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Vol. 30, No. 5, 2012
Issue release date: October 2012
Section title: Viral Hepatitis
Dig Dis 2012;30:445–452
(DOI:10.1159/000341688)

Promotion of Hepatocellular Carcinoma by Hepatitis C Virus

Bühler S. · Bartenschlager R.
Department of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany

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Article / Publication Details

First-Page Preview
Abstract of Viral Hepatitis

Published online: 10/24/2012

Number of Print Pages: 8
Number of Figures: 2
Number of Tables: 1

ISSN: 0257-2753 (Print)
eISSN: 1421-9875 (Online)

For additional information: http://www.karger.com/DDI

Abstract

Persistent infection with the hepatitis C virus (HCV) is a major global health problem. Around 2–3% of the world’s population are chronically infected, and infected individuals are at high risk of developing steatosis, fibrosis, and liver cirrhosis. The latter is a major predisposing factor for the development of hepatocellular carcinoma (HCC). It is generally accepted that an inflammatory response triggered by persistent HCV infection leads to increased cell proliferation and fibrogenesis that in turn promotes cirrhosis and ultimately HCC development. This indirect mechanism of tumor induction would explain the long incubation period from primary HCV infection to HCC and the requirement for additional cofactors such as toxins or drugs (most notably alcohol), metabolic liver diseases, steatosis, nonalcoholic liver disease, or diabetes. With the advent of adequate cell culture systems for HCV it is, however, becoming increasingly clear that the virus also contributes directly to HCC formation. Examples are the continuous induction of stress response or the massive accumulation of intracellular lipids. Moreover, viral proteins can bind to and sequester cell cycle control factors such as the retinoblastoma protein or the tumor suppressor DDX3. Thus, HCV-associated liver cancer is most likely promoted by the combined action of long-term chronic inflammation and targeted perturbations of cellular key pathways involved in metabolic homeostasis as well as cell cycle control.


Article / Publication Details

First-Page Preview
Abstract of Viral Hepatitis

Published online: 10/24/2012

Number of Print Pages: 8
Number of Figures: 2
Number of Tables: 1

ISSN: 0257-2753 (Print)
eISSN: 1421-9875 (Online)

For additional information: http://www.karger.com/DDI


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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