hMLH1-93G>A启动子多态性与胃癌发生风险的研究

目的:探讨碱基错配修复(mismatch repair,MMR)基因hMLH1启动子多态性位点-93G>A与中国江苏人群胃癌发生风险的关联性?方法:以554例胃癌患者和582例年龄(±5岁)?性别相匹配的非胃癌患者(对照组)作为研究对象,用 TaqMan MGB(minor grove binder)探针对hMLH1-93G>A多态性进行基因分型,分析不同基因型与胃癌发生风险的关联性?通过分层分析探讨不同基因型与胃癌临床病理特征之间的关联性?结果:hMLH1-93G>A的突变型GA和AA基因型频率在病例组和对照组的分布无显著关联性,病例组:GA 262例(47.3%),AA 187例(33.8%);对照组:GA 269例(46.2%),AA 190例(32.7%);P值分别为0.636和0.398,合并突变基因型GA+AA与野生型GG相比并不显著增加胃癌的发生风险(调整OR=1.11,95%CI=0.82~1.51,P=0.487)?不同基因型与胃癌临床病理特征之间亦无显著关联性?结论:hMLH1基因-93G>A多态性与胃癌发生风险无显著关联?

The association between hMLH1-93G>A promoter polymorphism and risk of gastric cancer

Objective:To evaluate the association between the mismatch repair gene hMLH1-93G>A promoter polymorphism and risk of gastric cancer in a population of Jiangsu province in China. Methods:Total of 554 patients with gastric cancer cases and 582 cancer-free controls frequency-matched by age(±5)and sex were recruited in the study. The genotypes of the hMLH1-93G>A polymorphism were detected by TaqMan MGB probe method. We further assessed its association with risk of gastric cancer and interaction with tumor clinic pathological characteristics. Results:There was no significant association of the frequencies of GA or AA among the case and control groups,for case group:GA 262(47.3%),AA 187(33.8%); for control group:GA 269(46.2%),AA 190(32.7%);P=0.636 and 0.398,respectively. The variant genotypes(GA+AA) did not significantly increase the risk of gastric cancer,compared with the GG genotypeadjusted odds ratio(OR)=1.11,95% confidence interval(CI)=0.82~1.51,P=0.487]. No significant association was observed between the variant genotypes of the hMLH1-93G>A polymorphism and the clinic pathological characteristics in gastric cancer. Conclusion:There was no significant association between the hMLH1-93G>A polymorphism and gastric cancer susceptibility.