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目的探讨抑癌基因p16和癌基因CDK4的遗传变异在人肝癌发生发展中的作用及其相互关系以及与HBV感染之间的关系。方法取手术切除的肝癌标本,用Southern杂交法对p16和CDK4基因以及HBV的状态进行检测,同时切片行病理检查。结果36例肝癌中4例有p16纯合性缺失,3例半合子丢失,总丢失率为19.4%,其中约1/3的p16丢失发生在肿瘤小于5cm的肝癌;在有HBV-DNA整合和无整合的病例中,p16的丢失率差异无显著性。37例肝癌中5例(13.2%)发生CDK4扩增,与p16的丢失无重叠;CDK4的扩增全部发生在有HBV整合的肝癌中。结论p16的丢失在部分肝癌的发生发展中起着一定的作用,但与HBV-DNA的整合无关;CDK4的扩增可能与HBV-DNA的整合以及肝癌的进展有关。
Objective To investigate the role of genetic variation of tumor suppressor gene p16 and oncogene CDK4 in the development of human hepatocellular carcinoma, their relationship and their relationship with HBV infection. Methods The specimens of surgically resected liver cancer were used to detect the status of p16 and CDK4 genes and HBV by Southern hybridization. Results Of the 36 patients with hepatocellular carcinoma, 4 were homozygous for p16, 3 were hemizygous for loss, and the total loss rate was 19.4%. About 1/3 of p16 loss occurred in liver cancer with tumor less than 5 cm; there was HBV-DNA. There was no significant difference in the loss rate of p16 in cases with and without integration. CDK4 amplification occurred in 5 cases (13.2%) of 37 cases of hepatocellular carcinoma, and there was no overlap with loss of p16; amplification of CDK4 occurred in liver cancer with HBV integration. Conclusion The loss of p16 may play a role in the development of some hepatocellular carcinomas, but it is not related to the integration of HBV-DNA. The amplification of CDK4 may be related to the integration of HBV-DNA and the progression of liver cancer.