Review
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World J Gastroenterol. Nov 28, 2011; 17(44): 4853-4857
Published online Nov 28, 2011. doi: 10.3748/wjg.v17.i44.4853
Hepatitis B virus infection and the risk of hepatocellular carcinoma
Ya-Jun Tan
Ya-Jun Tan, Department of Laboratory Medicine, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China
Author contributions: Tan YJ wrote the paper.
Correspondence to: Ya-Jun Tan, MS, Department of Laboratory Medicine, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China. tyj7713@163.com
Telephone: +86-571-87236383 Fax: +86-571-87236383
Received: March 20, 2011
Revised: July 6, 2011
Accepted: July 13, 2011
Published online: November 28, 2011
Abstract

Epidemiological studies have provided overwhelming evidence for a causal role of chronic hepatitis B virus (HBV) infection in the development of hepatocellular carcinoma (HCC). However, the pathogenesis of HBV infection and carcinogenesis of HBV-associated HCC are still elusive. This review will summarize the current knowledge on the mechanisms involved in HBV-related liver carcinogenesis. The role of HBV in tumor formation appears to be complex, and may involve both direct and indirect mechanisms. Integration of HBV DNA into the host genome occurs at early steps of clonal tumor expansion, and it has been shown to enhance the host chromosomal instability, leading to large inverted duplications, deletions and chromosomal translocations. It has been shown that the rate of chromosomal alterations is increased significantly in HBV-related tumors. Prolonged expression of the viral regulatory HBV x protein may contribute to regulating cellular transcription, protein degradation, proliferation, and apoptotic signaling pathways, and it plays a critical role in the development of hepatocellular carcinoma.

Keywords: Hepatocellular carcinoma; Hepatitis B virus infection; Hepatitis B virus genotypic variations; Hepatitis B virus x protein