Li Fuqiang, Xu Bing, Yang Zili, Wu Yijun, Dong Shuai, Qian Jiajie
Department of Gastrointestinal Surgery, The First Affiliated Hospital, Zhejiang University, 79# Qingchun Road, Hangzhou, 310003, Zhejiang Province, China.
Tumour Biol. 2013 Jun;34(3):1825-31. doi: 10.1007/s13277-013-0723-1. Epub 2013 Mar 19.
Studies investigating the association between cytochrome glutathione S-transferase P1 (GSTP1) Ala114Val polymorphism and colorectal cancer (CRC) risk report conflicting results. The aim of this study was to quantitatively summarize the evidence for such a relationship. Two investigators independently searched the Medline, Embase, China National Knowledge Infrastructure, and Chinese Biomedicine databases. Summary odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for GSTP1 polymorphism and CRC were calculated in a fixed effects model (the Mantel-Haenszel method) and a random effects model (the DerSimonian and Laird method) when appropriate. The pooled ORs were performed for co-dominant model (ValVal vs. AlaAla, AlaVal vs. AlaAla), dominant model (ValVal + AlaVal vs. AlaAla), and recessive model (ValVal vs. AlaVal + AlaAla). This meta-analysis included seven case-control studies, which included 3,173 CRC cases and 3,323 controls. Overall, the variant genotypes (ValVal and AlaVal) of the Ala114Val were not associated with CRC risk when compared with the wild-type AlaAla homozygote. Similarly, no associations were found in the dominant and recessive models. When stratifying for ethnicity, Hardy-Weinberg equilibrium in controls, study sample size, and source of controls, a significantly increased risk was observed among Asians (AlaVal vs. AlaAla, OR=1.67, 95 % CI=1.08-2.59; dominant model, OR=1.74, 95 % CI=1.14-2.67). No heterogeneity or publication bias was found in the present study. This meta-analysis suggests that the GSTP1 Ala114Val polymorphism may not be associated with CRC risk, while the observed increase in risk of CRC may be due to small-study bias.
研究细胞色素谷胱甘肽S-转移酶P1(GSTP1)Ala114Val多态性与结直肠癌(CRC)风险之间关联的研究报告了相互矛盾的结果。本研究的目的是定量总结这种关系的证据。两名研究者独立检索了Medline、Embase、中国知网和中国生物医学数据库。在适当情况下,采用固定效应模型(Mantel-Haenszel法)和随机效应模型(DerSimonian和Laird法)计算GSTP1多态性与CRC的汇总比值比(OR)和95%置信区间(95%CI)。对共显性模型(ValVal vs. AlaAla,AlaVal vs. AlaAla)、显性模型(ValVal + AlaVal vs. AlaAla)和隐性模型(ValVal vs. AlaVal + AlaAla)进行汇总OR分析。该荟萃分析纳入了7项病例对照研究,包括3173例CRC病例和3323例对照。总体而言,与野生型AlaAla纯合子相比,Ala114Val的变异基因型(ValVal和AlaVal)与CRC风险无关。同样,在显性和隐性模型中未发现关联。按种族、对照中的Hardy-Weinberg平衡、研究样本量和对照来源分层时,亚洲人中有显著增加的风险(AlaVal vs. AlaAla,OR = 1.67,95%CI = 1.08 - 2.59;显性模型,OR = 1.74,95%CI = 1.14 - 2.67)。本研究未发现异质性或发表偏倚。该荟萃分析表明,GSTP1 Ala114Val多态性可能与CRC风险无关,而观察到的CRC风险增加可能是由于小研究偏倚。