XPA gene rs1800975 single nucleotide polymorphism and lung cancer risk: a meta-analysis

XPA gene rs1800975 single nucleotide polymorphism and lung cancer risk: a meta-analysis
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XPA 基因 rs1800975 单核苷酸多态性与肺癌风险:荟萃分析。

DOI:
10.1007/s13277-014-1824-1
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发表时间:
2014-07-01
期刊:
影响因子:
--
通讯作者:
Han, Baohui
Han, Baohui
中科院分区:
其他
文献类型:
--
作者:
Lou, Yuqing;Li, Rong;Han, Baohui

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XPA基因rs 1800975多态性和肺癌风险尚未达成明确的共识。我们进行了荟萃分析,试图系统地探索可能的关联。我们在2013年11月之前对PubMed、Embase、万方、中国国家知识基础设施平台和VIP数据库进行了计算机检索。还筛选了检索到的文章的参考文献。将固定效应和随机效应模型应用于二分结局,以联合收割机合并个体研究的结果。根据纳入标准,最终纳入10篇文献(11项研究)。总体而言,rs 1800975基因多态性与肺癌在隐性遗传模型中存在统计学关联[AA vs.(AG + GG):P = 0.02,OR = 1.16,95%CI 1.02-1.31,P(异质性)= 0.14,固定效应模型]。在东亚人群中,等位基因比较模型发现显著关联(A vs. G:P = 0.03,OR = 1.13,95% CI 1.01-1.26,P(异质性)= 0.39,固定效应模型),在隐性遗传模型中[AA vs.(AG + GG):P = 0.005,OR = 1.30,95% CI 1.08-1.56,P(异质性)= 0.58,固定效应模型]和纯合子比较(AA vs. GG:P = 0.02,OR = 1.30,95% CI 1.04-1.63,P(异质性)= 0.39,固定效应模型)。没有证据表明rs 1800975多态性与其他种族的肺癌相关。按组织学类型分层分析表明,AA基因型可能是鳞状细胞癌的危险因素[AA vs.(AG + GG):P = 0.01,OR = 1.42,95%CI 1.08-1.86,P(异质性)= 0.27,固定效应模型; AA vs. GG:P = 0.03,OR = 1.43,95% CI 1.04-1.96,P(异质性)= 0.21,固定效应模型]。在腺癌亚组中未观察到相关性。我们的研究表明,XPA rs 1800975多态性可能与总体和东亚人的肺癌风险相关。这种多态性也可能与鳞状细胞癌有关。
No clear consensus has been reached on the XPA gene rs1800975 polymorphism and lung cancer risk. We performed a meta-analysis in an effort to systematically explore the possible association. We conducted a computer retrieval of PubMed, Embase, Wanfang, China National Knowledge Infrastructure Platform, and VIP databases prior to November 2013. References of retrieved articles were also screened. The fixed- and the random-effects model were applied for dichotomous outcomes to combine the results of the individual studies. According to the inclusion criteria, 10 articles (11 studies) were finally included. In overall, statistical association could be found between rs1800975 polymorphism and lung cancer in recessive genetic model [AA vs. (AG + GG): P = 0.02, OR = 1.16, 95% CI 1.02-1.31, P (heterogeneity) = 0.14, fixed-effects model]. In the East Asians, significant association was found in allele comparison model (A vs. G: P = 0.03, OR = 1.13, 95% CI 1.01-1.26, P (heterogeneity) = 0.39, fixed-effects model), in recessive genetic model [AA vs. (AG + GG): P = 0.005, OR = 1.30, 95% CI 1.08-1.56, P (heterogeneity) = 0.58, fixed-effects model] and in the homozygote comparison (AA vs. GG: P = 0.02, OR = 1.30, 95% CI 1.04-1.63, P (heterogeneity) = 0.39, fixed-effects model). No evidence suggested that rs1800975 polymorphism might associate with lung cancer in other ethnicities. Stratification analysis performed by histologic types indicated that AA genotype might represent a risk factor for squamous cell carcinoma [AA vs. (AG + GG): P = 0.01, OR = 1.42, 95% CI 1.08-1.86, P (heterogeneity) = 0.27, fixed-effects model; AA vs. GG: P = 0.03, OR = 1.43, 95% CI 1.04-1.96, P (heterogeneity) = 0.21, fixed-effects model]. No association was observed in adenocarcinoma subgroup. Our study suggested that XPA rs1800975 polymorphism might associate with lung cancer risk in overall and in East Asians. This polymorphism might also associate with squamous cell carcinoma.