actions, including the correlation of actions and effects of drugs with their chemical structure; also, such effects on the actions of a particular drug or drugs. [EU] Pharmacogenetics: A branch of genetics which deals with the genetic components of variability in individual responses to and metabolism (biotransformation) of drugs. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenyl: Ingredient used in cold and flu remedies. [NIH]
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Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phenylbutyrate: An anticancer drug that belongs to the family of drugs called differentiating agents. [NIH] Phorbol: Class of chemicals that promotes the development of tumors. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylates: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Photoreceptors: Cells specialized to detect and transduce light. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Phytotoxin: A substance which is toxic for plants. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pigments: Any normal or abnormal coloring matter in plants, animals, or micro-organisms. [NIH]
Pilot Projects: Small-scale tests of methods and procedures to be used on a larger scale if the pilot study demonstrates that these methods and procedures can work. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pineal gland: A tiny organ located in the cerebrum that produces melatonin. Also called pineal body or pineal organ. [NIH] Piroxicam: 4-Hydroxy-2-methyl-N-2-pyridyl-2H-1,2-benzothiazine-3-carboxamide 1,1dioxide. A non-steroidal anti-inflammatory agent that is well established in the treatment of rheumatoid arthritis and osteoarthritis. Its usefulness has also been demonstrated in the treatment of musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily. The drug has also been shown to be effective if administered rectally. Gastrointestinal complaints are the most frequently reported side effects. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth
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day of gestation when the blastocyst adheres to the decidua. [NIH] Plana: The radiographic term applied to a vertebral body crushed to a thin plate. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plastids: Self-replicating cytoplasmic organelles of plant and algal cells that contain pigments and may synthesize and accumulate various substances. Plastids are used in phylogenetic studies. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Count: A count of the number of platelets per unit volume in a sample of venous blood. [NIH] Platelet Transfusion: The transfer of blood platelets from a donor to a recipient or reinfusion to the donor. [NIH] Platelet-Derived Growth Factor: Mitogenic peptide growth hormone carried in the alphagranules of platelets. It is released when platelets adhere to traumatized tissues. Connective tissue cells near the traumatized region respond by initiating the process of replication. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Pleura: The thin serous membrane enveloping the lungs and lining the thoracic cavity. [NIH] Pneumonia: Inflammation of the lungs. [NIH]
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Podophyllotoxin: The main active constituent of the resin from the roots of may apple or mandrake (Podophyllum peltatum and P. emodi). It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives. [NIH] Point Mutation: A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair. [NIH] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polyneuritis: Inflammation of several peripheral nerves at the same time. [NIH] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Population Density: Number of individuals in a population relative to space. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postoperative: After surgery. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potentiate: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiating: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis,
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therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Preleukemia: Conditions in which the abnormalities in the peripheral blood or bone marrow represent the early manifestations of acute leukemia, but in which the changes are not of sufficient magnitude or specificity to permit a diagnosis of acute leukemia by the usual clinical criteria. [NIH] Premalignant: A term used to describe a condition that may (or is likely to) become cancer. Also called precancerous. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Presumptive: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Prickle: Several layers of the epidermis where the individual cells are connected by cell bridges. [NIH] Primary tumor: The original tumor. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or
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severity. [EU] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Prokaryotic Cells: Cells, such as those of bacteria and the blue green algae, which lack a nuclear membrane so that the nuclear material is either scattered in the cytoplasm or collected in a nucleoid region. [NIH] Prolactin: Pituitary lactogenic hormone. A polypeptide hormone with a molecular weight of about 23,000. It is essential in the induction of lactation in mammals at parturition and is synergistic with estrogen. The hormone also brings about the release of progesterone from lutein cells, which renders the uterine mucosa suited for the embedding of the ovum should fertilization occur. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promotor: In an operon, a nucleotide sequence located at the operator end which contains all the signals for the correct initiation of genetic transcription by the RNA polymerase holoenzyme and determines the maximal rate of RNA synthesis. [NIH] Promyelocytic leukemia: A type of acute myeloid leukemia, a quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. [NIH]
Prone: Having the front portion of the body downwards. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19-
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hydroxy derivatives are found in many organs and tissues. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein Isoforms: Different forms of a protein that may be produced from different genes, or from the same gene by alternative splicing. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycan: A molecule that contains both protein and glycosaminoglycans, which are a type of polysaccharide. Proteoglycans are found in cartilage and other connective tissues. [NIH]
Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Proton Pump: Integral membrane proteins that transport protons across a membrane against a concentration gradient. This transport is driven by hydrolysis of ATP by H(+)transporting ATP synthase. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity. [NIH] Proto-Oncogene Proteins c-mos: Cellular proteins encoded by the c-mos genes. They function in the cell cycle to maintain maturation promoting factor in the active state and have protein-serine/threonine kinase activity. Oncogenic transformation can take place when c-mos proteins are expressed at the wrong time. [NIH] Proto-Oncogenes: Normal cellular genes homologous to viral oncogenes. The products of proto-oncogenes are important regulators of biological processes and appear to be involved
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in the events that serve to maintain the ordered procession through the cell cycle. Protooncogenes have names of the form c-onc. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Provirus: Virus that is integrated into the chromosome of a host cell and is transmitted in that form from one host cell generation to another without leading to the lysis of the host cells. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Pruritic: Pertaining to or characterized by pruritus. [EU] Pseudotumor Cerebri: A condition marked by raised intracranial pressure and characterized clinically by headaches; nausea; papilledema, peripheral constriction of the visual fields, transient visual obscurations, and pulsatile tinnitus. Obesity is frequently associated with this condition, which primarily affects women between 20 and 44 years of age. Chronic papilledema may lead to optic nerve injury (optic nerve diseases) and visual loss (blindness). [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Pteroylpolyglutamic Acids: Derivatives of folic acid (pteroylglutamic acid). In gammaglutamyl linkage they are found in many tissues. They are converted to folic acid by the action of pteroylpolyglutamate hydrolase or synthesized from folic acid by the action of folate polyglutamate synthetase. Synthetic pteroylpolyglutamic acids, which are in alphaglutamyl linkage, are active in bacterial growth assays. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Pulmonary: Relating to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulmonary Fibrosis: Chronic inflammation and progressive fibrosis of the pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from oxygen lack or right heart failure. [NIH]
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Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purifying: Respiratory equipment whose function is to remove contaminants from otherwise wholesome air. [NIH] Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pyoderma: Any purulent skin disease (Dorland, 27th ed). [NIH] Pyoderma Gangrenosum: An idiopathic, rapidly evolving, and severely debilitating disease occurring most commonly in association with chronic ulcerative colitis. It is characterized by the presence of boggy, purplish ulcers with undermined borders, appearing mostly on the legs. The majority of cases are in people between 40 and 60 years old. Its etiology is unknown. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quaternary: 1. Fourth in order. 2. Containing four elements or groups. [EU] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Racemic: Optically inactive but resolvable in the way of all racemic compounds. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation Oncology: A subspecialty of medical oncology and radiology concerned with the radiotherapy of cancer. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radioimmunotherapy: Radiotherapy where cytotoxic radionuclides are linked to antibodies in order to deliver toxins directly to tumor targets. Therapy with targeted radiation rather than antibody-targeted toxins (immunotoxins) has the advantage that adjacent tumor cells, which lack the appropriate antigenic determinants, can be destroyed by radiation cross-fire. Radioimmunotherapy is sometimes called targeted radiotherapy, but this latter term can also refer to radionuclides linked to non-immune molecules (radiotherapy). [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign
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conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Ras gene: A gene that has been found to cause cancer when it is altered (mutated). Agents that block its activity may stop the growth of cancer. A ras peptide is a protein fragment produced by the ras gene. [NIH] Reactivation: The restoration of activity to something that has been inactivated. [EU] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombinant Proteins: Proteins prepared by recombinant DNA technology. [NIH] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Reconstitution: 1. A type of regeneration in which a new organ forms by the rearrangement of tissues rather than from new formation at an injured surface. 2. The restoration to original form of a substance previously altered for preservation and storage, as the restoration to a liquid state of blood serum or plasma that has been dried and stored. [EU] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflex: An involuntary movement or exercise of function in a part, excited in response to a
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stimulus applied to the periphery and transmitted to the brain or spinal cord. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [NIH]
Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Remission Induction: Therapeutic act or process that initiates a response to a complete or partial remission level. [NIH] Remission induction therapy: The initial chemotherapy a person receives to bring about a remission. [NIH] Renal tubular: A defect in the kidneys that hinders their normal excretion of acids. Failure to excrete acids can lead to weak bones, kidney stones, and poor growth in children. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes, which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] Repressor Proteins: Proteins which are normally bound to the operator locus of an operon, thereby preventing transcription of the structural genes. In enzyme induction, the substrate of the inducible enzyme binds to the repressor protein, causing its release from the operator and freeing the structural genes for transcription. In enzyme repression, the end product of the enzyme sequence binds to the free repressor protein, the resulting complex then binds to the operator and prevents transcription of the structural genes. [NIH] Reproductive cells: Egg and sperm cells. Each mature reproductive cell carries a single set of 23 chromosomes. [NIH] Reproductive History: An important aggregate factor in epidemiological studies of women's health. The concept usually includes the number and timing of pregnancies and their outcomes, the incidence of breast feeding, and may include age of menarche and menopause, regularity of menstruation, fertility, gynecological or obstetric problems, or contraceptive usage. [NIH] Research Support: Financial support of research activities. [NIH] Resection: Removal of tissue or part or all of an organ by surgery. [NIH] Residual disease: Cancer cells that remain after attempts have been made to remove the cancer. [NIH] Resolving: The ability of the eye or of a lens to make small objects that are close together, separately visible; thus revealing the structure of an object. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary,
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4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory Burst: A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (granulomatous disease, chronic) often die as a result of recurrent bacterial infections. [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [NIH] Response Elements: Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promotor and enhancer regions. [NIH]
Restitution: The restoration to a normal state. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinal Detachment: Separation of the inner layers of the retina (neural retina) from the pigment epithelium. Retinal detachment occurs more commonly in men than in women, in eyes with degenerative myopia, in aging and in aphakia. It may occur after an uncomplicated cataract extraction, but it is seen more often if vitreous humor has been lost during surgery. (Dorland, 27th ed; Newell, Ophthalmology: Principles and Concepts, 7th ed, p310-12). [NIH] Retinal Ganglion Cells: Cells of the innermost nuclear layer of the retina, the ganglion cell layer, which project axons through the optic nerve to the brain. They are quite variable in size and in the shapes of their dendritic arbors, which are generally confined to the inner plexiform layer. [NIH] Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retinoid: Vitamin A or a vitamin A-like compound. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retrobulbar: Behind the pons. [EU] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH]
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Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Reverse Transcriptase Inhibitors: Inhibitors of reverse transcriptase (RNA-directed DNA polymerase), an enzyme that synthesizes DNA on an RNA template. [NIH] Reversion: A return to the original condition, e. g. the reappearance of the normal or wild type in previously mutated cells, tissues, or organisms. [NIH] Rhabdomyosarcoma: A malignant tumor of muscle tissue. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Ribonuclease: RNA-digesting enzyme. [NIH] Ribonucleoproteins: Proteins conjugated with ribonucleic acids (RNA) or specific RNA. Many viruses are ribonucleoproteins. [NIH] Ribonucleoside Diphosphate Reductase: An enzyme of the oxidoreductase class that catalyzes the formation of 2'-deoxyribonucleotides from the corresponding ribonucleotides using NADPH as the ultimate electron donor. The deoxyribonucleoside diphosphates are used in DNA synthesis. (From Dorland, 27th ed) EC 1.17.4.1. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Ribosomal Proteins: Proteins found in ribosomes. They are believed to have a catalytic function in reconstituting biologically active ribosomal subunits. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Ricin: A protein phytotoxin from the seeds of Ricinus communis, the castor oil plant. It agglutinates cells, is proteolytic, and causes lethal inflammation and hemorrhage if taken internally. [NIH] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rituximab: A type of monoclonal antibody used in cancer detection or therapy. Monoclonal antibodies are laboratory-produced substances that can locate and bind to cancer cells. [NIH] RNA: Ribonucleic acid. One of the two types of nucleic acids found in cells. The other is DNA (deoxyribonucleic acid). RNA plays a role in sending information from DNA to the protein-forming system of the cell. [NIH] Rodenticides: Substances used to destroy or inhibit the action of rats, mice, or other rodents.
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[NIH]
Roentgenography: Production of an image of an object on film, or other kind of sensitized plate, usually by means of X-radiation or gamma radiation, the contrast between different areas of the image being the result of differential interaction of the radiation in the object. [NIH]
Rosiglitazone: A drug taken to help reduce the amount of sugar in the blood. Rosiglitazone helps make insulin more effective and improves regulation of blood sugar. It belongs to the family of drugs called thiazolidinediones. [NIH] Salicylate: Non-steroidal anti-inflammatory drugs. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saphenous: Applied to certain structures in the leg, e. g. nerve vein. [NIH] Saphenous Vein: The vein which drains the foot and leg. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Sargramostim: A colony-stimulating factor that stimulates the production of blood cells, especially platelets, during chemotherapy. It is a cytokine that belongs to the family of drugs called hematopoietic (blood-forming) agents. Also called GM-CSF. [NIH] Scatter: The extent to which relative success and failure are divergently manifested in qualitatively different tests. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Secondary tumor: Cancer that has spread from the organ in which it first appeared to
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another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedimentation: The act of causing the deposit of sediment, especially by the use of a centrifugal machine. [EU] Segmental: Describing or pertaining to a structure which is repeated in similar form in successive segments of an organism, or which is undergoing segmentation. [NIH] Segmentation: The process by which muscles in the intestines move food and wastes through the body. [NIH] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senescence: The bodily and mental state associated with advancing age. [NIH] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensory loss: A disease of the nerves whereby the myelin or insulating sheath of myelin on the nerves does not stay intact and the messages from the brain to the muscles through the nerves are not carried properly. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serrata: The serrated anterior border of the retina located approximately 8.5 mm from the limbus and adjacent to the pars plana of the ciliary body. [NIH] Serrated: Having notches or teeth on the edge as a saw has. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Sickness: Immune complex disease caused by the administration of foreign serum or serum proteins and characterized by fever, lymphadenopathy, arthralgia, and urticaria. When they are complexed to protein carriers, some drugs can also cause serum sickness
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when they act as haptens inducing antibody responses. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Shiga Toxin: A toxin produced by Shigella dysenteriae. It is the protype of class of toxins that inhibit protein synthesis by blocking the interaction of ribosomal RNA with peptide elongation factors. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to immunophilins. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Small cell lung cancer: A type of lung cancer in which the cells appear small and round when viewed under the microscope. Also called oat cell lung cancer. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH]
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Smoldering leukemia: Disease in which the bone marrow does not function normally. Also called preleukemia or myelodysplastic syndrome. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Work: The use of community resources, individual case work, or group work to promote the adaptive capacities of individuals in relation to their social and economic environments. It includes social service agencies. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium salicylate: A drug that belongs to the family of drugs called nonsteroidal antiinflammatory drugs. Sodium salicylate may be tolerated by people who are sensitive to aspirin. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Soft tissue sarcoma: A sarcoma that begins in the muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatic cells: All the body cells except the reproductive (germ) cells. [NIH] Spastic: 1. Of the nature of or characterized by spasms. 2. Hypertonic, so that the muscles are stiff and the movements awkward. 3. A person exhibiting spasticity, such as occurs in spastic paralysis or in cerebral palsy. [EU] Spasticity: A state of hypertonicity, or increase over the normal tone of a muscle, with heightened deep tendon reflexes. [EU] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by
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refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Speech Disorders: Acquired or developmental conditions marked by an impaired ability to comprehend or generate spoken forms of language. [NIH] Speech pathologist: A specialist who evaluates and treats people with communication and swallowing problems. Also called a speech therapist. [NIH] Sperm: The fecundating fluid of the male. [NIH] Sphenoid: An unpaired cranial bone with a body containing the sphenoid sinus and forming the posterior part of the medial walls of the orbits. [NIH] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] Spina bifida: A defect in development of the vertebral column in which there is a central deficiency of the vertebral lamina. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinal Cord Diseases: Pathologic conditions which feature spinal cord damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord. [NIH] Spinal Cord Vascular Diseases: Hypoxic-ischemic and hemorrhagic disorders of the spinal cord. Arteriosclerosis, emboli, and vascular malformations are potential causes of these conditions. [NIH] Spinal Nerves: The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [NIH] Spinal tap: A procedure in which a needle is put into the lower part of the spinal column to collect cerebrospinal fluid or to give anticancer drugs intrathecally. Also called a lumbar puncture. [NIH] Spinous: Like a spine or thorn in shape; having spines. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Splenomegaly: Enlargement of the spleen. [NIH] Spondylitis: Inflammation of the vertebrae. [EU] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Spores: The reproductive elements of lower organisms, such as protozoa, fungi, and cryptogamic plants. [NIH] Squamous: Scaly, or platelike. [EU] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells
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resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Stabilization: The creation of a stable state. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Standard therapy: A currently accepted and widely used treatment for a certain type of cancer, based on the results of past research. [NIH] Stasis: A word termination indicating the maintenance of (or maintaining) a constant level; preventing increase or multiplication. [EU] Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be expected to happen by chance alone. [NIH] Staurosporine: A drug that belongs to the family of drugs called alkaloids. It is being studied in the treatment of cancer. [NIH] Stem Cell Factor: Hematopoietic growth factor and the ligand of the c-kit receptor CD117 (proto-oncogene protein C-kit). It is expressed during embryogenesis and provides a key signal in multiple aspects of mast-cell differentiation and function. [NIH] Stem cell transplantation: A method of replacing immature blood-forming cells that were destroyed by cancer treatment. The stem cells are given to the person after treatment to help the bone marrow recover and continue producing healthy blood cells. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Stereotactic: Radiotherapy that treats brain tumors by using a special frame affixed directly to the patient's cranium. By aiming the X-ray source with respect to the rigid frame, technicians can position the beam extremely precisely during each treatment. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Steroid therapy: Treatment with corticosteroid drugs to reduce swelling, pain, and other symptoms of inflammation. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are
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coiled together. [NIH] Streptococcal: Caused by infection due to any species of streptococcus. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH] Structure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups. Other factors contributing to structure-activity relationship include chemical reactivity, electronic effects, resonance, and inductive effects. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Suction: The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure. [NIH] Sulindac: A sulfinylindene derivative whose sulfinyl moiety is converted in vivo to an active anti-inflammatory analgesic that undergoes enterohepatic circulation to maintain constant blood levels without causing gastrointestinal side effects. [NIH] Sunburn: An injury to the skin causing erythema, tenderness, and sometimes blistering and resulting from excessive exposure to the sun. The reaction is produced by the ultraviolet radiation in sunlight. [NIH] Superinfection: A frequent complication of drug therapy for microbial infection. It may result from opportunistic colonization following immunosuppression by the primary pathogen and can be influenced by the time interval between infections, microbial physiology, or host resistance. Experimental challenge and in vitro models are sometimes
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used in virulence and infectivity studies. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Supportive care: Treatment given to prevent, control, or relieve complications and side effects and to improve the comfort and quality of life of people who have cancer. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Symphysis: A secondary cartilaginous joint. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Syncytium: A living nucleated tissue without apparent cellular structure; a tissue composed of a mass of nucleated protoplasm without cell boundaries. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synthetic retinoid: A substance related to vitamin A that is produced in a laboratory. [NIH] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tachypnea: Rapid breathing. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Telomerase: Essential ribonucleoprotein reverse transcriptase that adds telomeric DNA to
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the ends of eukaryotic chromosomes. Telomerase appears to be repressed in normal human somatic tissues but reactivated in cancer, and thus may be necessary for malignant transformation. EC 2.7.7.-. [NIH] Telomere: A terminal section of a chromosome which has a specialized structure and which is involved in chromosomal replication and stability. Its length is believed to be a few hundred base pairs. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Teratoma: A type of germ cell tumor that may contain several different types of tissue, such as hair, muscle, and bone. Teratomas occur most often in the ovaries in women, the testicles in men, and the tailbone in children. Not all teratomas are malignant. [NIH] Terminator: A DNA sequence sited at the end of a transcriptional unit that signals the end of transcription. [NIH] Testicle: The male gonad where, in adult life, spermatozoa develop; the testis. [NIH] Testicular: Pertaining to a testis. [EU] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalamus: Paired bodies containing mostly gray substance and forming part of the lateral wall of the third ventricle of the brain. The thalamus represents the major portion of the diencephalon and is commonly divided into cellular aggregates known as nuclear groups. [NIH]
Thalidomide: A pharmaceutical agent originally introduced as a non-barbiturate hypnotic, but withdrawn from the market because of its known tetratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of tumor necrosis factor alpha from monocytes, and modulates other cytokine action. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Thiotepa: A very toxic alkylating antineoplastic agent also used as an insect sterilant. It
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causes skin, gastrointestinal, CNS, and bone marrow damage. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), thiotepa may reasonably be anticipated to be a carcinogen (Merck Index, 11th ed). [NIH] Thoracic: Having to do with the chest. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Thorium: Thorium. A radioactive element of the actinide series of metals. It has an atomic symbol Th, atomic number 90, and atomic weight 232.04. It is used as fuel in nuclear reactors to produce fissionable uranium isotopes. Because of its radioopacity, various thorium compounds are used to facilitate visualization in roentgenography. [NIH] Thorium Compounds: Inorganic compounds that contain thorium as an integral part of the molecule. [NIH] Thorium Dioxide: Thorium oxide (ThO2). A radiographic contrast agent that was used in the early 1930s through about 1954. High rates of mortality have been linked to its use and it has been shown to cause liver cancer. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [NIH] Thrombocytopenia: A decrease in the number of blood platelets. [NIH] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombopoietin: A humoral factor that controls blood platelet production through stimulation of megakaryocyte populations. Bone marrow megakaryocytes increase in both size and number in response to exposure to thrombopoietin. [NIH] Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thrush: A disease due to infection with species of fungi of the genus Candida. [NIH] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [NIH] Tiazofurin: An anticancer drug being studied to stop cell growth. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts plasminogen to plasmin. It has fibrin-binding activity and is
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immunologically different from urinary plasminogen activator. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases. EC 3.4.21.68. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tolmetin: An anti-inflammatory antipyretic and analgesic similar in mode of action to indomethacin. It has been proposed as an antirheumatic agent. [NIH] Tome: A zone produced by a number of irregular spaces contained in the outermost layer of denture of the root of a tooth. [NIH] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonicity: The normal state of muscular tension. [NIH] Topical: On the surface of the body. [NIH] Topoisomerase inhibitors: A family of anticancer drugs. The topoisomerase enzymes are responsible for the arrangement and rearrangement of DNA in the cell and for cell growth and replication. Inhibiting these enzymes may kill cancer cells or stop their growth. [NIH] Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA topoisomerase. [NIH] Total-body irradiation: Radiation therapy to the entire body. Usually followed by bone marrow or peripheral stem cell transplantation. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH]
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Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transgenes: Genes that are introduced into an organism using gene transfer techniques. [NIH]
Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocate: The attachment of a fragment of one chromosome to a non-homologous chromosome. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]
Trees: Woody, usually tall, perennial higher plants (Angiosperms, Gymnosperms, and some Pterophyta) having usually a main stem and numerous branches. [NIH] Tretinoin: An important regulator of gene expression, particularly during growth and development and in neoplasms. Retinoic acid derived from maternal vitamin A is essential for normal gene expression during embryonic development and either a deficiency or an excess can be teratogenic. It is also a topical dermatologic agent which is used in the treatment of psoriasis, acne vulgaris, and several other skin diseases. It has also been approved for use in promyelocytic leukemia. [NIH] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Trisomy: The possession of a third chromosome of any one type in an otherwise diploid cell. [NIH]
Troglitazone: A drug used in diabetes treatment that is being studied for its effect on reducing the risk of cancer cell growth in fat tissue. [NIH] Trophoblast: The outer layer of cells of the blastocyst which works its way into the endometrium during ovum implantation and grows rapidly, later combining with mesoderm. [NIH] Troxacitabine: A drug being studied for use as an anticancer agent. [NIH] Trypanosomiasis: Infection with protozoa of the genus Trypanosoma. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tubulin: A microtubule subunit protein found in large quantities in mammalian brain. It has also been isolated from sperm flagella, cilia, and other sources. Structurally, the protein is a dimer with a molecular weight of approximately 120,000 and a sedimentation coefficient of 5.8S. It binds to colchicine, vincristine, and vinblastine. [NIH]
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Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumor suppressor gene: Genes in the body that can suppress or block the development of cancer. [NIH] Tumorigenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH]
Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]
Type 2 diabetes: Usually characterized by a gradual onset with minimal or no symptoms of metabolic disturbance and no requirement for exogenous insulin. The peak age of onset is 50 to 60 years. Obesity and possibly a genetic factor are usually present. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Ultraviolet radiation: Invisible rays that are part of the energy that comes from the sun. UV radiation can damage the skin and cause melanoma and other types of skin cancer. UV radiation that reaches the earth's surface is made up of two types of rays, called UVA and UVB rays. UVB rays are more likely than UVA rays to cause sunburn, but UVA rays pass deeper into the skin. Scientists have long thought that UVB radiation can cause melanoma and other types of skin cancer. They now think that UVA radiation also may add to skin damage that can lead to skin cancer and cause premature aging. For this reason, skin specialists recommend that people use sunscreens that reflect, absorb, or scatter both kinds of UV radiation. [NIH] Unconditioned: An inborn reflex common to all members of a species. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Uranium: A radioactive element of the actinide series of metals. It has an atomic symbol U, atomic number 92, and atomic weight 238.03. U-235 is used as the fissionable fuel in nuclear weapons and as fuel in nuclear power reactors. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
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Uridine Diphosphate: A uracil nucleotide containing a pyrophosphate group esterified to C5 of the sugar moiety. [NIH] Uridine Diphosphate Glucuronic Acid: A nucleoside diphosphate sugar which serves as a source of glucuronic acid for polysaccharide biosynthesis. It may also be epimerized to UDP iduronic acid, which donates iduronic acid to polysaccharides. In animals, UDP glucuronic acid is used for formation of many glucosiduronides with various aglycones. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Plasminogen Activator: A proteolytic enzyme that converts plasminogen to plasmin where the preferential cleavage is between arginine and valine. It was isolated originally from human urine, but is found in most tissues of most vertebrates. EC 3.4.21.73. [NIH]
Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Uvea: The middle coat of the eyeball, consisting of the choroid in the back of the eye and the ciliary body and iris in the front of the eye. [NIH] Uveitis: An inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (the sclera and cornea, and the retina). [EU] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginitis: Inflammation of the vagina characterized by pain and a purulent discharge. [NIH] Varicella: Chicken pox. [EU] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH]
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Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertebral: Of or pertaining to a vertebra. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Villous: Of a surface, covered with villi. [NIH] Vinblastine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. It is a mitotic inhibitor. [NIH] Vinca Alkaloids: A class of alkaloids from the genus of apocyanaceous woody herbs including periwinkles. They are some of the most useful antineoplastic agents. [NIH] Vincristine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. [NIH] Vinorelbine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. [NIH] Vinyl Chloride: A gas that has been used as an aerosol propellant and is the starting material for polyvinyl resins. Toxicity studies have shown various adverse effects, particularly the occurrence of liver neoplasms. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral Hepatitis: Hepatitis caused by a virus. Five different viruses (A, B, C, D, and E) most commonly cause this form of hepatitis. Other rare viruses may also cause hepatitis. [NIH] Virion: The infective system of a virus, composed of the viral genome, a protein core, and a protein coat called a capsid, which may be naked or enclosed in a lipoprotein envelope called the peplos. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Virus Diseases: A general term for diseases produced by viruses. [NIH] Virus Replication: The process of intracellular viral multiplication, consisting of the synthesis of proteins, nucleic acids, and sometimes lipids, and their assembly into a new infectious particle. [NIH] Vitelline Membrane: The plasma membrane of the egg. [NIH] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] Vitreous Humor: The transparent, colorless mass of gel that lies behind the lens and in front of the retina and fills the center of the eyeball. [NIH]
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Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Warts: Benign epidermal proliferations or tumors; some are viral in origin. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Yolk Sac: An embryonic membrane formed from endoderm and mesoderm. In reptiles and birds it incorporates the yolk into the digestive tract for nourishing the embryo. In placental mammals its nutritional function is vestigial; however, it is the source of most of the intestinal mucosa and the site of formation of the germ cells. It is sometimes called the vitelline sac, which should not be confused with the vitelline membrane of the egg. [NIH] Zebrafish: A species of North American fishes of the family Cyprinidae. They are used in embryological studies and to study the effects of certain chemicals on development. [NIH] Zoledronate: A drug that belongs to the family of drugs called bisphosphonates. It is used to prevent bone fractures and reduce bone pain in people who have cancer that has spread to the bone. [NIH] Zoster: A virus infection of the Gasserian ganglion and its nerve branches, characterized by discrete areas of vesiculation of the epithelium of the forehead, the nose, the eyelids, and the cornea together with subepithelial infiltration. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
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515
INDEX 9 9-cis retinoic acid, 379, 419 A Abdomen, 419, 431, 449, 467, 469, 470, 472, 474, 483, 484, 485, 502, 503, 507 Abdominal, 419, 467, 483, 485, 510 Abdominal Pain, 419, 510 Aberrant, 29, 55, 58, 59, 65, 156, 419 Abortion, 419, 436 Acantholysis, 419, 484 Accelerated phase, 127, 324, 419 Acceptor, 315, 419, 482 ACE, 419 Acetylcholine, 419, 436, 479 Acidosis, 99, 419 Acne, 292, 419, 509 Acne Vulgaris, 419, 509 Acquired Immunodeficiency Syndrome, 299, 419 Actin, 214, 420 Acute lymphocytic leukemia, 5, 25, 53, 57, 99, 122, 167, 190, 197, 214, 233, 263, 271, 277, 287, 300, 305, 333, 359, 420 Acute nonlymphocytic leukemia, 306, 420 Acyclovir, 5, 345, 420 Adaptability, 420, 434 Adduct, 176, 420 Adenine, 301, 420 Adenocarcinoma, 106, 311, 313, 420, 480 Adenosine, 11, 420, 484, 486 Adenosine Deaminase, 420, 484 Adenovirus, 72, 100, 142, 244, 420 Adjuvant, 49, 107, 149, 170, 223, 228, 262, 420, 455 Adjuvant Therapy, 149, 420 Adolescence, 41, 344, 420 Adsorption, 299, 420 Adsorptive, 421 Adverse Effect, 301, 302, 343, 421, 500, 512 Aerobic, 47, 421, 475 Aerosol, 421, 512 Afferent, 421, 481 Affinity, 11, 15, 244, 421, 427, 472, 501 Agar, 421, 438, 442, 487 Age of Onset, 337, 421, 431, 510 Ageing, 50, 421 Aggressiveness, 290, 306, 421 Agonist, 289, 292, 421
Airway, 421, 500 Alanine, 301, 421 Algorithms, 421, 429 Alimentary, 421, 484 Alkaline, 322, 419, 421, 422, 423, 432 Alkaline Phosphatase, 322, 422 Alkaloid, 214, 285, 422, 432, 438, 461 Alkylating Agents, 9, 41, 289, 295, 422, 432, 436 Alleles, 64, 96, 422, 470 Allo, 295, 296, 422 Allogeneic bone marrow transplantation, 27, 30, 49, 98, 106, 113, 121, 149, 155, 176, 296, 404, 422 Allograft, 338, 422, 460 Allylamine, 422 Alopecia, 289, 422, 442 Alpha Particles, 422, 493 Alternative medicine, 371, 422 Alternative Splicing, 77, 135, 422, 491 Amikacin, 178, 422 Amine, 308, 422, 460 Amino Acid Motifs, 423, 440 Amino Acid Sequence, 294, 304, 423, 424, 440, 451, 455, 472 Ammonia, 420, 422, 423, 505 Amplification, 104, 183, 188, 195, 207, 298, 423 Amsacrine, 220, 423 Anabolic, 314, 423, 445 Anabolic Steroids, 314, 423 Anaesthesia, 423, 464 Anal, 423, 449, 452 Analgesic, 328, 423, 450, 462, 473, 478, 504, 508 Analog, 11, 161, 234, 285, 302, 336, 368, 420, 423, 453 Analogous, 26, 423, 446, 509 Analytes, 398, 423 Anaphylatoxins, 423, 439 Anaplastic, 213, 423 Anatomical, 105, 423, 427, 436, 464, 498 Anchorage, 93, 423 Anemia, 75, 133, 160, 255, 262, 264, 271, 278, 290, 300, 333, 372, 405, 424, 453, 458, 477 Aneuploidy, 55, 127, 424 Angiogenesis, 285, 313, 424, 473
516 Leukemia
Angioplasty, 292, 424 Animal model, 17, 23, 28, 32, 38, 50, 56, 58, 59, 61, 368, 424 Anions, 424, 467 Annealing, 424, 488 Anorexia, 388, 424 Antecedent, 336, 424 Anterior chamber, 144, 424, 467 Anthracycline, 424, 443, 449, 463 Antiangiogenic, 100, 424 Antibacterial, 231, 424, 434, 437, 502 Antibiotic, 285, 312, 422, 424, 431, 435, 437, 443, 446, 449, 454, 463, 468, 480, 502, 506 Antibody therapy, 153, 155, 251, 254, 260, 268, 424 Anticoagulant, 424, 491 Antidote, 425, 469 Antifungal, 282, 312, 425, 453, 480, 500 Antigen-Antibody Complex, 425, 439 Antigen-presenting cell, 309, 425, 444 Anti-infective, 425, 436 Anti-Inflammatory Agents, 425, 427, 441 Antimetabolite, 420, 425, 428, 453, 475 Antineoplastic Agents, 41, 422, 423, 425, 484, 512 Antioxidant, 87, 210, 425, 454 Antiproliferative, 211, 282, 308, 320, 425 Antipyretic, 425, 473, 478, 508 Antiseptic, 425, 433 Antiserum, 425, 428 Antiviral, 67, 274, 282, 303, 305, 420, 425, 466 Antiviral Agents, 274, 303, 425 Anuria, 302, 425, 468 Anus, 423, 425, 431, 438 Aorta, 7, 425, 441, 512 Aphakia, 426, 496 Aplasia, 51, 160, 426 Aplastic anemia, 51, 63, 426 Apnea, 426 Apoptosis, 6, 8, 9, 10, 11, 21, 22, 23, 31, 48, 50, 53, 61, 68, 69, 70, 75, 82, 83, 86, 91, 96, 102, 104, 106, 108, 109, 116, 118, 119, 123, 128, 135, 137, 138, 145, 160, 168, 178, 180, 188, 189, 190, 193, 194, 195, 196, 197, 200, 201, 208, 209, 211, 212, 215, 219, 223, 225, 228, 230, 245, 288, 289, 292, 295, 302, 319, 320, 324, 325, 326, 328, 331, 336, 426, 433 Appendicitis, 97, 426 Applicability, 45, 426 Approximate, 278, 426
Aqueous, 426, 428, 443, 448, 469 Arachidonic Acid, 426, 490 Arenavirus, 426, 471 Aromatic, 14, 426, 486 Arsenic trioxide, 102, 159, 164, 178, 179, 182, 189, 196, 262, 378, 426 Arterial, 422, 426, 462, 491, 505 Arteries, 425, 426, 430, 441, 475, 478 Arterioles, 426, 430, 432 Artery, 424, 426, 430, 441, 448, 483, 493, 512 Arthralgia, 403, 426, 499 Articular, 426, 482 Asbestos, 426, 472, 474 Aseptic, 426, 471, 482, 503 Asparaginase, 102, 225, 374, 379, 426 Aspartate, 426, 427 Aspergillosis, 148, 235, 427 Aspirate, 4, 427 Aspiration, 427 Aspirin, 301, 369, 427, 501 Assay, 13, 17, 25, 60, 293, 427 Astatine, 334, 427 Astringent, 427, 433 Astrocytes, 427, 459, 466 Astrocytoma, 427, 456 Asymptomatic, 137, 306, 427 Ataxia, 402, 403, 427, 506 Atopic, 292, 294, 310, 427 Atrium, 427, 512 Atrophy, 292, 419, 427, 479 Augmerosen, 378, 427 Aural, 100, 427 Auricular, 148, 427 Autacoids, 427, 464 Autoimmune disease, 279, 283, 294, 299, 300, 310, 312, 316, 337, 428, 477 Autoimmunity, 8, 428 Autologous, 13, 41, 181, 183, 205, 215, 219, 220, 221, 295, 296, 298, 428, 459, 485 Autologous bone marrow transplantation, 41, 296, 428, 459 Autonomic, 419, 428, 477, 485, 505 Autonomic Nervous System, 428, 485, 505 Avidity, 71, 428 Axons, 428, 481, 496 Azacitidine, 249, 428 B Bacteremia, 68, 96, 103, 104, 370, 428 Bacterial Infections, 428, 458, 496 Bacteriophage, 428, 487, 508 Barbiturate, 428, 506
Index 517
Basal Ganglia, 427, 428, 431, 454, 456 Basal Ganglia Diseases, 427, 428 Base, 9, 16, 41, 42, 285, 306, 420, 428, 442, 443, 444, 455, 468, 488, 506 Basement Membrane, 429, 451, 469 Basophil, 429, 460 Benign, 209, 285, 306, 429, 431, 433, 452, 454, 471, 474, 479, 483, 493, 513 Beta-Thromboglobulin, 429, 466 Bifida, 429 Bilateral, 106, 429, 483 Bile, 429, 448, 454, 457, 461, 468, 470, 503 Bile Pigments, 429, 468 Bilirubin, 429, 457, 462 Binding Sites, 288, 429 Bioassay, 60, 429 Biological response modifier, 41, 429, 466 Biological therapy, 250, 429, 458 Biomarkers, 12, 125, 429 Biopsy, 429, 450 Biotechnology, 20, 63, 97, 323, 360, 371, 387, 429 Biotransformation, 430, 485 Bispecific antibodies, 163, 430 Bladder, 147, 159, 292, 430, 440, 464, 477, 491, 510, 511 Blast Crisis, 9, 28, 52, 69, 104, 134, 137, 142, 149, 307, 324, 430 Blast phase, 335, 419, 430, 437 Blastocyst, 310, 430, 440, 487, 509 Blasts, 10, 39, 49, 57, 118, 120, 143, 167, 264, 306, 337, 340, 430 Blister, 430, 484 Blood Cell Count, 337, 398, 430, 458 Blood Coagulation, 430, 432, 507 Blood Glucose, 339, 430, 459, 466 Blood Groups, 430, 457 Blood Platelets, 430, 473, 487, 507 Blood Preservation, 430, 445 Blood pressure, 430, 433, 462, 476, 501 Blot, 12, 430 Body Fluids, 286, 429, 430, 432, 501, 510 Body Mass Index, 430, 482 Bone marrow aspiration, 256, 431 Bone Marrow Cells, 35, 54, 172, 431, 438, 458, 473, 477 Bone marrow metastases, 334, 431 Bone Morphogenetic Proteins, 124, 431 Bowel, 338, 339, 423, 431, 445, 448, 465, 467, 503, 510 Bowel Movement, 431, 445, 503 Brachytherapy, 431, 466, 467, 493, 513
Brain Neoplasms, 14, 431, 506 Brain Stem, 431, 435 Branch, 279, 282, 413, 431, 443, 471, 483, 485, 492, 501, 506 Breakdown, 276, 431, 445, 454, 481 Broad-spectrum, 422, 431, 434 Bronchial, 431, 460 Buccal, 18, 257, 431, 471 Buffers, 312, 431 Burns, 404, 431 Burns, Electric, 431 Busulfan, 41, 250, 269, 360, 374, 404, 432 Bypass, 48, 432 C Cachexia, 274, 432 Calcium, 69, 210, 275, 426, 432, 439, 462, 469, 473, 500 Camptothecin, 192, 199, 226, 285, 432, 467 Candidiasis, 5, 117, 432, 453 Candidosis, 432 Capillary, 126, 236, 432, 433, 512 Capillary Fragility, 236, 432, 433 Capsaicin, 210, 230, 432 Capsid, 81, 432, 480, 512 Capsules, 188, 195, 432, 455 Carbohydrate, 13, 334, 338, 339, 432, 441, 457, 488 Carbon Dioxide, 432, 443, 452, 454, 486, 495, 511 Carboplatin, 252, 263, 432 Carboxy, 79, 139, 432 Carboxy-terminal, 139, 432 Carcinogen, 420, 433, 473, 477, 507 Carcinogenic, 422, 433, 465, 481, 490, 503, 510 Carcinoid, 224, 433 Carcinoma, 8, 121, 136, 212, 223, 235, 292, 311, 325, 433, 480, 502, 503 Cardiac, 422, 433, 448, 449, 454, 463, 478, 503 Cardiorespiratory, 47, 433 Cardiotoxic, 423, 433 Cardiotoxicity, 433, 449 Cardiovascular, 47, 292, 328, 433 Cardiovascular disease, 292, 328, 433 Carotene, 106, 433, 496 Case report, 3, 4, 106, 107, 108, 110, 131, 135, 169, 189, 196, 224, 433 Case series, 217, 433 Caspase, 106, 119, 129, 130, 190, 193, 197, 200, 211, 433 Castor Oil, 433, 497
518 Leukemia
Cataract, 426, 433, 496 Catechin, 208, 433 Catechol, 221, 433 Catheter, 70, 257, 433, 448 Catheterization, 424, 433 Cations, 434, 467 Caudal, 434, 462, 488 Causal, 59, 299, 434, 449, 459 Cause of Death, 314, 434 CDC2, 336, 434 Ceftazidime, 178, 434 Cell Differentiation, 9, 22, 34, 39, 65, 72, 84, 86, 89, 112, 434, 500, 503 Cell Division, 55, 92, 428, 434, 443, 450, 458, 467, 473, 474, 476, 487, 499 Cell Lineage, 304, 434 Cell motility, 434, 460 Cell proliferation, 24, 38, 65, 79, 230, 275, 277, 284, 285, 289, 292, 305, 311, 434, 466, 500 Cell Respiration, 434, 475, 496 Cell Size, 109, 434, 453 Cell Survival, 54, 69, 434, 458 Cellulitis, 96, 126, 434 Cellulose, 434, 454, 487 Centrosome, 55, 434, 476 Cephaloridine, 434, 435 Ceramide, 220, 435 Cerebellar, 427, 435, 494 Cerebellum, 431, 435, 494 Cerebral, 404, 427, 428, 431, 435, 449, 456, 501 Cerebral Cortex, 427, 435 Cerebral hemispheres, 428, 431, 435, 456 Cerebral Palsy, 404, 435, 501 Cerebrospinal, 184, 257, 435, 471, 502 Cerebrospinal fluid, 184, 257, 435, 471, 502 Cerebrovascular, 428, 433, 435, 506 Cerebrum, 435, 486 Cervical, 292, 435 Cervix, 292, 419, 435 Character, 435, 443 Chemokines, 279, 283, 316, 435 Chemoprevention, 16, 435 Chemopreventive, 435, 452 Chemotactic Factors, 435, 439 Chemotherapeutic agent, 50, 320, 435 Chemotherapeutics, 10, 435 Chimera, 332, 436 Chimeric Proteins, 25, 26, 34, 66, 247, 332, 436 Chin, 436, 474
Chlorambucil, 302, 360, 374, 436 Chlorhexidine, 5, 436 Chlorine, 436, 462 Chloroform, 312, 436 Chlorophyll, 436, 454 Cholesterol, 429, 436, 441, 503 Cholinergic, 275, 436 Chondrocytes, 436, 452 Choriocarcinoma, 311, 436, 456, 461, 476 Chromatin, 55, 58, 80, 157, 177, 229, 300, 426, 436, 480 Chromosome Aberrations, 158, 436 Chronic Disease, 432, 436 Chronic granulocytic leukemia, 350, 436, 437 Chronic leukemia, 34, 52, 116, 149, 179, 269, 305, 306, 348, 358, 406, 436, 458 Chronic phase, 24, 28, 102, 156, 165, 228, 307, 324, 335, 404, 419, 437 Ciliary, 437, 499, 511 Ciliary Body, 437, 499, 511 Cirrhosis, 314, 437 CIS, 59, 81, 312, 401, 402, 437, 463, 496 Cisplatin, 62, 153, 190, 193, 197, 200, 203, 212, 228, 437 C-kit receptor, 437, 503 Cladribine, 138, 161, 220, 374, 380, 381, 437 Clavulanic Acid, 178, 437 Cleave, 287, 437 Clinical Medicine, 119, 140, 163, 437, 489 Clinical Protocols, 30, 33, 45, 46, 437 Clinical resistance, 71, 172, 437 Clinical trial, 6, 11, 14, 15, 16, 19, 22, 27, 32, 34, 37, 39, 40, 41, 42, 45, 47, 48, 57, 95, 249, 271, 278, 282, 285, 356, 387, 437, 441, 442, 473, 484, 491, 494 Clone, 6, 9, 12, 25, 36, 38, 133, 139, 163, 275, 281, 310, 437 Cloning, 19, 26, 34, 38, 52, 55, 71, 83, 245, 297, 299, 429, 437, 465 Cluster Analysis, 163, 438 Coagulation, 108, 166, 430, 438 Codon, 145, 438, 455 Coenzyme, 238, 438, 469 Cofactor, 60, 438, 491, 507 Cohort Studies, 438, 449 Colchicine, 438, 509 Colitis, 121, 292, 310, 438 Collagen, 288, 423, 429, 433, 438, 451, 452, 454, 473, 490 Collapse, 431, 438, 500
Index 519
Colon, 26, 48, 106, 223, 234, 276, 282, 292, 295, 296, 313, 314, 368, 438, 439, 465, 469, 510 Colon Polyps, 48, 438 Colony-Stimulating Factors, 288, 326, 331, 438 Colorectal, 32, 313, 439 Colorectal Cancer, 32, 439 Combination chemotherapy, 193, 200, 213, 215, 227, 228, 251, 252, 253, 254, 255, 263, 264, 265, 267, 271, 439 Combination Therapy, 216, 298, 369, 439 Communis, 433, 439, 497 Compassionate, 132, 439 Complement, 35, 284, 423, 439, 455, 468, 472 Complementary and alternative medicine, 205, 240, 439 Complementary medicine, 205, 439 Complementation, 25, 439 Complete remission, 5, 9, 28, 153, 211, 215, 269, 320, 439, 495 Complete response, 440 Compliance, 46, 188, 195, 440 Computational Biology, 387, 440 Conception, 419, 436, 440, 452, 456, 476, 503 Concomitant, 95, 121, 193, 200, 228, 233, 440 Condoms, 363, 440 Cones, 25, 440, 496 Confounding, 23, 440 Conjugated, 380, 381, 440, 442, 497 Connective Tissue, 431, 434, 438, 440, 452, 454, 471, 474, 491, 497, 498, 504, 505 Consciousness, 423, 440, 444, 446, 492 Consensus Sequence, 75, 320, 423, 440 Conserved Sequence, 423, 440 Constitutional, 112, 157, 206, 440 Consumption, 440, 444, 482 Contamination, 440, 459, 460 Continuous infusion, 62, 220, 440 Contraindications, ii, 440 Contralateral, 440, 452, 481, 494 Contrast Sensitivity, 441, 481 Control group, 18, 47, 441 Controlled study, 5, 441 Conventional therapy, 57, 441 Conventional treatment, 441 Cooperative group, 12, 14, 32, 39, 62, 63, 441 Coordination, 43, 46, 403, 435, 441, 477
Cornea, 192, 199, 424, 441, 468, 498, 511, 513 Coronary, 159, 433, 441, 475, 478 Coronary Artery Bypass, 159, 441 Coronary heart disease, 433, 441 Coronary Thrombosis, 441, 475, 478 Cortical, 241, 441, 499, 506 Corticosteroid, 441, 489, 503 Cortisone, 441, 444, 489 Cranial, 435, 442, 450, 467, 479, 481, 483, 485, 502 Crossing-over, 442, 494 Cross-Sectional Studies, 442, 449 Croton Oil, 325, 442 Cryostat, 442, 453 Culture Media, 309, 334, 421, 442 Cultured cells, 55, 442 Curative, 27, 30, 275, 314, 338, 442, 506 Cutaneous, 72, 98, 113, 117, 181, 207, 432, 442, 469, 471 Cyclic, 80, 442, 490 Cyclin, 58, 59, 65, 66, 77, 78, 135, 168, 194, 201, 336, 442 Cyclosporine, 132, 162, 442, 463 Cyst, 427, 442 Cytarabine, 130, 132, 147, 162, 165, 216, 217, 220, 222, 224, 228, 232, 255, 267, 270, 375, 442 Cytidine, 428, 442 Cytochrome, 12, 442, 443, 496 Cytochrome b, 443, 496 Cytogenetic Analysis, 33, 143, 318, 443 Cytokine, 33, 61, 120, 245, 279, 284, 299, 318, 328, 335, 443, 452, 466, 498, 500, 506 Cytomegalovirus, 79, 117, 443 Cytopenia, 103, 135, 443 Cytoplasm, 48, 65, 293, 295, 299, 336, 426, 443, 449, 490, 497 Cytosine, 120, 153, 210, 232, 329, 442, 443 Cytoskeleton, 244, 443, 475 Cytotoxicity, 6, 21, 64, 145, 153, 180, 189, 194, 196, 211, 212, 224, 225, 422, 437, 443, 468 D Data Collection, 47, 443 Daunorubicin, 162, 216, 224, 255, 375, 443, 446 De novo, 88, 113, 114, 166, 209, 233, 264, 307, 315, 443 Decarboxylation, 443, 460 Decidua, 443, 487 Decitabine, 22, 169, 255, 256, 443
520 Leukemia
Degenerative, 280, 443, 459, 482, 496 Deletion, 31, 33, 52, 57, 71, 78, 92, 114, 151, 316, 426, 443, 470 Dementia, 420, 443 Denaturation, 444, 488 Dendrites, 444, 479 Dendritic, 21, 69, 101, 114, 133, 143, 167, 177, 183, 444, 473, 496 Dendritic cell, 21, 69, 101, 114, 133, 143, 167, 177, 183, 444 Density, 56, 430, 444, 453, 481 Dental Care, 444, 484 Dentists, 4, 371, 444 Deoxycytidine, 169, 379, 380, 444 Deoxyribonucleic, 444, 497 Deoxyribonucleic acid, 444, 497 Depolarization, 444, 500 Depsipeptide, 21, 444 Dermatitis, 154, 292, 294, 310, 444, 447 Dermatosis, 205, 444 Detoxification, 444, 457 Deuterium, 444, 461 Developed Countries, 339, 444 Developing Countries, 314, 444 Dexamethasone, 191, 198, 206, 213, 216, 221, 232, 444 Diabetes Mellitus, 339, 444, 456, 459, 484 Diagnostic procedure, 269, 273, 371, 444 Diastolic, 444, 462 Digestion, 421, 429, 431, 445, 467, 470, 484, 503, 511 Digestive system, 272, 445, 477 Digestive tract, 445, 500, 502, 503, 513 Dihydrotestosterone, 445, 494 Dihydroxyacetone, 276, 445 Dihydroxyacetone Phosphate, 276, 445 Dilatation, 419, 424, 445, 489 Dilution, 49, 445 Dimerization, 32, 34, 82, 445 Dimethyl, 312, 445 Dimethyl Sulfoxide, 312, 445 Diphtheria, 51, 445 Diphtheria Toxin, 51, 445 Diploid, 424, 439, 445, 476, 487, 509 Direct, iii, 11, 20, 24, 50, 54, 286, 320, 338, 373, 407, 437, 445, 470, 494 Discrete, 445, 513 Discrimination, 363, 445 Disease Progression, 61, 86, 209, 445 Disease-Free Survival, 10, 40, 41, 221, 296, 445 Disparity, 338, 368, 445
Disposition, 102, 192, 199, 446 Dissection, 60, 446 Dissociation, 421, 446, 467 Distal, 85, 301, 441, 446, 492 Dorsal, 446, 488, 502 Dose-dependent, 7, 446 Dosimetry, 280, 446 Doxorubicin, 12, 214, 220, 375, 446, 449 Drive, ii, vi, 4, 7, 9, 35, 187, 334, 343, 350, 361, 446 Drug Combinations, 219, 446 Drug Design, 308, 377, 446 Drug Interactions, 377, 446 Drug Resistance, 10, 29, 45, 60, 116, 127, 210, 231, 242, 338, 350, 446 Drug Tolerance, 446, 508 Duodenum, 429, 447, 503 Dyes, 447, 453 Dynein, 55, 447 Dysmenorrhea, 301, 447, 478, 486 Dysplasia, 94, 119, 120, 153, 172, 447 Dyspnea, 447, 492 E Ectopic, 25, 447 Eczema, 292, 447 Edema, 181, 447, 467, 477 Effector, 21, 29, 419, 439, 447, 448, 468 Effector cell, 21, 447, 468 Efficacy, 10, 11, 12, 21, 26, 30, 45, 74, 112, 120, 289, 446, 447, 509 Effusion, 447, 471 Elastin, 438, 447, 451 Elective, 172, 447 Electrocoagulation, 438, 447 Electrolyte, 380, 441, 447, 468, 501 Electroplating, 433, 447 Emaciation, 420, 447 Embryo, 7, 24, 84, 419, 430, 434, 447, 448, 455, 464, 474, 477, 513 Embryogenesis, 447, 503 Emetic, 442, 447 Empirical, 178, 447 Emulsion, 447, 452 Encapsulated, 448, 470 Endarterectomy, 424, 448 Endemic, 448, 502 Endocarditis, 74, 432, 448 Endoderm, 448, 513 Endogenous, 8, 29, 293, 308, 447, 448, 457, 508 Endothelial cell, 284, 448, 452, 466, 507 Endotoxic, 448, 470
Index 521
Endotoxin, 448, 510 Enhancer, 39, 62, 67, 68, 72, 90, 92, 448, 496 Enterocolitis, 125, 448 Enterohepatic, 448, 504 Enterohepatic Circulation, 448, 504 Environmental Exposure, 14, 18, 314, 448, 481 Environmental Health, 13, 259, 386, 388, 448 Enzymatic, 21, 287, 423, 432, 433, 439, 448, 460, 488, 496 Enzyme Induction, 448, 495 Enzyme Repression, 448, 495 Eosinophil, 448, 458, 466 Eosinophilia, 110, 449 Eosinophilic, 121, 208, 448, 449 Epidemic, 449, 502 Epidemiologic Studies, 107, 245, 449 Epidemiological, 449, 495 Epidermal, 449, 468, 473, 513 Epidermis, 419, 430, 449, 468, 484, 489, 493 Epidural, 150, 449 Epigastric, 449, 483 Epinephrine, 449, 479, 510 Epirubicin, 170, 449 Epithelial, 87, 142, 149, 242, 288, 420, 437, 443, 449, 460, 466, 469, 483 Epithelial Cells, 87, 142, 242, 449, 460, 466, 469 Epithelium, 429, 436, 449, 454, 467, 496, 513 Epitope, 49, 78, 449 Erythema, 449, 504, 511 Erythrocyte Indices, 430, 449 Erythrocyte Membrane, 449, 457 Erythrocytes, 307, 424, 430, 431, 445, 450, 459, 483, 494 Erythroid Progenitor Cells, 450, 478 Erythroleukemia, 70, 72, 76, 78, 81, 82, 83, 84, 85, 91, 146, 189, 196, 244, 264, 265, 266, 267, 450 Erythropoietin, 122, 289, 307, 450 Esophagus, 292, 445, 450, 503 Estrogen, 369, 450, 490 Estrogen receptor, 369, 450 Ethanol, 450, 452 Ether, 312, 450 Ethmoid, 450, 483 Ethylmaleimide, 192, 199, 222, 450 Etodolac, 290, 301, 450 Eukaryotic Cells, 307, 434, 450, 464, 480, 482
Evaluable patients, 43, 450 Exatecan mesylate, 192, 199, 226, 450 Excisional, 5, 450 Excisional biopsy, 5, 450 Excitation, 451, 453, 479 Excrete, 425, 451, 468, 495 Exocrine, 451, 483 Exocytosis, 451, 460 Exogenous, 287, 310, 339, 421, 430, 447, 448, 451, 455, 457, 510 Exon, 14, 32, 321, 336, 422, 451 Expiration, 451, 495 Extensor, 451, 492 External-beam radiation, 451, 467, 493, 513 Extracellular, 93, 113, 297, 427, 440, 451, 452, 473, 501 Extracellular Matrix, 297, 440, 451, 452, 473 Extracellular Matrix Proteins, 451, 473 Extracellular Space, 451 Extraction, 3, 426, 451, 496 Extremity, 451, 483 Eye Infections, 420, 451 F Facial, 121, 451, 483 Family Planning, 387, 451 Fat, 83, 426, 431, 433, 435, 441, 451, 470, 477, 482, 497, 501, 509 Fatigue, 388, 403, 416, 451, 458 Fatty acids, 451, 490 Femoral, 403, 452 Femur, 452 Fenretinide, 154, 452 Fermentation, 334, 452 Ferritin, 95, 452 Fetus, 419, 450, 452, 486, 489, 511 Fibrin, 430, 452, 487, 507 Fibroblast Growth Factor, 219, 452 Fibroblasts, 108, 279, 284, 452, 466 Fibrosarcoma, 311, 452 Fibrosis, 121, 122, 310, 422, 452, 492, 498 Filgrastim, 250, 251, 252, 253, 261, 266, 380, 452 Filtration, 302, 452, 468 Finasteride, 15, 452 Fixation, 293, 452 Flaccid, 229, 453 Flavopiridol, 194, 201, 266, 453 Flow Cytometry, 33, 45, 217, 453, 463 Fluconazole, 81, 113, 453
522 Leukemia
Fludarabine, 128, 132, 216, 252, 257, 258, 266, 269, 295, 301, 302, 375, 380, 453 Fluorescence, 20, 29, 49, 52, 98, 128, 129, 155, 176, 193, 200, 214, 222, 247, 318, 453 Fluorescent Dyes, 453 Fluorouracil, 223, 238, 311, 453 Folate, 148, 167, 242, 244, 453, 492 Fold, 14, 49, 60, 315, 453, 474 Folic Acid, 203, 453, 469, 492 Follicles, 453 Fossa, 344, 435, 453 Fovea, 452, 453 Fractionation, 298, 325, 453 Free Radicals, 425, 446, 453 Frozen Sections, 98, 453 Fungemia, 107, 169, 454 Fungi, 425, 427, 451, 454, 475, 477, 502, 507, 513 Fungus, 286, 432, 454, 477 G Gait, 47, 454 Gallate, 208, 454 Gallbladder, 419, 445, 454 Gamma Rays, 454, 477, 493, 494 Gamma-Glutamyl Hydrolase, 192, 199, 454 Ganglia, 419, 428, 454, 479, 485, 505 Ganglion, 454, 496, 513 Gas, 423, 432, 436, 454, 461, 477, 480, 496, 504, 511, 512 Gas exchange, 454, 496, 511 Gastric, 121, 131, 449, 454, 460, 481, 484 Gastric Juices, 454, 484 Gastric Mucosa, 454, 484 Gastrin, 454, 461 Gastrointestinal, 16, 282, 286, 289, 426, 433, 449, 450, 454, 486, 504, 507, 510 Gastrointestinal tract, 289, 450, 454, 510 Gelatin, 442, 454, 457 Gemcitabine, 60, 193, 200, 206, 226, 228, 270, 455 Gene Fusion, 66, 68, 455 Gene Rearrangement, 29, 110, 152, 307, 455 Gene Targeting, 76, 455 Gene Therapy, 21, 82, 100, 108, 126, 171, 192, 199, 229, 242, 297, 315, 368, 401, 420, 455 Gene-modified, 108, 455 Genetic Code, 455, 480 Genetic Engineering, 429, 437, 455 Genetic testing, 269, 455, 488
Genital, 116, 292, 455, 511 Genotype, 12, 14, 23, 37, 68, 455, 485 Germ Cells, 59, 322, 455, 473, 482, 501, 506, 513 Germ Layers, 323, 448, 455 Germline mutation, 54, 455, 460 Gestation, 455, 487 Gestational, 194, 201, 233, 456, 476 Gestational trophoblastic disease, 194, 201, 233, 456, 476 Gestational trophoblastic neoplasia, 456, 476 Gestational trophoblastic tumor, 456, 476 Giant Cells, 456, 498 Gingival Hyperplasia, 4, 456 Ginseng, 238, 239, 240, 456 Gland, 372, 441, 456, 460, 462, 471, 483, 486, 491, 499, 503, 507 Glioblastoma, 147, 276, 296, 456 Glomerular, 302, 456, 468 Glomerulus, 456 Glucocorticoid, 135, 168, 218, 292, 351, 444, 456, 489 Glucose, 213, 276, 430, 434, 444, 456, 457, 459, 465, 498 Glucose Intolerance, 444, 456 Glucuronic Acid, 456, 457, 511 Glucuronides, 193, 200, 227, 456, 457 Glutamate, 148, 457 Glutamic Acid, 453, 454, 457, 479, 490 Glycine, 423, 457, 479, 499 Glycolysis, 276, 445, 457 Glycophorin, 275, 457 Glycoprotein, 95, 130, 139, 220, 304, 313, 450, 456, 457, 458, 469, 472, 507, 510 Glycosaminoglycans, 451, 457, 491 Glycosidic, 457 Gonad, 7, 457, 506 Gonadal, 457, 503 Gonadotropin, 436, 457 Gout, 236, 438, 457, 478 Governing Board, 457, 489 Grade, 5, 146, 457 Graft Rejection, 296, 457, 464, 475 Grafting, 159, 441, 457 Graft-versus-host disease, 33, 155, 300, 458 Gram-negative, 434, 448, 458 Granule, 49, 245, 458, 497 Granulocyte-Macrophage ColonyStimulating Factor, 289, 307, 438, 458 Granulomatous Disease, Chronic, 458, 496
Index 523
Growth factors, 8, 288, 295, 458 Guanine, 78, 458 Guinea Pigs, 458, 471 H Hair follicles, 289, 458 Hairy cell leukemia, 102, 115, 135, 148, 291, 305, 365, 406, 458 Half-Life, 13, 312, 427, 458, 486 Haploid, 458, 487 Haptens, 421, 458, 500 Heart attack, 328, 433, 458 Heart failure, 458, 492 Helix-loop-helix, 34, 458 Hematocrit, 430, 449, 458 Hematologic malignancies, 27, 36, 56, 63, 179, 295, 296, 459 Hematopoietic growth factors, 47, 136, 289, 459 Hematopoietic Stem Cell Transplantation, 123, 218, 459 Hematopoietic Stem Cells, 7, 53, 156, 178, 248, 289, 295, 296, 297, 298, 326, 331, 459, 478 Hematopoietic tissue, 30, 431, 459 Hematuria, 147, 459 Heme, 95, 212, 429, 442, 443, 459, 483 Hemodialysis, 459, 468 Hemoglobin, 125, 300, 424, 430, 449, 450, 459 Hemoglobinopathies, 455, 459 Hemoglobinuria, 51, 459 Hemolysis, 51, 450, 459 Hemophilia, 344, 372, 459 Hemorrhage, 447, 459, 493, 497, 504 Heparan Sulfate Proteoglycan, 139, 459 Hepatic, 32, 301, 459 Hepatitis, 301, 459, 460, 512 Hepatitis A, 301, 459 Hepatocyte, 173, 275, 459, 460 Hepatocyte Growth Factor, 173, 460 Hepatoma, 313, 314, 460 Hepato-splenomegaly, 290, 460 Hepatovirus, 459, 460 Hereditary, 62, 216, 455, 457, 459, 460, 479, 496 Hereditary mutation, 455, 460 Heredity, 419, 455, 460 Herpes, 420, 460 Heterodimer, 431, 460 Heterogeneity, 17, 36, 107, 136, 157, 161, 173, 278, 421, 460 Hidradenitis, 121, 460
Histamine, 284, 377, 423, 460 Histamine Release, 284, 423, 460 Histidine, 299, 460 Histiocytosis, 233, 361, 460 Histocompatibility, 70, 222, 460, 475 Histocompatibility Antigens, 222, 460, 475 Histone Deacetylase, 21, 65, 74, 461 Homeobox, 29, 60, 77, 83, 133, 301, 461 Homeostasis, 50, 461 Homogeneous, 23, 275, 461 Homoharringtonine, 206, 228, 378, 379, 461 Homologous, 24, 26, 93, 310, 327, 422, 442, 455, 461, 477, 491, 499, 505, 509 Homosexuality, 363, 461 Hormonal, 285, 427, 441, 461 Hormone, 50, 284, 285, 289, 292, 309, 318, 420, 422, 429, 441, 449, 450, 454, 461, 465, 487, 489, 490, 497, 500, 506, 507 Hormone therapy, 309, 420, 461 Hospice, 404, 461 Humoral, 71, 288, 326, 331, 457, 461, 507 Humour, 461 Hybrid, 58, 59, 60, 108, 189, 196, 206, 275, 317, 437, 461 Hybridization, 33, 123, 193, 200, 222, 299, 317, 461, 480 Hybridomas, 275, 293, 331, 334, 461, 466 Hydatidiform Mole, 436, 461 Hydrogen, 311, 419, 422, 428, 431, 432, 444, 451, 461, 476, 480, 482, 491 Hydrolysis, 420, 430, 437, 454, 461, 486, 491 Hydroxamic Acids, 311, 462 Hydroxylamine, 311, 462 Hydroxylysine, 438, 462 Hydroxyproline, 423, 438, 462 Hydroxyurea, 99, 116, 375, 404, 462 Hyperbilirubinemia, 462, 468 Hypercalcemia, 157, 462 Hyperglycemia, 229, 462 Hyperlipidemia, 162, 462 Hyperplasia, 4, 452, 462 Hypersensitivity, 67, 236, 449, 462, 497 Hypertension, 47, 433, 462, 467 Hyperthermia, 153, 462 Hyperthyroidism, 427, 462 Hypertrophy, 462 Hypnotic, 428, 462, 506 Hypochlorous Acid, 213, 462 Hypogammaglobulinemia, 302, 462 Hypoglycemia, 230, 462
524 Leukemia
Hypothalamus, 428, 431, 462, 486 Hypothyroidism, 403, 462 I Ibuprofen, 301, 462 Id, 41, 202, 235, 278, 398, 399, 400, 401, 402, 404, 405, 412, 414, 463 Idarubicin, 41, 162, 210, 224, 232, 375, 380, 463 Idiopathic, 216, 460, 463, 493, 498 Idiotype, 163, 463 Ileitis, 292, 463 Ileum, 463 Immune adjuvant, 262, 463 Immune function, 463, 464 Immunity, 30, 49, 66, 71, 167, 305, 330, 345, 419, 421, 463 Immunization, 68, 463, 464 Immunoconjugates, 319, 463 Immunodeficiency, 5, 86, 88, 90, 281, 299, 344, 364, 419, 462, 463 Immunodeficiency syndrome, 344, 364, 463 Immunofluorescence, 293, 463 Immunogenic, 69, 71, 463, 470 Immunoglobulin, 146, 159, 181, 185, 330, 424, 463, 476 Immunologic, 40, 352, 435, 463, 494 Immunophenotyping, 39, 127, 463 Immunophilins, 463, 500 Immunosuppressant, 422, 453, 463, 464, 475, 500 Immunosuppressive, 78, 294, 299, 337, 442, 456, 464, 484 Immunosuppressive Agents, 294, 464 Immunosuppressive therapy, 464 Immunotherapy, 80, 123, 184, 278, 309, 319, 399, 429, 464 Immunotoxin, 94, 379, 464 Impairment, 344, 427, 451, 464, 474 Implant radiation, 464, 466, 467, 493, 513 In situ, 20, 46, 52, 98, 128, 129, 155, 176, 193, 200, 222, 280, 318, 464 In Situ Hybridization, 20, 98, 128, 129, 155, 176, 193, 200, 222, 280, 318, 464 Incision, 464, 467 Incontinence, 464, 477 Indicative, 229, 345, 464, 483, 511 Indolent, 3, 182, 193, 200, 227, 278, 319, 464 Indomethacin, 301, 464, 508 Induction therapy, 10, 191, 198, 218, 220, 221, 234, 464
Infancy, 41, 324, 464 Infarction, 464 Infiltration, 4, 106, 131, 147, 290, 324, 340, 465, 513 Inflammatory bowel disease, 372, 465 Influenza, 457, 465, 471 Informed Consent, 43, 465 Infusion, 13, 220, 226, 298, 465 Initiation, 7, 14, 22, 465, 490, 508 Inlay, 465, 496 Inorganic, 274, 303, 437, 462, 465, 477, 507 Insecticides, 465, 485 Insertional, 19, 59, 245, 465 Insight, 26, 59, 61, 465 Insomnia, 345, 465 Insulator, 465, 477 Insulin, 322, 339, 465, 468, 498, 510 Insulin-dependent diabetes mellitus, 465 Intercalating Agents, 289, 466 Interferon, 71, 75, 82, 102, 110, 120, 130, 156, 165, 220, 228, 233, 289, 349, 380, 404, 466, 471 Interferon-alpha, 102, 120, 156, 220, 228, 466 Interleukin-1, 79, 81, 228, 466 Interleukin-10, 79, 466 Interleukin-2, 252, 254, 255, 264, 267, 466 Interleukin-3, 284, 438, 466 Interleukin-5, 95, 466 Interleukin-6, 328, 466 Interleukin-8, 285, 318, 466 Interleukins, 307, 464, 466 Internal Medicine, 15, 21, 37, 53, 63, 190, 192, 197, 199, 340, 459, 466, 473 Internal radiation, 466, 467, 493, 513 Interphase, 143, 280, 434, 467, 480 Interstitial, 431, 451, 466, 467, 513 Intestinal, 310, 313, 372, 433, 448, 467, 513 Intestinal Mucosa, 448, 467, 513 Intestine, 276, 431, 439, 448, 467, 469 Intoxication, 467, 513 Intracellular, 8, 22, 89, 192, 199, 210, 212, 245, 295, 299, 322, 465, 467, 490, 500, 512 Intracranial Hypertension, 209, 467, 483 Intrahepatic, 32, 467 Intraperitoneal, 89, 467 Intravascular, 51, 108, 166, 467 Intravenous, 10, 74, 454, 465, 467 Intrinsic, 145, 156, 330, 421, 429, 467 Invasive, 148, 214, 235, 461, 463, 467, 472 Ionization, 467
Index 525
Ionizing, 188, 191, 195, 198, 206, 422, 448, 467, 472, 493 Ions, 274, 303, 428, 431, 446, 447, 461, 467 Irinotecan, 60, 226, 267, 467 Iris, 144, 424, 441, 467, 493, 511 Irradiation, 98, 258, 467, 513 Ischemia, 427, 467, 477 Islet, 300, 322, 468 J Jaundice, 388, 462, 468 Joint, 355, 403, 426, 468, 482, 505 K Kanamycin, 422, 468 Karyotype, 113, 133, 176, 181, 182, 310, 461, 468 Kb, 165, 280, 300, 317, 386, 468 Keratin, 468 Keratinocytes, 87, 284, 285, 318, 466, 468 Keratitis, 192, 199, 468 Kidney Disease, 272, 372, 386, 468 Kidney Failure, 287, 468 Kidney Failure, Acute, 468 Kidney Failure, Chronic, 468 Killer Cells, 64, 90, 468 Kinetic, 467, 468 L Labile, 302, 439, 468 Lactate Dehydrogenase, 80, 469 Lactation, 469, 490 Laminin, 288, 429, 451, 469 Language Disorders, 344, 469 Large Intestine, 439, 445, 467, 469, 494, 500 Larynx, 276, 292, 469, 508 Latency, 59, 82, 145, 469 Latent, 82, 299, 469, 489 Lectin, 286, 288, 469 Leiomyosarcoma, 311, 469 Leishmaniasis, 469, 484 Lens, 426, 433, 469, 495, 512 Lethal, 21, 31, 33, 75, 275, 295, 296, 298, 337, 369, 445, 469, 477, 497 Lethargy, 462, 469 Leucocyte, 448, 469, 471 Leucovorin, 145, 469 Leukocytes, 73, 279, 323, 430, 431, 435, 464, 466, 469, 483, 510 Leukoencephalopathy, 164, 469 Leukopenia, 4, 469 Leukoplakia, 5, 470 Library Services, 412, 470 Life Expectancy, 278, 337, 470 Ligament, 470, 491
Ligands, 8, 130, 156, 243, 470 Ligation, 82, 118, 470 Linkage, 19, 26, 454, 470, 492 Lipid, 193, 200, 245, 246, 292, 338, 339, 445, 465, 470, 477, 509 Lipid A, 338, 470 Lipopolysaccharides, 470 Liposomal, 66, 162, 216, 229, 321, 470 Liver cancer, 470, 507 Liver Neoplasms, 470, 512 Liver Transplantation, 100, 470 Localization, 37, 48, 50, 59, 60, 82, 84, 91, 121, 208, 246, 470 Localized, 26, 147, 299, 445, 448, 452, 465, 469, 470, 477, 487, 510, 511 Locomotion, 470, 487 Loop, 71, 92, 470 Loss of Heterozygosity, 82, 148, 470 Lucida, 469, 470 Lumbar, 171, 256, 470, 471, 502 Lumbar puncture, 171, 256, 471, 502 Lupus, 294, 344, 471, 505 Lutein Cells, 471, 490 Lymph, 278, 290, 302, 407, 435, 448, 461, 471, 477, 480, 498, 499 Lymph node, 278, 302, 407, 435, 471, 477, 480, 498 Lymphadenopathy, 471, 499 Lymphatic, 292, 310, 319, 365, 465, 471, 474, 501, 502, 507 Lymphatic system, 292, 471, 501, 502, 507 Lymphoblasts, 22, 43, 47, 102, 330, 420, 471 Lymphocyte Count, 278, 419, 471 Lymphocyte Subsets, 86, 471 Lymphocytic Choriomeningitis Virus, 48, 471 Lymphocytosis, 69, 79, 81, 83, 88, 160, 290, 306, 471 Lymphoproliferative, 27, 40, 80, 87, 104, 207, 437, 471, 484 Lymphosarcoma, 72, 306, 471 Lymphotoxin, 336, 471 Lysine, 21, 64, 462, 472 M Macrophage, 95, 96, 135, 216, 279, 284, 307, 438, 458, 466, 472 Macrophage Colony-Stimulating Factor, 135, 307, 438, 472 Magnetic Resonance Imaging, 192, 199, 221, 472 Maintenance therapy, 220, 472
526 Leukemia
Major Histocompatibility Complex, 8, 82, 91, 460, 472, 475 Malignancy, 4, 22, 23, 26, 33, 42, 55, 146, 151, 181, 302, 306, 321, 472 Malignant fibrous histiocytoma, 115, 472 Malignant mesothelioma, 472, 474 Malignant tumor, 55, 313, 436, 471, 472, 477, 482, 497 Malnutrition, 427, 432, 472 Mammary, 242, 350, 441, 472 Man-made, 433, 472 Mannans, 454, 472 Mastication, 472 Masticatory, 4, 472 Matched-Pair Analysis, 181, 472 Matrix metalloproteinase, 119, 473 Maxillary, 473, 483 Median survival time, 339, 473 Mediate, 30, 33, 58, 89, 92, 335, 468, 473 Mediator, 466, 473 Medical Oncology, 32, 149, 224, 234, 473, 493 Medical Records, 473, 496 Medicament, 308, 327, 473 MEDLINE, 387, 473 Medullary, 56, 473 Mefenamic Acid, 301, 473 Megakaryocytes, 307, 329, 431, 473, 507 Meiosis, 59, 473, 477, 505 Melanin, 467, 473, 486, 510 Melanocytes, 473 Melanoma, 15, 16, 275, 282, 284, 286, 305, 311, 313, 325, 473, 510 Melphalan, 41, 98, 120, 191, 198, 221, 473 Memory, 424, 444, 473 Menarche, 473, 495 Meninges, 434, 474, 502 Meningioma, 310, 474 Meningitis, 453, 471, 474 Menopause, 474, 488, 495 Menstruation, 443, 447, 474, 495 Mental, iv, 5, 47, 272, 345, 386, 389, 404, 435, 436, 443, 446, 451, 462, 473, 474, 492, 498, 499, 510 Mental Disorders, 272, 474, 492 Mental Health, iv, 5, 47, 272, 386, 389, 474, 492 Mental Processes, 446, 474, 492 Mental Retardation, 404, 474 Mercaptopurine, 102, 118, 360, 376, 474 Mercury, 453, 474 Mesenchymal, 21, 287, 458, 461, 472, 474
Mesoderm, 474, 509, 513 Mesonephros, 7, 474 Mesothelioma, 63, 311, 472, 474 Meta-Analysis, 107, 474 Metabolite, 60, 285, 297, 430, 445, 448, 469, 474, 489 Metaphase, 280, 474 Metaplasia, 101, 474 Metastasis, 55, 214, 473, 474, 475 Metastatic, 12, 214, 285, 289, 309, 431, 475, 499 Methanol, 293, 475 Methionine, 445, 475 Methylprednisolone, 105, 475 Methyltransferase, 428, 475 MI, 129, 185, 319, 417, 475 Microbe, 475, 508 Microbiology, 7, 59, 104, 113, 189, 196, 351, 354, 427, 475 Microorganism, 305, 438, 475, 483, 513 Microscopy, 214, 293, 350, 429, 475, 480 Microtubules, 282, 475, 476, 483 Migration, 33, 279, 284, 285, 318, 475 Minor Histocompatibility Antigens, 30, 460, 475 Minor Histocompatibility Loci, 475 Mitochondria, 11, 119, 475, 482 Mitosis, 55, 426, 434, 435, 476 Mitotic, 55, 102, 163, 190, 197, 211, 282, 289, 435, 450, 476, 477, 512 Mitotic Spindle Apparatus, 435, 476 Mitoxantrone, 194, 201, 220, 222, 224, 232, 233, 376, 378, 476 Modeling, 446, 476 Modification, 58, 310, 313, 423, 455, 476, 493 Modulator, 53, 58, 226, 328, 476 Molar pregnancy, 456, 476 Molecular mass, 312, 476 Monitor, 16, 101, 231, 257, 476, 480 Monocyte, 95, 111, 279, 313, 472, 476 Mononuclear, 69, 94, 211, 279, 472, 476, 510 Monophosphate, 80, 329, 476 Monosomy, 103, 424, 476 Monotherapy, 226, 476 Morphological, 25, 229, 322, 330, 421, 447, 454, 473, 476 Morphology, 6, 36, 108, 141, 144, 205, 329, 350, 433, 459, 477 Morula, 430, 477 Motility, 464, 477
Index 527
Mucocutaneous, 4, 292, 469, 477 Mucor, 184, 477 Mucosa, 131, 454, 465, 471, 477, 478, 490, 504 Mucositis, 5, 477 Mucus, 477, 510 Multidrug resistance, 130, 148, 166, 223, 226, 477 Multiple Myeloma, 128, 164, 172, 366, 398, 477 Multiple sclerosis, 294, 310, 327, 477, 481 Multivalent, 428, 477 Muscular Diseases, 477, 483 Mustard Gas, 477 Mutagen, 19, 67, 477 Mutagenic, 314, 422, 477 Mycosis, 184, 190, 197, 211, 477 Mycosis Fungoides, 190, 197, 211, 477 Myelin, 477, 499 Myelitis, 327, 477 Myelodysplasia, 51, 63, 99, 115, 149, 151, 172, 477 Myelofibrosis, 101, 184, 236, 478 Myeloid Cells, 35, 38, 142, 288, 307, 325, 326, 478 Myeloid Progenitor Cells, 69, 307, 478 Myeloma, 234, 292, 293, 311, 368, 399, 405, 406, 478 Myeloproliferative Disorders, 40, 169, 236, 429, 478 Myelosuppression, 423, 478 Myocardial infarction, 207, 429, 441, 475, 478 Myocarditis, 445, 478 Myocardium, 475, 478 Myopia, 478, 495, 496 Myristate, 246, 478 N Naive, 302, 331, 478 Naphthoquinones, 445, 478 Naproxen, 301, 478 Nasal Cavity, 478, 483 Natural killer cells, 87, 478 Need, 3, 5, 57, 285, 290, 300, 311, 314, 315, 330, 343, 344, 350, 361, 363, 371, 377, 388, 401, 405, 406, 408, 421, 473, 479, 508 Neonatal, 68, 78, 126, 479 Neoplasia, 45, 108, 280, 306, 479 Neoplasm, 14, 28, 305, 479, 483, 498, 510 Neoplastic, 39, 41, 51, 287, 295, 340, 344, 461, 470, 471, 479 Nephropathy, 468, 479
Nerve Growth Factor, 257, 479 Nervous System, 80, 106, 210, 247, 327, 348, 419, 421, 428, 431, 434, 454, 456, 457, 473, 477, 479, 481, 484, 485, 505 Networks, 16, 58, 479 Neural, 30, 216, 421, 461, 479, 496 Neuritis, 479, 481 Neuroblastoma, 12, 39, 40, 41, 42, 47, 171, 308, 403, 479 Neurodegenerative Diseases, 292, 428, 479 Neurologic, 155, 291, 456, 479 Neurology, 46, 62, 150, 155, 210, 479 Neuronal, 275, 323, 479 Neurons, 320, 323, 444, 454, 479, 505 Neuropathy, 234, 479 Neurosurgery, 46, 62, 479 Neurotoxicity, 138, 151, 192, 199, 479 Neurotransmitter, 419, 420, 423, 457, 460, 479, 500, 504 Neutrons, 422, 467, 480, 493 Neutrophil, 94, 279, 480 Nitrogen, 422, 442, 451, 452, 468, 473, 476, 480, 509 Node-positive, 223, 228, 480 Non-small cell lung cancer, 50, 325, 480 Nuclear, 7, 24, 26, 35, 48, 55, 56, 59, 60, 65, 68, 72, 77, 80, 82, 84, 87, 88, 177, 228, 232, 320, 428, 432, 450, 454, 456, 472, 480, 490, 496, 506, 507, 510 Nuclear Matrix, 55, 480 Nuclear Pore, 480 Nucleates, 435, 480 Nuclei, 55, 193, 200, 280, 422, 455, 472, 476, 480, 481, 491 Nucleic Acid Hybridization, 461, 480 Nucleic Acid Probes, 280, 323, 480 Nucleocapsid, 79, 143, 244, 274, 303, 480 Nucleolus, 88, 480, 497 Nursing Care, 116, 480 Nystatin, 5, 480 O Occupational Exposure, 151, 481 Odour, 426, 481 Oliguria, 302, 468, 481 Omeprazole, 192, 199, 222, 481 Oncogenic, 8, 19, 25, 29, 32, 56, 59, 61, 85, 306, 481, 491 Opacity, 433, 444, 481 Operon, 481, 490, 495 Ophthalmology, 106, 164, 192, 199, 452, 481, 496 Opportunistic Infections, 27, 345, 420, 481
528 Leukemia
Opsin, 481, 496, 497 Optic Chiasm, 462, 481 Optic disc, 481 Optic Nerve, 106, 481, 492, 496, 498 Optic Neuritis, 327, 481 Oral Health, 482 Oral Hygiene, 5, 482 Oral Manifestations, 3, 4, 482 Orbit, 482 Orbital, 106, 159, 439, 481, 482 Orderly, 37, 62, 482 Organ Culture, 53, 482, 507 Organ Transplantation, 149, 482 Organelles, 55, 443, 473, 482, 487 Osteoarthritis, 338, 339, 450, 482, 486 Osteogenic sarcoma, 482 Osteoporosis, 47, 482 Osteosarcoma, 44, 159, 482 Ototoxic, 422, 482 Ovary, 276, 334, 457, 482, 504 Overall survival, 10, 482 Overweight, 202, 339, 482 Ovum, 443, 456, 477, 482, 489, 490, 509, 513 Oxidation, 419, 425, 430, 442, 482 Oxygen Consumption, 482, 496 Oxygenase, 212, 483 P P53 gene, 6, 43, 483 Paclitaxel, 193, 200, 212, 219, 228, 235, 239, 245, 483 Palliative, 5, 32, 483, 506 Palsy, 105, 483 Pancreas, 147, 276, 296, 300, 419, 429, 445, 465, 468, 483, 510 Pancreatic, 160, 310, 322, 449, 483 Pancreatic cancer, 310, 449, 483 Pancytopenia, 51, 483 Papilloma, 292, 483 Paralysis, 93, 229, 483, 501 Paranasal Sinuses, 109, 483 Paraparesis, 291, 483 Parietal, 481, 483 Parotid, 483, 498 Partial remission, 483, 495 Parturition, 483, 490 Patch, 470, 483 Pathogen, 483, 504 Pathologic, 160, 337, 338, 419, 426, 429, 432, 441, 462, 483, 492, 502 Pathologic Processes, 426, 483 Pathologies, 361, 484
Pathologist, 484 Pathophysiology, 19, 28, 54, 160, 358, 361, 484 Patient Education, 402, 410, 412, 417, 484 PDQ, 398, 399, 484 Pediatric Dentistry, 5, 484 Pedigree, 26, 484 Pelvic, 484, 491 Pelvis, 419, 469, 470, 484, 511 Pemphigus, 230, 419, 484 Penis, 440, 484, 485 Pentamidine, 345, 484 Pentostatin, 148, 369, 376, 379, 484 Pepsin, 484 Pepsin A, 484 Peptic, 302, 484 Peptic Ulcer, 302, 484 Peptide, 49, 113, 184, 231, 277, 279, 306, 422, 452, 468, 484, 485, 487, 491, 494, 500, 507 Peptide Elongation Factors, 485, 500 Perennial, 485, 509 Pericarditis, 75, 485 Pericardium, 485, 505 Peripheral Nervous System, 327, 479, 483, 485, 504 Peripheral Nervous System Diseases, 483, 485 Peripheral stem cell transplantation, 252, 254, 255, 257, 258, 260, 266, 267, 485, 508 Peripheral stem cells, 266, 458, 485 Peritoneal, 467, 485 Peritoneal Cavity, 467, 485 Pesticides, 18, 465, 485 Phagocyte, 472, 485 Phallic, 452, 485 Pharmacodynamics, 11, 45, 221, 225, 485 Pharmacogenetics, 138, 246, 485 Pharmacokinetic, 10, 22, 63, 192, 199, 226, 485 Pharmacologic, 10, 22, 40, 44, 50, 56, 59, 427, 442, 458, 485, 508 Phenotype, 7, 19, 24, 26, 29, 49, 54, 59, 79, 144, 163, 176, 223, 287, 295, 439, 485 Phenyl, 336, 485 Phenylalanine, 484, 486, 510 Phenylbutyrate, 249, 486 Phorbol, 67, 230, 246, 325, 486 Phospholipases, 486, 500 Phosphorus, 432, 486 Phosphorylated, 24, 131, 299, 321, 438, 445, 486
Index 529
Phosphorylates, 93, 486 Phosphorylation, 9, 25, 71, 112, 299, 340, 486 Photocoagulation, 438, 486 Photoreceptors, 440, 486 Physical Examination, 256, 403, 486 Physiologic, 421, 458, 474, 486, 490, 494 Physiology, 48, 62, 459, 486, 504 Phytotoxin, 486, 497 Pigmentation, 292, 486 Pigments, 429, 433, 486, 487, 496 Pilot Projects, 44, 486 Pilot study, 162, 193, 200, 227, 486 Pineal gland, 436, 486 Piroxicam, 301, 486 Pituitary Gland, 441, 452, 486 Placenta, 301, 486, 489 Plana, 487, 499 Plants, 280, 286, 325, 334, 422, 432, 433, 456, 469, 477, 486, 487, 498, 502, 508, 509 Plaque, 5, 424, 436, 487 Plasma cells, 424, 477, 478, 487 Plasmid, 298, 487, 511 Plasmin, 487, 507, 511 Plasminogen, 487, 507, 511 Plastids, 482, 487 Platelet Activation, 487, 500 Platelet Count, 278, 398, 487 Platelet Transfusion, 171, 487 Platelet-Derived Growth Factor, 94, 141, 487 Platelets, 245, 307, 407, 429, 478, 483, 487, 498, 507 Platinum, 437, 470, 487 Pleura, 125, 487 Pneumonia, 75, 440, 484, 487 Podophyllotoxin, 450, 488 Point Mutation, 7, 57, 65, 206, 488 Polymerase, 5, 29, 84, 89, 123, 165, 173, 190, 197, 211, 222, 299, 308, 425, 488, 490, 495, 497 Polymerase Chain Reaction, 5, 29, 84, 89, 123, 165, 173, 222, 488 Polymorphic, 12, 436, 488 Polymorphism, 87, 145, 209, 488 Polyneuritis, 445, 488 Polyposis, 439, 488 Polysaccharide, 286, 425, 434, 488, 491, 511 Population Density, 14, 488 Posterior, 344, 423, 427, 435, 446, 467, 481, 483, 488, 498, 502 Postmenopausal, 482, 488
Postnatal, 488, 503 Postoperative, 228, 450, 454, 486, 488 Postsynaptic, 488, 500 Potentiate, 108, 488 Potentiating, 194, 201, 488 Potentiation, 87, 227, 488, 500 Practicability, 488, 509 Practice Guidelines, 389, 404, 488 Precancerous, 292, 435, 489 Preclinical, 60, 289, 489 Predisposition, 26, 92, 489 Prednisolone, 105, 225, 475, 489 Prednisone, 218, 232, 302, 489 Preleukemia, 478, 489, 501 Premalignant, 73, 292, 295, 489 Prenatal, 280, 447, 489 Presumptive, 165, 184, 274, 303, 489 Prevalence, 94, 137, 489 Prickle, 419, 468, 489 Primary tumor, 308, 489 Probe, 52, 280, 298, 489 Prodrug, 28, 190, 197, 211, 285, 489 Progesterone, 489, 490, 503 Prognostic factor, 101, 168, 181, 233, 346, 489 Progression, 24, 25, 48, 49, 55, 59, 78, 86, 88, 89, 134, 287, 306, 308, 322, 324, 340, 424, 489 Projection, 481, 490, 494 Prokaryotic Cells, 334, 490 Prolactin, 146, 490 Proline, 48, 438, 462, 490 Promoter, 12, 24, 59, 130, 139, 177, 190, 197, 214, 298, 300, 333, 490 Promotor, 490, 496 Prone, 26, 490 Prophylaxis, 210, 327, 338, 425, 490, 511 Prospective study, 25, 166, 231, 490 Prostaglandin, 176, 279, 283, 316, 490 Prostaglandins A, 464, 490 Prostate, 15, 16, 63, 102, 276, 282, 292, 296, 306, 310, 325, 338, 339, 429, 452, 491, 510 Protease, 27, 65, 439, 491, 507 Protein C, 74, 274, 286, 293, 303, 321, 333, 423, 428, 438, 452, 468, 491, 499, 512 Protein Conformation, 274, 303, 423, 468, 491 Protein Isoforms, 422, 491 Protein S, 27, 50, 51, 245, 277, 332, 360, 425, 430, 440, 445, 455, 485, 491, 497, 500, 506 Proteinuria, 477, 491
530 Leukemia
Proteoglycan, 330, 491 Proteolytic, 431, 439, 487, 491, 497, 507, 511 Protocol, 4, 5, 13, 15, 20, 32, 39, 41, 43, 44, 45, 46, 166, 206, 218, 234, 327, 491 Proton Pump, 481, 491 Protons, 422, 461, 467, 491, 493 Proto-Oncogene Proteins, 483, 491 Proto-Oncogene Proteins c-mos, 483, 491 Proto-Oncogenes, 295, 491 Protozoa, 276, 469, 475, 492, 502, 509 Provirus, 72, 77, 137, 245, 281, 291, 306, 492 Proximal, 14, 167, 177, 446, 478, 492 Pruritic, 447, 492 Pseudotumor Cerebri, 467, 492 Psoriasis, 137, 279, 283, 292, 294, 310, 313, 316, 403, 477, 492, 509 Psychiatric, 323, 474, 492 Psychiatry, 452, 492 Psychic, 474, 492, 499 Psychoactive, 492, 513 Psychology, 4, 46, 446, 492 Pteroylpolyglutamic Acids, 454, 492 Public Health, 13, 14, 259, 355, 358, 389, 492 Public Policy, 387, 492 Pulmonary, 88, 106, 164, 224, 292, 430, 436, 440, 449, 468, 492, 512 Pulmonary Edema, 436, 468, 492 Pulmonary Fibrosis, 292, 492 Pulse, 227, 476, 493 Pupil, 441, 481, 493 Purifying, 324, 493 Purpura, 110, 216, 416, 493 Purulent, 493, 511 Pyoderma, 108, 493 Pyoderma Gangrenosum, 108, 493 Q Quality of Life, 16, 47, 63, 175, 245, 406, 493, 505 Quaternary, 491, 493 R Race, 166, 175, 468, 473, 475, 493 Racemic, 473, 493 Radiation, 9, 14, 16, 43, 46, 62, 63, 69, 188, 191, 195, 198, 206, 258, 260, 274, 278, 286, 289, 295, 296, 298, 299, 302, 314, 319, 337, 340, 357, 402, 420, 448, 451, 453, 454, 462, 466, 467, 472, 493, 498, 508, 510, 513 Radiation Oncology, 16, 63, 493
Radioactive, 427, 458, 461, 464, 466, 467, 472, 476, 480, 481, 493, 507, 510, 513 Radioimmunotherapy, 463, 493, 494 Radiolabeled, 183, 260, 467, 493, 513 Radiology, 46, 50, 115, 159, 189, 191, 192, 196, 198, 199, 357, 493 Radiotherapy, 42, 151, 309, 319, 343, 431, 467, 493, 503, 513 Randomized clinical trial, 45, 494 Ras gene, 287, 295, 494 Reactivation, 335, 494 Reactive Oxygen Species, 106, 230, 494 Reagent, 13, 287, 436, 450, 494 Recombinant Proteins, 299, 494 Recombination, 24, 84, 93, 159, 242, 310, 455, 494 Reconstitution, 91, 124, 167, 494 Rectum, 425, 431, 438, 439, 445, 454, 464, 465, 469, 491, 494 Recurrence, 100, 147, 435, 494 Red blood cells, 407, 450, 478, 483, 494, 498 Red Nucleus, 427, 494 Reductase, 11, 83, 87, 161, 167, 452, 475, 494 Refer, 1, 296, 431, 439, 452, 454, 460, 470, 478, 480, 493, 494, 508 Reflex, 494, 510 Refraction, 478, 495, 502 Refractory, 10, 30, 41, 111, 126, 132, 137, 142, 161, 162, 169, 188, 189, 194, 195, 196, 201, 206, 207, 216, 217, 222, 225, 226, 233, 251, 252, 255, 256, 260, 261, 262, 264, 265, 266, 267, 268, 269, 270, 271, 369, 447, 495 Regeneration, 452, 494, 495 Regimen, 98, 132, 162, 206, 211, 225, 233, 253, 262, 265, 295, 437, 447, 495 Reliability, 322, 495 Remission Induction, 105, 495 Remission induction therapy, 105, 495 Renal tubular, 99, 495 Repressor, 57, 77, 178, 300, 333, 481, 495 Repressor Proteins, 300, 495 Reproductive cells, 455, 460, 495 Reproductive History, 18, 495 Research Support, 20, 495 Resection, 314, 495 Resolving, 125, 495 Respiration, 109, 426, 432, 476, 495 Respiratory Burst, 284, 496 Respiratory failure, 160, 496
Index 531
Response Elements, 320, 496 Restitution, 320, 496 Restoration, 292, 494, 496, 513 Retina, 437, 440, 469, 478, 481, 496, 499, 511, 512 Retinal, 87, 292, 445, 481, 496, 497 Retinal Detachment, 292, 496 Retinal Ganglion Cells, 481, 496 Retinoblastoma, 280, 311, 496 Retinoid, 50, 58, 72, 84, 96, 154, 170, 292, 320, 337, 496 Retinol, 203, 496, 497 Retrobulbar, 481, 496 Retrospective, 148, 496 Retrospective study, 148, 496 Retroviral vector, 35, 281, 315, 455, 497 Retrovirus, 28, 51, 64, 67, 68, 77, 83, 85, 86, 89, 90, 96, 281, 299, 306, 497 Reverse Transcriptase Inhibitors, 175, 497 Reversion, 133, 497 Rhabdomyosarcoma, 62, 497 Rheumatism, 166, 462, 497 Rheumatoid, 166, 279, 283, 294, 310, 316, 338, 339, 344, 403, 450, 478, 486, 497 Rheumatoid arthritis, 166, 279, 283, 294, 310, 316, 338, 339, 344, 403, 450, 478, 486, 497 Rhinitis, 310, 497 Rhodopsin, 481, 496, 497 Ribonuclease, 38, 497 Ribonucleoproteins, 480, 497 Ribonucleoside Diphosphate Reductase, 462, 497 Ribose, 190, 197, 211, 420, 442, 497 Ribosomal Proteins, 48, 497 Ribosome, 497, 509 Ricin, 147, 380, 381, 497 Rigidity, 487, 497 Risk factor, 12, 18, 107, 314, 367, 449, 490, 497 Rituximab, 128, 170, 216, 219, 261, 497 Rodenticides, 485, 497 Roentgenography, 498, 507 Rosiglitazone, 339, 498 S Salicylate, 261, 498, 501 Salivary, 443, 445, 483, 498 Salivary glands, 443, 445, 498 Saphenous, 441, 498 Saphenous Vein, 441, 498 Saponins, 498, 503 Sarcoidosis, 135, 498
Sarcoma, 44, 62, 73, 106, 159, 292, 297, 310, 472, 498, 501 Sargramostim, 252, 379, 498 Scatter, 498, 510 Schizoid, 498, 513 Schizophrenia, 498, 513 Schizotypal Personality Disorder, 498, 513 Sclera, 498, 511 Sclerosis, 105, 178, 477, 498 Screening, 6, 171, 288, 300, 307, 325, 326, 329, 333, 437, 484, 498 Secondary tumor, 475, 498 Secretion, 33, 51, 120, 140, 146, 419, 436, 441, 460, 461, 462, 466, 469, 477, 481, 499, 511 Secretory, 481, 499 Sedimentation, 499, 509 Segmental, 26, 280, 499 Segmentation, 499 Segregation, 55, 494, 499 Seizures, 192, 199, 221, 456, 499 Semen, 208, 491, 499 Semisynthetic, 432, 434, 450, 499 Senescence, 58, 499 Senile, 482, 499 Sensory loss, 477, 499, 506 Sepsis, 70, 122, 125, 234, 310, 454, 499 Septic, 403, 426, 499 Sequencing, 488, 499 Serine, 95, 491, 499, 507 Serous, 487, 499 Serrata, 237, 437, 499 Serrated, 499 Serum, 13, 42, 48, 76, 151, 301, 403, 423, 425, 439, 457, 468, 494, 499, 510 Serum Sickness, 403, 499 Sex Characteristics, 420, 500, 506 Shiga Toxin, 67, 305, 500 Shock, 500, 509 Signal Transduction, 24, 38, 53, 61, 173, 174, 242, 245, 246, 277, 289, 295, 335, 500 Signs and Symptoms, 371, 372, 495, 500 Sirolimus, 312, 463, 500 Skeletal, 477, 500 Skeleton, 420, 452, 468, 490, 500 Skull, 482, 500, 506 Sleep apnea, 224, 500 Small cell lung cancer, 500 Small intestine, 447, 461, 463, 467, 500, 512 Smoldering leukemia, 478, 501 Smooth muscle, 422, 423, 427, 460, 477, 501, 504
532 Leukemia
Social Environment, 493, 501 Social Work, 363, 501 Sodium, 194, 201, 245, 247, 261, 285, 301, 380, 457, 478, 501, 505 Sodium salicylate, 261, 501 Soft tissue, 62, 372, 431, 452, 472, 500, 501 Soft tissue sarcoma, 62, 452, 501 Solid tumor, 21, 41, 43, 45, 60, 61, 62, 229, 296, 305, 312, 317, 423, 424, 446, 501 Solvent, 324, 436, 445, 450, 475, 501 Soma, 182, 501 Somatic, 6, 19, 23, 51, 308, 420, 447, 461, 473, 476, 485, 501, 506 Somatic cells, 6, 19, 308, 473, 476, 501 Spastic, 291, 501 Spasticity, 501 Specialist, 400, 403, 407, 501, 502 Specificity, 25, 27, 304, 331, 421, 489, 501 Spectrum, 7, 18, 289, 320, 340, 501 Speech Disorders, 344, 502 Speech pathologist, 343, 502 Sperm, 436, 455, 460, 495, 502, 509 Sphenoid, 483, 502 Sphincter, 469, 502 Spina bifida, 404, 502 Spinal cord, 257, 427, 431, 434, 435, 436, 449, 454, 474, 477, 479, 483, 485, 495, 502, 505 Spinal Cord Diseases, 483, 502 Spinal Cord Vascular Diseases, 477, 502 Spinal Nerves, 485, 502 Spinal tap, 256, 471, 502 Spinous, 449, 468, 502 Spleen, 85, 139, 278, 288, 293, 302, 326, 331, 443, 460, 471, 498, 502 Splenomegaly, 416, 502 Spondylitis, 450, 502 Sporadic, 7, 26, 479, 496, 502 Spores, 477, 502 Squamous, 480, 502 Squamous cell carcinoma, 480, 502 Stabilization, 60, 218, 503 Staging, 278, 319, 503 Standard therapy, 36, 256, 503 Stasis, 154, 503 Statistically significant, 40, 503 Staurosporine, 117, 503 Stem Cell Factor, 307, 437, 503 Stereotactic, 43, 503 Sterility, 442, 503 Steroid, 50, 170, 253, 292, 302, 441, 457, 498, 503
Steroid therapy, 253, 503 Stimulant, 460, 503 Stimulus, 427, 446, 447, 451, 466, 469, 495, 503, 507 Stomach, 193, 200, 230, 282, 292, 313, 419, 445, 450, 454, 461, 484, 485, 500, 502, 503 Stool, 438, 464, 469, 503 Strand, 152, 154, 299, 302, 488, 503 Streptococcal, 234, 504 Streptococcus, 504 Stress, 48, 129, 428, 432, 489, 497, 504, 511 Stroke, 272, 292, 386, 433, 504 Stromal, 18, 154, 297, 326, 331, 431, 504 Stromal Cells, 154, 326, 331, 431, 504 Structure-Activity Relationship, 117, 504 Subacute, 465, 504 Subclinical, 94, 149, 465, 499, 504 Subcutaneous, 434, 447, 504 Subspecies, 501, 504 Substance P, 474, 494, 499, 504 Substrate, 245, 317, 495, 504 Suction, 452, 504 Sulindac, 301, 504 Sunburn, 299, 337, 504, 510 Superinfection, 281, 504 Superoxide, 496, 505 Supplementation, 102, 505 Support group, 344, 345, 505 Supportive care, 44, 484, 505 Suppression, 31, 48, 56, 67, 77, 88, 91, 135, 174, 230, 289, 296, 441, 505 Survival Rate, 101, 179, 482, 505 Sweat, 96, 460, 505 Sympathetic Nervous System, 428, 479, 505 Symphysis, 436, 491, 505 Synaptic, 479, 500, 505 Syncytium, 76, 139, 456, 505 Synergistic, 194, 201, 219, 230, 304, 313, 484, 490, 505 Synthetic retinoid, 320, 452, 505 Systemic disease, 4, 372, 505 Systemic lupus erythematosus, 310, 403, 505 Systolic, 462, 505 T Tachycardia, 428, 505 Tachypnea, 428, 505 Telangiectasia, 216, 402, 403, 505 Telomerase, 89, 98, 308, 505 Telomere, 89, 92, 156, 176, 506 Temporal, 7, 18, 506
Index 533
Teratogenic, 422, 506, 509 Teratoma, 436, 506 Terminator, 438, 506 Testicle, 457, 506 Testicular, 282, 506 Testis, 436, 506 Testosterone, 423, 452, 494, 506 Tetracycline, 29, 54, 506 Thalamic, 427, 506 Thalamic Diseases, 427, 506 Thalamus, 431, 506 Thalidomide, 56, 251, 506 Therapeutics, 16, 45, 56, 102, 105, 110, 112, 173, 180, 377, 506 Thermal, 426, 446, 480, 488, 506 Thigh, 452, 506 Thiotepa, 206, 506 Thoracic, 15, 63, 487, 507, 513 Thorax, 419, 470, 507 Thorium, 314, 507 Thorium Compounds, 507 Thorium Dioxide, 314, 507 Threshold, 7, 34, 462, 507 Thrombin, 452, 491, 507 Thrombocytes, 487, 507 Thrombocytopenia, 4, 290, 507 Thrombomodulin, 491, 507 Thrombopoietin, 95, 307, 507 Thrombosis, 429, 491, 504, 507 Thrush, 432, 507 Thymus, 76, 463, 471, 507 Thyroid, 50, 125, 294, 462, 507, 510 Thyrotropin, 462, 507 Tiazofurin, 142, 378, 507 Tissue Culture, 34, 48, 60, 281, 507 Tissue Plasminogen Activator, 292, 507 Tolerance, 31, 420, 456, 508 Tolmetin, 301, 508 Tome, 240, 508 Tomography, 213, 508 Tone, 103, 482, 501, 508 Tonicity, 459, 508 Topical, 5, 292, 427, 436, 445, 450, 508, 509 Topoisomerase inhibitors, 450, 467, 508 Topotecan, 60, 188, 194, 195, 201, 206, 207, 233, 252, 263, 376, 508 Total-body irradiation, 258, 260, 508 Toxicity, 11, 22, 30, 74, 120, 213, 243, 285, 289, 292, 296, 320, 433, 446, 463, 474, 508, 512 Toxicology, 208, 211, 357, 388, 508 Toxin, 297, 305, 306, 445, 448, 500, 508
Trachea, 469, 507, 508 Transcriptase, 35, 145, 173, 244, 298, 299, 497, 505, 508 Transcription Factors, 23, 25, 34, 35, 37, 39, 50, 117, 274, 299, 303, 323, 496, 508 Transduction, 27, 28, 38, 54, 500, 508 Transfection, 281, 429, 455, 509 Transgenes, 25, 509 Translation, 16, 48, 81, 422, 509 Translational, 31, 34, 41, 48, 509 Translocate, 48, 509 Trauma, 403, 428, 506, 509 Treatment Outcome, 34, 100, 509 Trees, 282, 325, 509 Tretinoin, 203, 253, 376, 378, 509 Triglyceride, 339, 509 Trisomy, 75, 93, 101, 143, 164, 177, 180, 424, 509 Troglitazone, 339, 509 Trophoblast, 430, 509 Troxacitabine, 161, 369, 509 Trypanosomiasis, 484, 509 Tryptophan, 438, 509 Tubulin, 42, 231, 282, 313, 475, 509 Tumor marker, 309, 429, 510 Tumor Necrosis Factor, 21, 73, 147, 219, 289, 328, 335, 471, 506, 510 Tumor suppressor gene, 59, 62, 295, 470, 483, 510 Tumorigenic, 75, 96, 321, 510 Tumour, 311, 328, 454, 510 Tunica, 448, 477, 510 Type 2 diabetes, 47, 338, 339, 510 U Ulcer, 116, 434, 484, 510 Ulcerative colitis, 294, 465, 493, 510 Ultraviolet radiation, 302, 504, 510 Unconditioned, 310, 510 Unconscious, 463, 510 Uranium, 182, 507, 510 Uremia, 468, 510 Urethra, 484, 491, 510, 511 Uridine Diphosphate, 457, 511 Uridine Diphosphate Glucuronic Acid, 457, 511 Urinary, 147, 464, 481, 508, 511 Urinary Plasminogen Activator, 508, 511 Urine, 84, 256, 425, 430, 438, 457, 459, 464, 468, 481, 491, 510, 511 Urogenital, 474, 511 Urticaria, 310, 499, 511
534 Leukemia
Uterus, 292, 419, 435, 443, 456, 469, 474, 476, 489, 511 Uvea, 511 Uveitis, 237, 310, 511 V Vaccination, 73, 114, 183, 244, 248, 511 Vaccine, 49, 68, 87, 262, 309, 359, 368, 420, 491, 511 Vacuoles, 482, 511 Vagina, 432, 435, 474, 511 Vaginitis, 432, 511 Varicella, 79, 99, 511 Vascular, 56, 140, 162, 173, 312, 328, 422, 465, 486, 502, 511 Vascular endothelial growth factor, 56, 140, 162, 173, 511 Vasodilator, 460, 511 Vector, 78, 281, 297, 300, 314, 315, 333, 465, 508, 511 Vein, 467, 480, 483, 498, 511 Venous, 429, 430, 487, 491, 511 Venous blood, 430, 487, 511 Ventricle, 462, 493, 505, 506, 512 Venules, 430, 432, 512 Vertebrae, 502, 512 Vertebral, 429, 487, 502, 512 Veterinary Medicine, 387, 512 Villi, 461, 512 Villous, 290, 512 Vinblastine, 509, 512 Vinca Alkaloids, 512 Vincristine, 41, 70, 191, 198, 213, 214, 216, 221, 225, 226, 229, 234, 243, 376, 509, 512 Vinorelbine, 193, 200, 206, 228, 512 Vinyl Chloride, 314, 512 Viral Hepatitis, 314, 512 Virion, 480, 512
Virulence, 505, 508, 512 Virus Diseases, 425, 512 Virus Replication, 152, 274, 303, 512 Vitelline Membrane, 512, 513 Vitreous, 469, 496, 512 Vitreous Humor, 496, 512 Vitro, 6, 8, 10, 11, 22, 23, 25, 27, 30, 31, 40, 41, 49, 51, 52, 53, 54, 55, 56, 58, 60, 73, 79, 85, 120, 142, 145, 172, 183, 191, 198, 215, 219, 242, 244, 245, 247, 287, 297, 310, 312, 313, 323, 326, 331, 455, 464, 488, 504, 507, 513 W Warts, 292, 325, 488, 513 White blood cell, 249, 252, 254, 255, 266, 267, 337, 340, 407, 419, 420, 424, 429, 430, 436, 437, 452, 458, 469, 471, 472, 476, 477, 478, 480, 487, 513 Windpipe, 507, 513 Withdrawal, 323, 513 Womb, 511, 513 Wound Healing, 279, 283, 285, 292, 316, 452, 473, 513 X Xenograft, 100, 424, 513 X-ray, 189, 196, 260, 366, 416, 453, 454, 467, 472, 477, 480, 493, 494, 503, 513 X-ray therapy, 467, 513 Y Yeasts, 432, 454, 485, 513 Yolk Sac, 7, 513 Z Zebrafish, 62, 513 Zoledronate, 232, 513 Zoster, 79, 460, 513 Zymogen, 491, 513
Index 535
536 Leukemia
