The summaries are free for public
use. The Chronic Liver Disease
Foundation will continue to add and
archive summaries of articles deemed
relevant to CLDF by the Board of
Trustees and its Advisors.
Abstract Details
Hepatitis C Virus-Associated Cancer
Lin MV1, King LY, Chung RT. Annu Rev Pathol. 2014 Nov 5. [Epub ahead of print]
Author information
1Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA 02114; email: mvlin@mgh.harvard.edu.
Abstract
Hepatitis C virus (HCV) is one of the major etiologic agents of liver cancer. HCV is an RNA virus that, unlike hepatitis B virus, is unable to integrate into the host genome. Through complex interactions between viral and host proteins that induce host responses and promote inflammation, fibrosis, and ultimately cirrhosis, HCV infection can result in the development of hepatocellular carcinoma (HCC). The HCV oncogenic process involves genetic and epigenetic alterations and oncogenic effects mediated by viral proteins in the activation of cellular oncogenes, inactivation of tumor-suppressor genes, and dysregulation of multiple signal-transduction pathways. Advances in genetics and gene expression profiling have enhanced our current understanding of the pathways involved in HCV-associated liver cancer development. In this review, we summarize the current understanding of mechanisms of hepatocarcinogenesis induced by HCV infection. Expected final online publication date for the Annual Review of Pathology: Mechanisms of Disease Volume 10 is January 24, 2015. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.