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Review
. 2012 Dec;18(4):347-56.
doi: 10.3350/cmh.2012.18.4.347. Epub 2012 Dec 21.

Hepatitis C virus and hepatocarcinogenesis

Affiliations
Review

Hepatitis C virus and hepatocarcinogenesis

Soung Won Jeong et al. Clin Mol Hepatol. 2012 Dec.

Abstract

Hepatitis C virus (HCV) is an RNA virus that is unable to integrate into the host genome. However, its proteins interact with various host proteins and induce host responses. The oncogenic process of HCV infection is slow and insidious and probably requires multiple steps of genetic and epigenetic alterations, the activation of cellular oncogenes, the inactivation of tumor suppressor genes, and dysregulation of multiple signal transduction pathways. Stellate cells may transdifferentiate into progenitor cells and possibly be linked to the development of hepatocellular carcinoma (HCC). Viral proteins also have been implicated in several cellular signal transduction pathways that affect cell survival, proliferation, migration and transformation. Current advances in gene expression profile and selective messenger RNA analysis have improved approach to the pathogenesis of HCC. The heterogeneity of genetic events observed in HCV-related HCCs has suggested that complex mechanisms underlie malignant transformation induced by HCV infection. Considering the complexity and heterogeneity of HCCs of both etiological and genetic aspects, further molecular classification is required and an understanding of these molecular complexities may provide the opportunity for effective chemoprevention and personalized therapy for HCV-related HCC patients in the future. In this review, we summarize the current knowledge of the mechanisms of hepatocarcinogenesis induced by HCV infection.

Keywords: Hepatitis C virus; Hepatocellular carcinoma; Molecular.

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Conflict of interest statement

The authors have no conflicts to disclose.

Figures

Figure 1
Figure 1
Cellular signaling pathways implicated in hepatitis C virus (HCV) core protein-related hepatocarcinogenesis. Blue boxes indicate key driving forces for carciniogenesis.
Figure 2
Figure 2
Hepatitis C virus and hepatocarcinogenesis.

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