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粘蛋白MUC1 568A/G SNP与辽宁地区人群胃癌遗传易感性的关系
引用本文:徐倩,孙丽萍,宫月华,徐莹,董楠楠,袁媛.粘蛋白MUC1 568A/G SNP与辽宁地区人群胃癌遗传易感性的关系[J].遗传,2008,30(9):1163-1168.
作者姓名:徐倩  孙丽萍  宫月华  徐莹  董楠楠  袁媛
作者单位:中国医科大学附属第一医院肿瘤研究所第三研究室暨普通外科研究所肿瘤病因与预防实验室,沈阳,110001
摘    要:为了探讨粘蛋白(MUC1)基因568位点A/G单核苷酸多态性与胃癌遗传易感性的关系, 采用序列特异性引物-聚合酶链反应(Sequence specific primers PCR, PCR-SSPs)检测来自辽宁地区人群138例胃癌患者及与其配比的131例对照个体MUC1 568 位点A/G多态性, 以ELISA法检测血清H. pylori IgG抗体。结果显示:(1)对照人群MUC1基因568位点AA、AG、GG 3种基因型分布频率分别为73.3%、22.1%、4.6%; (2)胃癌组MUC1 AA基因型携带频率显著高于正常对照组(P=0.03), 携带MUC1 AA基因型个体胃癌的发病风险增高到1.92倍; (3)以MUC1 AG+GG基因型并血清幽门螺杆菌(H. pylori)IgG抗体阴性的个体为对照, AG+GG基因型并H. pylori IgG抗体阳性个体、AA基因型并H. pylori IgG抗体阴性个体、AA基因型并H. pylori IgG抗体阳性个体胃癌患病风险增高, 但3组各组间差异均无统计学意义(P>0.05)。说明MUC1基因568位点A/G多态与胃癌的遗传易感性相关; MUC1 A/G基因多态性和H. pylori感染在胃癌发生发展过程未见交互作用。

关 键 词:基因多态性  粘蛋白MUC1  胃癌  幽门螺杆菌
收稿时间:2007-12-25
修稿时间:2008-02-19

The relationship between the polymorphism of MUC1 and suscepti-bility to gastric cancer in Liaoning region
XU Qian,SUN Li-Ping,GONG Yue-Hua,XU Ying,DONG Nan-Nan,YUAN Yuan.The relationship between the polymorphism of MUC1 and suscepti-bility to gastric cancer in Liaoning region[J].Hereditas,2008,30(9):1163-1168.
Authors:XU Qian  SUN Li-Ping  GONG Yue-Hua  XU Ying  DONG Nan-Nan  YUAN Yuan
Institution:Cancer Control Laboratory of Cancer Institute and General Surgery Institute, the First Affiliated Hospital of China Medical University, Shenyang 110001, China E-mail: xuqian820101@163.com.
Abstract:Analyzed the relationship between 568 site A/G polymorphism in mucin 1(MUC1) gene in a population from Liaoning Province and susceptibility to gastric cancer. Sequence specific primers-polymerase chain reaction(PCR-SSPs) were performed to analyze the genotype of the A/G polymorphism in its 568 site of exon 2 for 138 gastric cancer cases and 131 normal ones tested, and ELISA was performed to test IgG antibody of H. pylori. We found that the distribution frequency of AA, AG, GG three genotypes were 73.3%, 22.1%, 4.6%, respectively. The frequency of AA genotype was statistically higher in the gastric cancer (GC) group compared to the control group(P=0.03), moreover, individuals with the MUC1 AA genotype increased 1.92 fold risk for gastric cancer. And compared with subjects carrying both AG+GG genotype and H. pylori-IgG negative, there was an obviously increased risk of developing gastric cancer for those who carried both AA genotype and H. pylori-IgG negative, both AG+GG genotype and H. pylori-IgG positive, and both AG+GG genotype and H. pylori-IgG negative, but there were no significantly differences between the every two of the latter three. Our results in-dicated that there was a relationship between MUC1 A/G polymorphism and susceptibility to gastric cancer. And there were probably no statistically interaction between the 568 site A/G polymorphism in MUC1 and H. pylori infection in the occur-rence and development process of gastric cancer.
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