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DNA Tumor Viruses: Oncogenic Mechanisms 1995 Edition
Contributor(s): Barbanti-Brodano, Giuseppe (Editor), Bendinelli, Mauro (Editor), Friedman, Herman (Editor)

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ISBN: 0306451514     ISBN-13: 9780306451515
Publisher: Springer
OUR PRICE: $208.99  

Binding Type: Hardcover - See All Available Formats & Editions
Published: January 1996
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Annotation: This single reference on DNA tumor viruses in animal models and humans presents the latest studies on mechanisms of virus transformation, their association with human tumors, and the possibility of prevention and control by vaccination. Chapters provide current information on the epidemiology and pathogenesis of virus-induced tumors and offer insights into future prospects of immunological intervention. Biomedical researchers, clinicians, and virologists will benefit from this key resource.

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Additional Information
BISAC Categories:
- Medical | Oncology - General
- Medical | Microbiology
- Science | Life Sciences - Botany
Dewey: 571.31
LCCN: 95042518
Series: Plenum Series in Social/Clinical Psychology
Physical Information: 1.19" H x 6" W x 9" L (1.86 lbs) 428 pages
Themes:
- Topical - Ecology
Features: Bibliography, Illustrated, Index
 
Descriptions, Reviews, Etc.
Publisher Description:
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.
 
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