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Annals of Clinical & Laboratory Science 33:39-54 (2003)
© 2003 Association of Clinical Scientists

Review

Hepatocellular Carcinoma and Hepatitis Virus

Richard B. Birrer1, Danielle Birrer1 and John V. Klavins2
1 St. Joseph’s Regional Medical Center, Paterson, New Jersey, and
2 Department of Pathology, Albert Einstein College of Medicine, New York City, New York

Address correspondence to Richard B. Birrer, M.D., St Joseph’s Regional Medical Center, 703 Main Street, Patterson, NJ 07503, USA; tel 973 754 4366; fax 973 754 2044; e-mail birrerr{at}sjhmc.org.

Integrated hepatitis B virus (HBV) DNA is present in many hepatocellular carcinomas (HCC), suggesting that HBV has a direct oncogenic effect through interaction with transformation-associated genes. Many genes involved in cell cycle regulation (cyclins, kinases, negative regulators, Wntbeta-catenin) and the transcriptome profile are deregulated or altered in most HCC patients. The HBx protein, potentially oncogenic via multistep carcinogenesis, modifies apoptosis, inhibits nucleotide excision and repair of damaged cellular DNA, and modulates transcriptional activation of cellular growth regulating genes. Hepatocyte transformation may be indirectly influenced by HBV DNA integration, by the generation of mutagenic oxygen reactive species, or by acquisition of mutations in association with necroinflammatory disease. HBV replication, which may occur in HCC, affects the long-term survival of patients. Prevention of HBV infection is expected to decrease the incidence of endemic HCC.

Keywords: hepatitis B virus, hepatocellular carcinoma




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