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与癌症风险相关的rs17655基因G>C多态性:来自60项研究的证据。

rs17655 G>C polymorphism associated with cancer risk: evidence from 60 studies.

作者信息

Zhao Jie, Chen Shanshan, Zhou Haixia, Zhang Ting, Liu Yang, He Jing, Zhu Jinhong, Ruan Jichen

机构信息

Department of Hematology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.

Department of Clinical Medicine Center, The First People's Hospital of Wenling, The Affiliated Wenling Hospital of Wenzhou Medical University, Wenling, Zhejiang 317500, China.

出版信息

Aging (Albany NY). 2018 May 20;10(5):1073-1088. doi: 10.18632/aging.101448.

Abstract

Xeroderma pigmentosum group G (XPG), a key component in nucleotide excision repair pathway, functions to cut DNA lesions during DNA repair. Genetic variations that alter DNA repair gene expression or function may decrease DNA repair ability and impair genome integrity, thereby predisposing to cancer. The association between rs17655 G>C polymorphism and cancer risk has been investigated extensively, but the results remain contradictory. To get a more accurate conclusion, we performed a comprehensive meta-analysis of 60 case-control studies, involving 27,098 cancer cases and 30,535 healthy controls. Crude odds ratios (ORs) and 95% confidence interval (CIs) were calculated to determine the association of interest. Pooled analysis indicated that the rs17655 G>C polymorphism increased the risk of overall cancer (CC vs. GG: OR=1.10, 95% CI=1.00-1.20; CG vs. GG: OR=1.06, 95% CI=1.02-1.11; CG+CC vs. GG: OR=1.07, 95% CI=1.02-1.12; C vs. G: OR=1.05, 95% CI=1.01-1.09). Stratification analysis by cancer type further showed that this polymorphism was associated with increased risk of gastric cancer and colorectal cancer. This meta-analysis indicated that the gene rs17655 G>C polymorphism was associated with increased overall cancer risk, especially the risk of gastric cancer and colorectal cancer. Further validation experiments are needed to strength our conclusion.

摘要

着色性干皮病G组(XPG)是核苷酸切除修复途径中的关键成分,在DNA修复过程中负责切割DNA损伤。改变DNA修复基因表达或功能的基因变异可能会降低DNA修复能力并损害基因组完整性,从而易患癌症。rs17655 G>C多态性与癌症风险之间的关联已得到广泛研究,但结果仍相互矛盾。为了得出更准确的结论,我们对60项病例对照研究进行了全面的荟萃分析,涉及27,098例癌症病例和30,535例健康对照。计算粗比值比(OR)和95%置信区间(CI)以确定感兴趣的关联。汇总分析表明,rs17655 G>C多态性增加了总体癌症风险(CC与GG相比:OR=1.10,95%CI=1.00-1.20;CG与GG相比:OR=1.06,95%CI=1.02-1.11;CG+CC与GG相比:OR=1.07,95%CI=1.02-1.12;C与G相比:OR=1.05,95%CI=1.01-1.09)。按癌症类型进行的分层分析进一步表明,这种多态性与胃癌和结直肠癌风险增加有关。这项荟萃分析表明,基因rs17655 G>C多态性与总体癌症风险增加有关,尤其是胃癌和结直肠癌风险。需要进一步的验证实验来强化我们的结论。

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