肝细胞肝癌细胞p53基因第2～3,4,11外显子纯合性缺失、杂合性缺失的分析

Homozygous deletion and loss of heterozygosity of p53 gene exon 2～3, 4 and 11 in human hepatocellular carcinoma

目的 研究非高发区肝细胞癌 (HCC) p5 3基因外显子 2～ 3、4和 11的纯合性、杂合性缺失 (L OH)。方法 应用 PCR为基础的微卫星多态性分析技术。结果 2 0例 HCC标本中 p5 3基因外显子 2～ 3(TP5 3.A )、外显子 4 (TP5 3.B)、外显子 11(TP5 3.G)纯合性缺失率分别为 0 %、30 %、10 % ;p5 3基因外显子 2～ 3(TP5 3.A)、外显子 4 (TP5 3.B)、外显子 11(TP5 3.G)杂合性缺失率分别为 2 0 %、30 %、0 %。 p5 3基因的缺失率与 HCC病理分级高低之间的差异无统计学意义。结论 以上结果提示 :p5 3基因第 4外显子的纯合性缺失及杂合性缺失在本组肝细胞癌的发生中可能起重要作用 ,而第 11、2～

Objective To analyze the homozygous deletion and the loss of heterozygosity (LOH) on p53 gene (exon2～3, 4 and 11) in human hepatocellular carcinoma (HCC) in non HCC prevalent area. Methods PCR-based microsatellite polymorphism analysis technique was used. Results The rates of homozygous deletion were as follows: 0% at TP53.A (exon 2～3), 30% at TP53.B (exon 4), 10% at TP53.G (exon 11); the rates of LOH at 20 cases were as follows: 20% at TP53.A, 30% at TP53.B and none at TP53.G. No significant relationship was found between the deletion and the pathological grade of HCC. Conclusions Homozygous deletion and/or LOH of p53 exon 4 may play an important role in the carcinogenesis of HCC, but the deletion of p53 exon11 and 2～3 may not play a major role in the pathogenesis of HCC in non HCC prevalent area.