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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.