HUMAN LIVER CARCINOGENESIS

B型和C型肝炎病毒协同作为肝细胞因子 癌（HCC）。 我们继续在高肝癌患者中进行分子流行病学研究， 中国启东市的风险地理区域。 和我们的老同事 孙宗堂，HBV和HCV具有累加效应的假说 在肝细胞癌发生中的作用正在测试中。 我们最近 分析了我们的病例对照研究的数据，涉及112例组织学 证实的HCC病例和225名年龄和性别匹配的对照。 的 结果与我们的假设一致。 值得注意的是， 启东市居民年龄调整的肝癌年死亡率 慢性HBV和HCV携带者估计为7%。 B型肝炎病毒与DNA修复。 我们和其他人以前曾报道过p53可以调节核苷酸水平， 切除修复 使用宿主再活化试验，我们的初步数据 表明HBx抑制再活化，即，修复 紫外线（UV-C，254 nm）损伤质粒。 这导致 HBx抑制p53与XPB或XPD DNA解旋酶结合的假说 在基础转录核苷酸切除修复复合物，TFIIH。 我们以前已经证明HBx蛋白在体外抑制p53 与XPB绑定。 然而，HBx不与XPB结合，HBx与XPB结合。 p53的羧基末端，也是XPB结合的位点。 我们 目前正在研究HBx与其他成员结合的假设， TFIIH多蛋白复合物的一部分。

Hepatitis B and C Viruses Cooperate as Factors of Hepatocellular Carcinoma (HCC). We continue to conduct molecular epidemiology studies in the high HCC risk geographic area in Qidong, China. With our longstanding coworker Zong-tang Sun, the hypothesis that HBV and HCV have additive effects in hepatocellular carcinogenesis is being tested. We have recently analyzed data from our case-control study involving 112 histologically proven HCC cases, and 225 age- and gender-matched controls. The results are consistent with our hypothesis. Remarkably, the age-adjusted annual HCC mortality rate for Qidong residents with chronic HBV and HCV carriers is estimated to be 7%. Hepatitis B Virus and DNA Repair. We and others have previously reported that p53 can modulate nucleotide excision repair. Using a host reactivation assay, our preliminary data indicate that HBx inhibits reactivation, i.e., repair of the ultraviolet light (UV-C, 254 nm) damage plasmid. This leads to the hypothesis that HBx inhibits p53 binding to XPB or XPD DNA helicases in the basal transcription-nucleotide excision repair complex, TFIIH. We have previously demonstrated that HBx protein inhibits in vitro p53 binding to XPB. Whereas, HBx did not bind to XPB, HBx does bind to the carboxyl terminus of p53 which also is the site of XPB binding. We are currently investigating the hypothesis that HBx binds to other members of the TFIIH multiprotein complex.