title: Molecular mechanism of hepatitis B virus-induced hepatocarcinogenesis.
abstract: Hepatitis B virus (HBV) infection is a global public health problem with approximately 2 billion people that have been exposed to the virus. HBV is a member of a family of small, enveloped DNA viruses called hepadnaviruses, and has a preferential tropism for hepatocytes of mammals and birds. Epidemiological studies have proved a strong correlation between chronic hepatitis B virus infection and the development of hepatocellular carcinoma (HCC). HCC is the fifth most common malignancy with about 700000 new cases each year, and more than 50% of them arise in HBV carriers. A large number of studies describe the way in which HBV can contribute to HCC development. Multiple mechanisms have been proposed, including the accumulation of genetic damage due to immune-mediated hepatic inflammation and the induction of oxidative stress. There is evidence of the direct effects of the viral proteins HBx and HBs on the cell biology. Integration of HBV-DNA into the human genome is considered an early event in the carcinogenic process and can induce, through insertional mutagenesis, the alteration of gene expression and chromosomal instability. HBV has also epigenetic effects through the modification of the genomic methylation status. Furthermore, the virus plays an important role in the regulation of microRNA expression. This review will summarize the many mechanisms involved in HBV-related liver carcinogenesis.
authors.affiliation: Mirko Tarocchi, Simone Polvani, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy.
authors.forename: Mirko
authors.initials: M
authors.lastname: Tarocchi
authors.affiliation: Mirko Tarocchi, Simone Polvani, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy.
authors.forename: Simone
authors.initials: S
authors.lastname: Polvani
authors.affiliation: Mirko Tarocchi, Simone Polvani, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy.
authors.forename: Giada
authors.initials: G
authors.lastname: Marroncini
authors.affiliation: Mirko Tarocchi, Simone Polvani, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy.
authors.forename: Andrea
authors.initials: A
authors.lastname: Galli
mesh_terms: D000818:Animals; D000998:Antiviral Agents / Q000627:therapeutic use; D006528:Carcinoma, Hepatocellular / Q000453:epidemiology / Q000276:immunology / Q000517:prevention & control / Q000821:virology*; D002472:Cell Transformation, Viral; D006509:Hepatitis B / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology / Q000821:virology*; D006515:Hepatitis B virus / Q000187:drug effects / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D008113:Liver Neoplasms / Q000453:epidemiology / Q000276:immunology / Q000473:pathology / Q000517:prevention & control / Q000821:virology*
chemical_list: D000998:Antiviral Agents
keywords: Cell biology; Chronic hepatitis B infection; Hepatitis B Virus; Hepatocarcinogenesis; Hepatocellular carcinoma