Hepatitis B virus infection and primary hepatocellular carcinoma.
For many years, epidemiological studies have demonstrated a strong link between chronic hepatitis B virus (HBV) infection and the development of primary hepatocellular carcinoma (PHC). Other hepatocarcinogens such as hepatitis C virus and aflatoxin also contribute to hepatocarcinogenesis either in conjunction with HBV infection or alone. Cellular and molecular biological studies are providing explanations for the HBV-PHC relationship, and models are now being formulated to further test the relative importance of various factors such as viral DNA integration, activation of oncogenes, genetic instability, loss of tumor suppressor genes, and trans-activating properties of HBV to the pathogenesis of PHC. Further research will probably define more than a single mechanism whereby chronic HBV infection results in PHC.
Feitelson
M
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Department of Pathology and Cell Biology, Jefferson Medical School, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
D006528:Carcinoma, Hepatocellular / Q000209:etiology*; D005260:Female; D015870:Gene Expression; D015321:Gene Rearrangement; D016147:Genes, Tumor Suppressor; D006509:Hepatitis B / Q000150:complications*; D006515:Hepatitis B virus / Q000235:genetics; D006801:Humans; D008113:Liver Neoplasms / Q000209:etiology*; D008242:Lysogeny; D008297:Male; D009857:Oncogenes