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Review
. 2011 Jun 28;305(2):123-43.
doi: 10.1016/j.canlet.2010.11.014. Epub 2010 Dec 18.

Hepatitis B and C virus hepatocarcinogenesis: lessons learned and future challenges

Michael J Bouchard  1 , Sonia Navas-Martin
Affiliations
Review

Hepatitis B and C virus hepatocarcinogenesis: lessons learned and future challenges

Michael J Bouchard et al. Cancer Lett. .

Abstract

Worldwide, hepatocellular carcinoma (HCC) is one of the most common cancers. It is thought that 80% of hepatocellular carcinomas are linked to chronic infections with the hepatitis B (HBV) or hepatitis C (HCV) viruses. Chronic HBV and HCV infections can alter hepatocyte physiology in similar ways and may utilize similar mechanisms to influence the development of HCC. There has been significant progress towards understanding the molecular biology of HBV and HCV and identifying the cellular signal transduction pathways that are altered by HBV and HCV infections. Although the precise molecular mechanisms that link HBV and HCV infections to the development of HCC are not entirely understood, there is considerable evidence that both inflammatory responses to infections with these viruses, and associated destruction and regeneration of hepatocytes, as well as activities of HBV- or HCV-encoded proteins, contribute to hepatocyte transformation. In this review, we summarize progress in defining mechanisms that may link HBV and HCV infections to the development of HCC, discuss the challenges of directly defining the processes that underlie HBV- and HCV-associated HCC, and describe areas that remain to be explored.

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Figures

Fig. 1
Fig. 1
Hepatitis B virus life cycle: See text for detailed description.
Fig. 2
Fig. 2
Hepatitis B virus genome: See text for detailed description. Inner arrows represent open reading frames. Outer arrows represent mRNAs. EN (Enhancer); DR (Direct Repeat); PC (Precore); TP (terminal protein); 1/3182 (nucleotide 1 and 3182 of circular genome).
Fig. 3
Fig. 3
Hepatitis B virus hepatocarcinogenesis: Summary of putative mechanisms that could link chronic HBV infections to the development of HCC. Circle connecting HBx activities suggests that more than one HBx activity likely contributes to HCC development. See text for details.
Fig. 4
Fig. 4
Hepatitis C virus genome organization and protein function: See text for detailed description. UTR (untranslated region).
Fig. 5
Fig. 5
Hepatitis C virus life cycle: See text for detailed description.
Fig. 6
Fig. 6
Hepatitis C virus hepatocarcinogenesis. Summary of putative mechanisms that could link chronic HCV infections to the development of HCC. See text for details
See this image and copyright information in PMC

References

    1. El-Serag HB, Rudolph KL. Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. Gastroenterology. 2007;132:2557–2576. - PubMed
    1. Wang XW, Hussain SP, Huo T, Wu CG, Forgues M, Hofseth LJ, Brechot C, Harris CC. Molecular pathogenesis of human hepatocellular carcinoma. Toxicology. 2002;181–182:43–47. - PubMed
    1. Guidotti LG, Chisari FV. Immunobiology and pathogenesis of viral hepatitis. Annu Rev Pathol. 2006;1:23–61. - PubMed
    1. Bartosch B, Thimme R, Blum HE, Zoulim F. Hepatitis C virus-induced hepatocarcinogenesis. J Hepatol. 2009;51:810–820. - PubMed
    1. Bouchard MJ, Schneider RJ. The enigmatic X gene of hepatitis B virus. J Virol. 2004;78:12725–12734. - PMC - PubMed

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