原发性肝癌染色体17P微卫星不稳定性及突变型P53蛋白的表达

目的　探讨微卫星不稳定性 (microsatelliteinstability ,MSI)及突变型P5 3蛋白在原发性肝癌 (hepatocellularcarci noma ,HCC)发生中的作用。方法　采用PCR为基础的方法及免疫组织化学技术检测了 48例手术切除肝癌标本染色体17P的MSI及突变型P5 3蛋白的表达。结果　肝癌MSI总阳性率为 8.3 %( 4 /4 8) ,突变型P5 3蛋白表达阳性率为 3 9.6%( 19/4 8) ,MSI在肝癌的不同发病年龄、性别 ,是否伴有肝硬化、血清HBsAg和AFP是否阳性及是否存在突变型P5 3蛋白的表达组无显著差异 (P >0 0 5 ) ,但AFP阳性肝癌突变型P5 3蛋白的表达阳性率明显高于AFP阴性肝癌 (P <0 0 1)。结论　MSI与大多数HCC发生无关 ,HCC中p5 3基因突变的致癌机制不是通过MSI病理途径。

Microsatellite instability of chromosome 17p and mutant P53 protein expression in hepatocellular carcinoma

Objective To evaluate the effects of microsatellite instability (MSI) and mutant P53 protein expression on the carcinogenesis of hepatocellular carcinoma (HCC). Methods MSI and mutant P53 protein expression in 48 surgical specimens of HCC were detected by using PCR based method and immunohistochemical method. Results MSI was detected in 4 (8 3%) specimens of HCC. Of the 48 specimens of HCC, 19 (39.6%) were positive for mutant P53. MSI was not associated with sex, age, liver cirrhosis, HBsAg, AFP of HCC, and mutant P53 protein expression ( P >0 05). However, P53 positive rate in AFP positive HCC was significantly higher than that in AFP negative HCC ( P <0 01). Conclusion MSI may not be involved in the genesis of HCC, and the carcinogenic mechanism of p53 gene mutation in most of the HCCs may not be realized through the pathological pathway of MSI.