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Glutathione S-transferase M1 polymorphism and esophagealcancer risk:An updated meta-analysis based on 37 studies 被引量:4
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作者 Quan-Jun Lu Ya-Cong Bo +7 位作者 Yan Zhao Er-Jiang Zhao Wolde Bekalo Sapa Ming-Jie Yao Dan-Dan Duan Yi-Wei Zhu Wei-Quan Lu Ling Yuan 《World Journal of Gastroenterology》 SCIE CAS 2016年第5期1911-1918,共8页
AIM: To evaluate the relationship between glutathione S-transferase M1(GSTM1) polymorphism and susceptibility to esophageal cancer(EC).METHODS: A comprehensive search of the United States National Library of Medicine ... AIM: To evaluate the relationship between glutathione S-transferase M1(GSTM1) polymorphism and susceptibility to esophageal cancer(EC).METHODS: A comprehensive search of the United States National Library of Medicine Pub Med database and the Elsevier, Springer, and China National Knowledge Infrastructure databases for all relevant studies was conducted using combinations of the following terms: "glutathione S-transferase M1", "GSTM1", "polymorphism", and "EC"(until November 1, 2014). The statistical analysis was performed using the SAS software(v.9.1.3; SAS Institute, Cary, NC, United States) and the Review Manager software(v.5.0; Oxford, England); crude odds ratios(ORs) with 95% confidence intervals(CIs) were used to assess the association between the GSTM1 null genotype and the risk of EC.RESULTS: A total of 37 studies involving 2236 EC cases and 3243 controls were included in this metaanalysis. We observed that the GSTM1 null genotype was a significant risk factor for EC in most populations(OR = 1.33, 95%CI: 1.12-1.57, P_(heterogeneity) < 0.000001, and I2 = 77.0%), particularly in the Asian population(OR = 1.53, 95%CI: 1.26-1.86, P_(heterogeneity)< 0.000001, and I2 = 77.0%), but not in the Caucasian population(OR = 1.02, 95%CI: 0.87-1.19, P_(heterogeneity) = 0.97, and I2 = 0%).CONCLUSION: The GSTM1 null polymorphism may be associated with an increased risk for EC in Asian but not Caucasian populations. 展开更多
关键词 META-ANALYSIS GLUTATHIONE S-transferasem1 POLYMORPHISM ESOPHAGEAL cancer DELETIONS
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P16基因甲基化和GSTM1基因多态性与非小细胞肺癌易感性研究 被引量:3
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作者 汪亚松 金永堂 +7 位作者 薛绍礼 于在诚 徐迎春 刘晓 田敏华 陶文虎 孔云明 侯勇 《现代预防医学》 CAS 北大核心 2007年第7期1207-1209,1212,共4页
[目的]研究P16基因甲基化、谷胱甘肽硫转移酶M1基因(GSTM1)多态性和环境暴露与非小细胞肺癌(NSCLC)的关系。[方法]采用病例对照研究方法选择47例NSCLC患者和94例对照,用甲基化特异性PCR(MSP)检测P16基因甲基化,GSTM1基因多态性用限制性... [目的]研究P16基因甲基化、谷胱甘肽硫转移酶M1基因(GSTM1)多态性和环境暴露与非小细胞肺癌(NSCLC)的关系。[方法]采用病例对照研究方法选择47例NSCLC患者和94例对照,用甲基化特异性PCR(MSP)检测P16基因甲基化,GSTM1基因多态性用限制性片断长度多态性PCR(PCR-RFLP)测定。[结果]肺癌组接触粉尘、毒物频率高于对照组(P﹤0.01),食用蔬菜水果、饮用消毒水频率肺癌组低于对照组(P﹤0.01);肺癌组织甲基化率44.7%,高于癌旁组织的17%(P﹤0.01),甲基化和吸烟高度相关(P﹤0.01);GSTM1多态性分布无统计学意义(P﹥0.05),粉尘接触、吸烟和GSTM1缺陷型有协同作用,P16甲基化和GSTM1多态性关系不明显。[结论]接触粉尘、毒物明显增加NSCLC危险性,食用蔬菜水果和消毒水降低NSCLC危险性;吸烟致P16基因甲基化参与NSCLC的形成,粉尘、吸烟可能增加GSTM1缺失型患NSCLC危险性,未发现P16甲基化和GSTM1多态性有交互作用。 展开更多
关键词 P16 谷胱甘肽硫转移酶M1(GSTM1) 甲基化 基因多态性 非小细胞肺癌
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