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Review
. 2010 Apr 22;29(16):2309-24.
doi: 10.1038/onc.2010.36. Epub 2010 Mar 15.

Viral hepatocarcinogenesis

W-L Tsai  1 , R T Chung
Affiliations
Review

Viral hepatocarcinogenesis

W-L Tsai et al. Oncogene. .

Abstract

Hepatocellular carcinoma (HCC) is the fifth most common cancer and the third leading cause of cancer death worldwide. Despite recent advances in the diagnosis and treatment of HCC, its prognosis remains dismal. Infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) are the major risk factors for HCC. Although both are hepatotropic viral infections, there are important differences between the oncogenic mechanisms of these two viruses. In addition to the oncogenic potential of its viral proteins, HBV, as a DNA virus, can integrate into host DNA and directly transform hepatocytes. In contrast, HCV, an RNA virus, is unable to integrate into the host genome, and viral protein expression has a more critical function in hepatocarcinogenesis. Both HBV and HCV proteins have been implicated in disrupting cellular signal transduction pathways that lead to unchecked cell growth. Most HCC develops in the cirrhotic liver, but the linkage between cirrhosis and HCC is likely multifactorial. In this review, we summarize current knowledge regarding the pathogenetic mechanisms of viral HCC.

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Figures

Figure 1
Figure 1
Cellular signaling pathways implicated in hepatitis B virus (HBV) X protein-related hepatocarcinogenesis. Bolded boxes indicate key driving forces for carcinogenesis.
Figure 2
Figure 2
Cellular signaling pathways implicated in hepatitis C virus (HCV) core protein-related hepatocarcinogenesis. Bolded boxes indicate key driving forces for carcinogenesis.
Figure 3
Figure 3
A unified model of viral hepatocarcinogenesis.
See this image and copyright information in PMC

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