Wang He-Ling, Zhou Ping-Yi, Liu Peng, Zhang Yu
Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, P. R. China.
PLoS One. 2014 Mar 14;9(3):e88779. doi: 10.1371/journal.pone.0088779. eCollection 2014.
We conducted a meta-analysis of case-control studies to determine whether ALDH2, ADH1 and ADH2 genetic polymorphisms contribute to the pathogenesis of gastric cancer.
The PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before November 1st, 2013 without any language restrictions. Meta-analysis was conducted using the STATA 12.0 software. We calculated crude odds ratios (ORs) with their 95% confidence intervals (95%CI) to evaluate their relationships under five genetic models. Seven case-control studies with a total of 2,563 gastric cancer patients and 4,192 healthy controls met the inclusion criteria. Nine common polymorphisms were evaluated, including rs671, rs16941667 and rs886205 in the ALDH2 gene, rs1230025, rs13123099, rs698 and rs1693482 in the ADH1 gene, and rs1229984 and rs17033 in the ADH2 gene.
The results of our meta-analysis suggested that ALDH2 genetic polymorphisms might be strongly correlated with an increased risk of gastric cancer (allele model: OR = 1.21, 95%CI: 1.11 ∼ 1.32, P<0.001; dominant model: OR = 1.23, 95%CI: 1.09 ∼ 1.39, P = 0.001; respectively), especially for rs671 polymorphism. Furthermore, we observed significant associations between ADH1 genetic polymorphisms and an increased risk of gastric cancer (allele model: OR = 1.21, 95%CI: 1.08 ∼ 1.36, P = 0.001; dominant model: OR = 10.52, 95%CI: 3.04 ∼ 36.41, P<0.001; respectively), especially for rs1230025 polymorphism. Nevertheless, no positive relationships were found between ADH2 genetic polymorphisms and gastric cancer risk (all P>0.05).
The current meta-analysis suggests that ALDH2 and ADH1 genetic polymorphisms may play crucial roles in the pathogenesis of gastric cancer. However, ADH2 genetic polymorphisms may not be important dominants of susceptibility to gastric cancer.
我们进行了一项病例对照研究的荟萃分析，以确定乙醛脱氢酶2（ALDH2）、乙醇脱氢酶1（ADH1）和乙醇脱氢酶2（ADH2）基因多态性是否与胃癌的发病机制有关。
检索了PubMed、CISCOM、CINAHL、Web of Science、谷歌学术、EBSCO、Cochrane图书馆和中国生物医学文献数据库，以查找2013年11月1日前发表的相关文章，无任何语言限制。使用STATA 12.0软件进行荟萃分析。我们计算了粗比值比（OR）及其95%置信区间（95%CI），以评估在五种遗传模型下它们之间的关系。七项病例对照研究，共2563例胃癌患者和4192例健康对照符合纳入标准。评估了九个常见的多态性，包括ALDH2基因中的rs671、rs16941667和rs886205，ADH1基因中的rs1230025、rs13123099、rs698和rs1693482，以及ADH2基因中的rs1229984和rs17033。
我们的荟萃分析结果表明，ALDH2基因多态性可能与胃癌风险增加密切相关（等位基因模型：OR = 1.21，95%CI：1.11 ∼ 1.32，P<0.001；显性模型：OR = 1.23，95%CI：1.09 ∼ 1.39，P = 0.001），尤其是rs671多态性。此外，我们观察到ADH1基因多态性与胃癌风险增加之间存在显著关联（等位基因模型：OR = 1.21，95%CI：1.08 ∼ 1.36，P = 0.001；显性模型：OR = 10.52，95%CI：3.04 ∼ 36.41，P<0.001），尤其是rs1230025多态性。然而，未发现ADH2基因多态性与胃癌风险之间存在正相关关系（所有P>0.05）。
当前的荟萃分析表明，ALDH2和ADH1基因多态性可能在胃癌发病机制中起关键作用。然而，ADH2基因多态性可能不是胃癌易感性的重要决定因素。
