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World J Gastroenterol. May 28, 2014; 20(20): 6236-6243
Published online May 28, 2014. doi: 10.3748/wjg.v20.i20.6236
Published online May 28, 2014. doi: 10.3748/wjg.v20.i20.6236
Role of hepatitis B virus DNA integration in human hepatocarcinogenesis
Hoang Hai, Akihiro Tamori, Norifumi Kawada, Department of Hepatology, Osaka City University Graduate School of Medicine, Osaka 5458585, Japan
Author contributions: Hai H wrote the manuscript; Tamori A and Kawada N revised the manuscript.
Correspondence to: Akihiro Tamori, MD, PhD, Associate Professor, Department of Hepatology, Osaka City University Graduate School of Medicine, 1-4-3, Asahimachi, Abeno-ku, Osaka 5458585, Japan. atamori@med.osaka-cu.ac.jp
Telephone: +81-6-66453811 Fax: +81-6-66461433
Received: November 2, 2013
Revised: December 14, 2013
Accepted: January 14, 2014
Published online: May 28, 2014
Revised: December 14, 2013
Accepted: January 14, 2014
Published online: May 28, 2014
Core Tip
Core tip: A high viral load is associated with an elevated risk of hepatocellular carcinoma (HCC), and the risk remains increased in hepatitis B surface antigen-negative hepatitis B virus (HBV) and occult infections. The ability of HBV to integrate into the infected host’s hepatocyte genome is one of the most important direct pro-oncogenic properties. The recent development of efficient tools for genome-wide analysis of gene expression and genetic defects has allowed a comprehensive overview of the changes occurring with HCC. Specific HBV features, including the integration of viral DNA into host chromosomes, may trigger increased genetic instability.