肝细胞癌基因P53异常的研究

Structural abnormalities of the p53 tumour suppressor gene in hepatocellular carcinoma

目的：分析我国重庆地区肝细胞癌Ｐ５３基因失活机制及突变谱。方法：采用ＰＣＲ—ＲＦＬＰＰＣＲＳＳＣＰ和ＰＣＲ直接测序技术对来自我国重庆地区２８例肝细胞癌Ｐ５３抑癌基因结构异常进行了分析。结果：６１．５１％的肝癌存在ｐ５３的杂合缺失：５０％肝癌伴有ｐ５３基因突变，其突变模式为突普通散在于５６７和８外显子，其中第７外显子２４９们密友情子突弯率最高（２１％）；具有突变的肝癌多同时伴夺缺失。伴有ｐ５３基因结构异常的肝癌均属进展期。结论：我国重庆地区肝癌存在Ｐ５３基因结构异常，Ｐ５３基因结构异常，ｐ５３基因突变模式反映了该地区肝癌发生可能与肝炎病互和黄贡互素两种因素及其相互作用有关；ｐ５３基因结构异常属肝癌晚期事件，可能参加与肝癌的进展过程。

Objective: to the mechanism of p53 gene inactivation and its mutationspectrum. Methods: PCR-RFLP< PCR-SSCP and PCR direct sequencing have been used to detect the mutation and deletion of P53 gene were found respectively The nutationscattered overexon5 6 7 and 8,but mutation rate is highest at codon 249 Mostof the HCC from Chongqing may be related to HBV AND AFB1,both deletion and nutationparticipate in inactivation of p53gene,and aberration of p53 gene is a late event in HCC,which may contribute to progression of HCC.