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人肝癌中p16和CDK4基因的遗传变异及其与HBV感染之间的关系
http://www.100md.com 《中华消化杂志》 1999年第1期
癌,肝细胞|基因|乙型肝炎病毒,关键词:
人肝癌中p16和CDK4基因的遗传变异及其与HBV感染之间的关系
人肝癌中p16和CDK4基因的遗传变异及其与HBV感染之间的关系

     王辉云 严瑞琪 吴秋良 龙江斌 梁启万 510060 广州,中山医科大学肿瘤防治中心肿瘤研究所(王辉云,严瑞琪,龙江斌,梁启万),肿瘤医院病理科(吴秋良) 中华消化杂志 1999 0 19 1


    关键词:癌,肝细胞;基因;乙型肝炎病毒 期刊 zhxhzz 0 论著 fur -->


    

【摘要】 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。

The genetic alteration of p16 and CDK4 genes and their relations to HBV infection in human hepatocellular carcinoma

    
WANG Huiyun,YAN Ruiqi,WU Qiuliang,et al.

    
Cancer Institute,Cancer Center,Sun Yat-Sen University of Medical Sciences,Guangzhou,
510060

Abstract Objective To explore the genetic alterations of the tumor suppressor gene p16 and oncogene CDK4,as well as their relations to HBV infection during the developmental process of human hepatocellular carcinoma (HCC).Methods 40 cases of fresh paired tumor and nontumor liver tissues obtained from surgical resections were used for genetic analysis of p16,CDK4 and HBV DNA with Southern blot and hybridization. These samples were also examined histologically.Results The homozygous deletions of p16 gene were detected in 4 of 36 cases and hemizygous deletions in another 3 cases. The frequency of p16 deletion was 19.4%.About one-third of p16 deletion was found in HCCs with tumor size < 5cm.The deletion of p16 was not correlated with the integration of HBV DNA.CDK4 amplifications were detected in 5 of 37 cases (13.2%),and the gene amplifications and p16 deletions did not appear in the same case. All of the cases with CDK4 amplifications were detected in the HCCs with HBV-DNA integration. The majority of amplifications were observed in HCCs with poorer differentiation, higher index of mitosis and larger size.Conclusion p16 deletion might play certain important role in a subset of HCCs and didn t correlate with the HBV DNA integration;CDK4 amplification could be correlated with HBV DNA integration and the progression of HCC.

    
Key words Carcinoma,hepatocellular Gene Hepatitis B virus

    


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