Department of Pharmaceutical Information Science, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
PLoS One. 2013 Aug 13;8(8):e71126. doi: 10.1371/journal.pone.0071126. eCollection 2013.
Several studies have investigated whether the polymorphisms in the prostaglandin endoperoxide synthase 1 (PTGS1) and PTGS2 genes and nonsteroidal anti-inflammatory drug (NSAID) use are associated with cancer risk; however, those studies have produced mixed results. Therefore, we performed a meta-analysis to evaluate the association between the PTGS1 and PTGS2 polymorphisms and the effect of NSAID use on the risk of developing cancer.
We conducted a comprehensive search in PubMed through March 2012. The odds ratios (ORs) with the corresponding 95% confidence intervals (CIs) were calculated using the fixed-effect model or the random-effect model.
The database search generated 13 studies that met the inclusion criteria. For PTGS1 rs3842787, NSAID users homozygous for the major allele (CC) had a significantly decreased cancer risk compared with non-NSAID users (OR = 0.73, 95% CI = 0.59-0.89). For PTGS2 rs5275 and rs20417, there were no significant differences between the gene polymorphism and NSAID use on cancer risk among the 8 and 7 studies, respectively. However, in the stratified analysis by the type of cancer or ethnicity population, NSAID users homozygous for the major allele (TT) in rs5275 demonstrated significantly decreased cancer risk compared with non-NSAID users in cancer type not involving colorectal adenoma (OR = 0.70, 95% CI = 0.59-0.83) and among the USA population (OR = 0.67, 95% CI = 0.56-0.82). NSAID users homozygous for the major allele (GG) in rs20417 displayed a significantly decreased cancer risk than non-NSAID users among the US population (OR = 0.72, 95% CI = 0.58-0.88). For the PTGS2 rs689466 and rs2745557 SNPs, there were no significant differences.
This meta-analysis suggests that the associations between PTGS polymorphisms and NSAID use on cancer risk may differ with regard to the type of cancer and nationality.
多项研究调查了前列腺素内过氧化物合酶 1（PTGS1）和 PTGS2 基因的多态性以及非甾体抗炎药（NSAID）的使用是否与癌症风险相关；然而，这些研究结果存在差异。因此，我们进行了荟萃分析，以评估 PTGS1 和 PTGS2 多态性与 NSAID 使用对癌症发病风险的影响。
我们通过 2012 年 3 月前的 PubMed 进行全面检索。使用固定效应模型或随机效应模型计算比值比（OR）及其相应的 95%置信区间（CI）。
数据库检索生成了 13 项符合纳入标准的研究。对于 PTGS1 rs3842787，与非 NSAID 用户相比，NSAID 用户中主要等位基因（CC）纯合子的癌症风险显著降低（OR=0.73，95%CI=0.59-0.89）。对于 PTGS2 rs5275 和 rs20417，分别有 8 项和 7 项研究的基因多态性与 NSAID 使用对癌症风险没有显著差异。然而，在按癌症类型或种族人群进行的分层分析中，rs5275 中主要等位基因（TT）纯合子的 NSAID 用户与非 NSAID 用户相比，在不涉及结直肠腺瘤的癌症类型（OR=0.70，95%CI=0.59-0.83）和美国人群中（OR=0.67，95%CI=0.56-0.82）的癌症风险显著降低。rs20417 中主要等位基因（GG）纯合子的 NSAID 用户与非 NSAID 用户相比，美国人群的癌症风险显著降低（OR=0.72，95%CI=0.58-0.88）。对于 PTGS2 rs689466 和 rs2745557 SNP，没有显著差异。
本荟萃分析表明，PTGS 多态性与 NSAID 使用对癌症风险的关联可能因癌症类型和国籍而异。
