期刊
HEPATOLOGY
卷 45, 期 1, 页码 16-21出版社
WILEY
DOI: 10.1002/hep.21445
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资金
- NCI NIH HHS [R01CA055578] Funding Source: Medline
- NCRR NIH HHS [R21RR027812] Funding Source: Medline
- NIDDK NIH HHS [P30DK026743] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA055578] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK026743] Funding Source: NIH RePORTER
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.
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