[HBV and hepatocellular carcinoma].
Significant research evidence has demonstrated an association between persistent infection with hepatitis B virus (HBV) and the generation of hepatocellular carcinoma (HCC). These findings are based on epidemiologic studies, molecular studies and studies of HBV like viruses. Epidemiologically, the geographic correlation between HBV infection and HCC, serum HBsAg in patients with HCC, familial clustering of HCC, prospective studies, and pathological studies are discussed. Molecular studies of HBV, the structure of HBV DNA as related to retroviruses and integration of HBV DNA into the host DNA are demonstrated. The structure and replication of HBV are somewhat similar to those of retroviruses. The incidence of HBV DNA integration into the host chromosome of the patients with HBV infection is high. The structure of integrated HBV DNA sequences and flanking sequences was analyzed in many cases. However, none of the classical mechanisms of viral oncogenesis has thus far been demonstrated. The role of HBV in HCC is not understood at the molecular level. HBV may act as just an initiator, or HBV DNA integration may have an active role in liver cancer. The woodchuck hepatitis virus (WHV) is the most oncogenic and suitable animal model. Using this model, we show some results of our experiments.
D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000209:etiology* / Q000276:immunology; D004273:DNA, Neoplasm / Q000032:analysis; D004279:DNA, Viral / Q000235:genetics; D005796:Genes; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications; D008113:Liver Neoplasms / Q000209:etiology* / Q000276:immunology; D008114:Liver Neoplasms, Experimental / Q000209:etiology / Q000276:immunology; D051379:Mice; D008819:Mice, Nude
D004273:DNA, Neoplasm; D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens