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DNA Tumor Viruses: Oncogenic Mechanisms PDF

440 Pages·1995·13.331 MB·English
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DNA Tumor Viruses Oncogenic Mechanisms Edited by Giuseppe Barbanti-Brodano University of Ferrara Ferrara, Italy Mauro Bendinelli University of Pisa Pisa, Italy and Herman Friedman University of South Florida Tampa, Florida Springer Science+Business Media, LLC Library of Congress Cataloging-in-Publication Data DNA tumor viruses . ancogenic mechanisms / edited by Giuseppe Barbanti -Brodano, Maure Bendlne 111, Herman Friedman. p. cm. — (Infectious agents and pathogenesis) Includes bibliographical references and index. ISBN 978-1-4899-1102-5 1. Oncogenic viruses. I. Barbant1-Brodano, Giuseppe. II. Bendinelli, Mauro. III. Friedman, Herman, 1931- IV. Series. [DNLM: 1. DNA Tumor Viruses—pathogenicity. 2. TumorVirus Infections—complications. 3. Neoplasms—etiology. 4. Cell Transformation, Neoplastic. 5. Viral Vaccines. QW 166D6289 1995] QR372.06D595 1995 616.99'4071--dc20 DNLM/DLC for Library of Congress 95-42518 CIP ISBN 978-1-4899-1102-5 ISBN 978-1-4899-1100-1 (eBook) DOI 10.1007/978-1-4899-1100-1 © Springer Science+Business Media New York 1995 Originally published by Plenum Press, New York in 1995 Softcover reprint of the hardcover 1st edition 1995 10 98765432 1 All rights reserved No part of this book may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher DNA Tumor Viruses Oncogenic Mechanisms INFECTIOUS AGENTS AND PATHOGENESIS Series Editors: Mauro Bendinelli, University of Pisa Herman Friedman, University of South Florida COXSACKIEVIRUSES A General Update Edited by Mauro Bendinelli and Herman Friedman DNA TUMOR VIRUSES Oncogenic Mechanisms Edited by Giuseppe Barbanti-Brodano, Mauro Bendinelli, and Herman Friedman FUNGAL INFECTIONS AND IMMUNE RESPONSES Edited by Juneann W. Murphy, Herman Friedman, and Mauro Bendinelli MYCOBACTERIUM TUBERCULOSIS Interactions with the Immune System Edited by Mauro Bendinelli and Herman Friedman NEUROPATHOGENIC VIRUSES AND IMMUNITY Edited by Steven Specter, Mauro Bendinelli, and Herman Friedman PSEUDOMONAS AERUGINOSA AS AN OPPORTUNISTIC PATHOGEN Edited by Mario Campa, Mauro Bendinelli, and Herman Friedman PULMONARY INFECTIONS AND IMMUNITY Edited by Herman Chmel, Mauro Bendinelli, and Herman Friedman VIRUS-INDUCED IMMUNOSUPPRESSION Edited by Steven Specter, Mauro Bendinelli, and Herman Friedman A Continuation Order Plan is available for this series. A continuation order will bring delivery of each new volume immediately upon publication. Volumes are billed only upon actual shipment. For further information please contact the publisher. Contributors LAURE AURELIAN • Virology/Immunology Laboratories, Department of Phar macology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201-1192; and Departments of Biochemistry and Comparative Medicine, The Johns Hopkins Medical Institutions, Bal timore, Maryland 21205 GIUSEPPE BARBANTI-BRODANO • Institute of Microbiology, School ofMedi cine, University of Ferrara, 1-44100 Ferrara, Italy MAURO BOIOCCHI • Division of Experimental Oncology 1, Centro di Riferi mento Oncologico, 33081 Aviano (PN), Italy MARIE ANNICK BUENDIA • Unite de Recombinaison et Expression Gene tique, INSERM U163, Departement des Retrovirus, Institut Pasteur, 75724 Paris Cedex 15, France M. SAVERIA CAMPO • The Beatson Institute for Cancer Research, CRC Beat son Laboratories, Bearsden, Glasgow G61 IBD, Scotland ANTONINO CARBONE • Division of Pathology, Centro di Riferimento Onco logico, 33081 Aviano (PN), Italy MICHELE CARBONE • Department of Pathology, University of Chicago, Chi cago, Illinois 60637 E. CASELLI • Institute of Microbiology, University of Ferrara, 1-44100 Ferrara, Italy E. CASSAI • Institute of Microbiology, University of Ferrara, 1-44100 Ferrara, Italy CHRISTA CERNI • Institute of Tumor Biology-Cancer Research, University of Vienna, 1090 Vienna, Austria DOROTHY H. CRAWFORD • Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, London WCIE 7HT, England LIONEL CRAWFORD • ICRF Tumour Virus Group, Department of Pathology, University of Cambridge, Cambridge CB2 lQP, England VALLI DE RE • Division of Experimental Oncology 1, Centro di Riferimento Oncologico, 33081 Aviano (PN), Italy v vi CONTRIBUTORS DARIO DI LUCA • Institute of Microbiology, University of Ferrara, 1-44100 Ferrara, Italy JOSEPH A. DiPAOLO • National Cancer Institute, Laboratory of Biology, Be thesda, Maryland 20892 RICCARDO DOLCETII • Division of Experimental Oncology 1, Centro di Riferimento Oncologico, 33081 Aviano (PN), Italy M. EICKMANN • Institut fur Virologie, Philipps-Universitat, D-35037 Marburg, Germany JEAN FEUNTEUN • Institut Gustave Roussy, Laboratoire d'Oncologie Mo leculaire, 94805 Villejuif, France ANNUNZIATA GLOGHINI • Division of Pathology, Centro di Riferimento On cologico, 33081 Aviano (PN), Italy MARIA E. JACKSON • The Beatson Institute for Cancer Research, CRC Beatson Laboratories, Bearsden, Glasgow G61 lBD, Scotland LAYLA KARIMI • Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, London WCIE 7HT, England H. KERN • Institut fUr Zellbiologie, Philipps-Universitat, D-35037 Marburg, Germany LAURA de LELLIS • Institute of Microbiology, School of Medicine, University of Ferrara, 1-44100 Ferrara, Italy PETER G. MEDVECZKY • Department of Medical Microbiology and Immunol ogy, University of South Florida, Tampa, Florida 33612-4799 T. MOCKENHAUPT • Institut fur Virologie, Philipps-Universitat, D-35037 Mar burg, Germany PAOLO MONINI • Institute of Microbiology, School of Medicine, University of Ferrara, 1-44100 Ferrara, Italy ANDREW J. MORGAN • Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, Bristol BS8 lTD, England MElHAN NONOYAMAt • Tampa Bay Research Institute, St. Petersburg, Flor ida 33716 JOSEPH S. PAGANO • Departments of Microbiology and Immunology and Medicine, UNC Lineberger Comprehensive Cancer Center, University of North Carolina, School of Medicine, Chapel Hill, North Carolina 27599-7295 HARVEY I. PASS • Thoracic Oncology Section, National Cancer Institute, Na tional Institutes of Health, Bethesda, Maryland 20892 PASCAL PINEAU • Unite de Recombinaison et Expression Genetique, INSERM U163, Departement des Retrovirus, Institut Pasteur, 75724 Paris Cedex 15, France K. RADSAK • Institut fur Virologie, Philipps-Universitat, D-35037 Marburg, Ger many F. ANDREW RAY • Life Sciences Division, Los Alamos National Laboratory, Los Alamos, New Mexico 87545; present address: Department of Microbiology, Im munology and Molecular Genetics, The Albany Medical College, Albany, New York 12208-3479 tDeceased. CONTRIBUTORS vii B. REIS • Institut fur Virologie, Philipps-Universitiit, D-35037 Marburg, Ger many M. RESCHKE • Institut fUr Virologie, Philipps-Universitiit, D-35037 Marburg, Germany ROBERT P. RICCIARDI • Department of Microbiology, School of Dental Medi cine, and Graduate Program in Microbiology and Virology, University of Penn sylvania, Philadelphia, Pennsylvania 19104 PAOlA RIZZO • Department of Pathology, University of Chicago, Chicago, Illinois 60637 SIEGFRIED SCHERNECK • Max-Delbruck-Centrum for Molecular Medicine, Tumorgenetics, 13122 Berlin, Germany CHRISTIAN SEELOS • Institute of Tumor Biology-Cancer Research, Univer sity of Vienna, 1090 Vienna, Austria DANIEL T. SIMMONS • Department of Biology, University of Delaware, New ark, Delaware, 19716 NANCY S. SUNG • Departments of Microbiology and Immunology and Medi cine, UNC Lineberger Comprehensive Cancer Center, University of North Carolina, School of Medicine, Chapel Hill, North Carolina 27599-7295 AKIKO TANAKA • Tampa Bay Research Institute, St. Petersburg, Florida 33716 CRAIG D. WOODWORTH • National Cancer Institute, Laboratory of Biology, Bethesda, Maryland 20892 Preface to the Series The mechanisms of disease production by infectious agents are presently the focus of an unprecedented flowering of studies. The field has undoubtedly received impetus from the considerable advances recently made in the understanding of the structure, biochemistry, and biology of viruses, bacteria, fungi, and other parasites. Another contributing factor is our improved knowledge of immune responses and other adaptive or constitutive mechanisms by which hosts react to infection. Fur thermore, recombinant DNA technology, monoclonal antibodies, and other newer methodologies have provided the technical tools for examining questions previ ously considered too complex to be successfully tackled. The most important incentive of all is probably the regenerated idea that infection might be the initiating event in many clinical entities presently classified as idiopathic or of uncertain origin. Infectious pathogenesis research holds great promise. As more information is uncovered, it is becoming increasingly apparent that our present knowledge of the pathogenic potential of infectious agents is often limited to the most noticeable effects, which sometimes represent only the tip of the iceberg. For example, it is now well appreciated that pathologic processes caused by infectious agents may emerge clinically after an incubation of decades and may result from genetic, immunologic, and other indirect routes more than from the infecting agent in itself. Thus, there is a general expectation that continued investigation will lead to the isolation of new agents of infection, the identification of hitherto unsuspected etiologic correla tions, and, eventually, more effective approaches to prevention and therapy. Studies on the mechanisms of disease caused by infectious agents demand a breadth of understanding across many specialized areas, as well as much coopera tion between clinicians and experimentalists. The series Infectious Agents and Patho genesis is intended not only to document the state of the art in this fascinating and challenging field but also to help lay bridges among diverse areas and people. Mauro Bendinelli Herman Friedman ix Preface DNA tumor viruses have long been useful experimental models of carcinogenesis and have elucidated several important mechanisms of cell transformation. Re search in recent years has shown that human tumors have a multifactorial nature and that some DNA tumor viruses may playa key role in their etiology. The aim of this book is to assess our knowledge of DNA tumor viruses by reviewing animal models, mechanisms of transformation, association with human tumors, and possi bilities of prevention and control by vaccination. Animal models of tumor virology have contributed significantly to our under standing of the epidemiology and pathogenesis of virus-induced tumors. Bovine papillomaviruses induce papillomas in the intestine of cattle. The papillomas undergo a transition to carcinomas in cows feeding on bracken fern, which pro duces a toxin with radiomimetic and immunosuppressive functions. This example of cooperation between a virus and chemical carcinogens parallels the cooperative role of human papillomaviruses (HPVs) and herpes simplex virus type 2 (HSV-2) with environmental carcinogens in the pathogenesis of cervical cancer. Likewise, hepatocarcinomas appearing in woodchucks chronically infected by woodchuck hepatitis virus (WIN) provide strong support for the relationship between hepatitis B virus (HBV) infection and human hepatocellular carcinoma. Also, the fact that WIN DNA integrates closely to cellular oncogenes suggests a possible molecular mechanism for the tumorigenesis induced by HBV. Two animal herpesviruses inducing Iymphoproliferative diseases, Marek's disease virus and Herpesvirus saimiri, are presented as models of lymphomas associated with the human herpesviruses, Epstein-Barr virus (EBV) , and human herpesvirus 6. Of particular interest is that the SeOL gene of Herpesvirus saimiri behaves as a viral oncogene like the LMP-l gene of EBV. Several chapters discuss the molecular mechanisms of transformation by DNA tumor viruses. Some important results have been contributed recently in this field. It was discovered that simian virus 40 (SV40) T antigen, a DNA-binding protein with pleiotropic functions, induces extensive and severe chromosomal lesions before the appearance of the transformed phenotype, suggesting that genomic damage is xi

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