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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 analyze the inactivation mechanism and mutation spectrum of P53 gene in hepatocellular carcinoma in Chongqing, China. METHODS: The structural abnormalities of P53 tumor suppressor gene in 28 cases of hepatocellular carcinoma from Chongqing, China were analyzed by PCR-RFLP PCRSSCP and PCR-direct sequencing. Results: 61.51% of liver cancers had p53 heterozygous deletion: 55% of liver cancers were accompanied by p53 gene mutations. The mutation pattern was sudden and common in 567 and 8 exons, of which the 7th exon 249 had close friendships. The highest burst rate was found (21%); liver cancers with mutations were associated with multiple deletions. The liver cancer with abnormal p53 gene structure is in an advanced stage. Conclusion: There is an abnormal P53 gene structure in the liver cancer in Chongqing area of China. The structure of P53 gene is abnormal. The p53 gene mutation pattern reflects that the occurrence of liver cancer in this area may be related to the interaction between Hepatitis and the two factors of huanggonine and its interaction; p53 gene structure is abnormal. It is a late event of liver cancer that may participate in the progression of liver cancer.