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端粒延长解旋酶1(RTEL1)rs6010620多态性会增加患神经胶质瘤的风险。

Regulator of telomere elongation helicase 1 (RTEL1) rs6010620 polymorphism contribute to increased risk of glioma.

作者信息

Zhao Wei, Bian Yusong, Zhu Wei, Zou Peng, Tang Guotai

机构信息

Department of Neurosurgery, Yuhuangding Hospital of Yantai, 20 Yuhuangding East Road, Yantai, 264000, Shandong, China.

出版信息

Tumour Biol. 2014 Jun;35(6):5259-66. doi: 10.1007/s13277-014-1684-8. Epub 2014 Feb 13.

Abstract

Regulator of telomere elongation helicase 1 (RTEL1) is critical for genome stability and tumor avoidance. Many studies have reported the associations of RTEL1 rs6010620 with glioma risk, but individually published results were inconclusive. This meta-analysis was performed to quantitatively summarize the evidence for such a relationship. The PubMed, Embase, and Web of Science were systematically searched to identify relevant studies. The odds ratio (OR) and 95 % confidence interval (95 % CI) were computed to estimate the strength of the association using a fixed or random effects model. Ten studies were eligible for meta-analysis including data on glioma with 6,490 cases and 9,288 controls. Overall, there was a significant association between RTEL1 rs6010620 polymorphism and glioma risk in all four genetic models (GG vs. AA: OR=1.87, 95 % CI=1.60-2.18, P heterogeneity=0.552; GA vs. AA: OR=1.30, 95 % CI=1.16-1.46, P heterogeneity=0.495; dominant model-GG+GA vs. AA: OR=1.46, 95 % CI=1.31-1.63, P heterogeneity=0.528; recessive model-GG vs. GA+AA: OR=1.36, 95 % CI=1.27-1.46, P heterogeneity=0.093). Subgroup analyses by ethnicity showed that RTEL1 rs6010620 polymorphism resulted in a higher risk of glioma among both Asians and Caucasians. In the stratified analysis by ethnicity and source of controls, significantly increased risk was observed for Asians and Europeans in all genetic models, population-based studies in all genetic models, and hospital-based studies in three genetic models (heterozygote comparison, homozygote comparison, and dominant model). Our meta-analysis suggested that RTEL1 rs6010620 polymorphism is likely to be associated with increased glioma risk, which lends further biological plausibility to these findings.

摘要

端粒延长解旋酶1调节因子(RTEL1)对基因组稳定性和肿瘤预防至关重要。许多研究报告了RTEL1 rs6010620与胶质瘤风险的关联,但单独发表的结果尚无定论。本荟萃分析旨在定量总结这种关系的证据。系统检索了PubMed、Embase和Web of Science以识别相关研究。使用固定效应或随机效应模型计算比值比(OR)和95%置信区间(95%CI)来估计关联强度。十项研究符合荟萃分析条件,包括6490例胶质瘤病例和9288例对照的数据。总体而言,在所有四种遗传模型中,RTEL1 rs6010620多态性与胶质瘤风险之间均存在显著关联(GG与AA:OR = 1.87,95%CI = 1.60 - 2.18,P异质性 = 0.552;GA与AA:OR = 1.30,95%CI = 1.16 - 1.46,P异质性 = 0.495;显性模型 - GG + GA与AA:OR = 1.46,95%CI = 1.31 - 1.63,P异质性 = 0.528;隐性模型 - GG与GA + AA:OR = 1.36,95%CI = 1.27 - 1.46,P异质性 = 0.(此处原文有误,应为0.093))。按种族进行的亚组分析表明,RTEL1 rs6010620多态性在亚洲人和高加索人中均导致较高的胶质瘤风险。在按种族和对照来源进行的分层分析中,在所有遗传模型中,亚洲人和欧洲人、所有遗传模型中的基于人群的研究以及三种遗传模型(杂合子比较、纯合子比较和显性模型)中的基于医院的研究均观察到风险显著增加。我们的荟萃分析表明,RTEL1 rs6010620多态性可能与胶质瘤风险增加有关,这为这些发现提供了进一步的生物学合理性。

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