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Hepatitis B virus promotes hepatocarcinogenesis in transgenic mice
Author(s) -
Zheng Yanyan,
Chen Wenling,
Louie Stan G.,
Yen T. S. Benedict,
Ou Jinghsiung James
Publication year - 2007
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.21445
Subject(s) - hepatocellular carcinoma , hepatitis b virus , carcinogen , genetically modified mouse , transgene , virus , inflammation , cancer research , medicine , hepadnaviridae , liver cancer , virology , immunology , biology , gene , genetics
HBV is a major risk factor for hepatocellular carcinoma (HCC). However, whether HBV can directly cause HCC or only indirectly via the induction of chronic liver inflammation has been controversial. By using transgenic mice carrying the entire HBV genome as a model, we now demonstrate that HBV by itself is an inefficient carcinogen. However, it can efficiently promote hepatocarcinogenesis initiated by the carcinogen diethylnitrosamine (DEN). This effect of HBV does not involve chronic liver inflammation, is apparently due to enhanced hepatocellular apoptosis and compensatory regeneration following DEN treatment, and does not require the HBV X protein. Conclusion : Our results demonstrate a direct role of HBV in a hepatocarcinogenesis pathway that involves the interaction between this virus and a dietary carcinogen. (H EPATOLOGY 2007;45:16–21.)