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作 者:徐倩[1] 孙丽萍[1] 宫月华[1] 徐莹[1] 董楠楠[1] 袁媛[1]
机构地区:[1]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
出 处:《遗传》2008年第9期1163-1168,共6页Hereditas(Beijing)
基 金:国家自然科学基金(编号:30572131)资助~~
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MUC1568位点A/G多态性,以ELISA法检测血清H.pyloriIgG抗体。结果显示:(1)对照人群MUC1基因568位点AA、AG、GG3种基因型分布频率分别为73.3%、22.1%、4.6%;(2)胃癌组MUC1AA基因型携带频率显著高于正常对照组(P=0.03),携带MUC1AA基因型个体胃癌的发病风险增高到1.92倍;(3)以MUC1AG+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.pyloriIgG抗体阳性个体、AA基因型并H.pyloriIgG抗体阴性个体、AA基因型并H.pyloriIgG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;MUC1A/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。Analyzed the relationship between 568 site A/G polymorphism in mucin I(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 fre- quency of AA, AG, GG three genotypes were 73.3%, 22.1%, 4.6%, respectively. The frequency of AA genotype was statis- tically 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 geno- type 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 geno- type and H. pylori-IgG negative, but there were no significantly differences between the every two of the latter three. Our results indicated 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 occurrence and development process of gastric cancer.
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