Abstract
BackgroundSeveral 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.MethodsWe 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.ResultsThe 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.ConclusionThis 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.
Highlights
Prostaglandin endoperoxide synthase 1 (PTGS1) and PTGS2, known as cyclooxygenase 1 (COX1) and COX2, catalyze the oxidative conversion of arachidonic acid to prostaglandin (PG) H2, which is subsequently metabolized to various biologically active metabolites, such as prostacyclin and thromboxane A2 [1]
Among the 38 excluded studies, 28 studies did not perform the analysis for recurring SNPs, and 10 studies did not provide the number of subjects to calculate for odds ratios (ORs)
For prostaglandin endoperoxide synthase 1 (PTGS1) rs3842787, nonsteroidal anti-inflammatory drug (NSAID) users homozygous for the major allele (CC) demonstrated a significantly decreased cancer risk compared with non-NSAID users (Fig. 2A, OR = 0.73, 95% confidence intervals (CIs) = 0.59–0.89)
Summary
Prostaglandin endoperoxide synthase 1 (PTGS1) and PTGS2, known as cyclooxygenase 1 (COX1) and COX2, catalyze the oxidative conversion of arachidonic acid to prostaglandin (PG) H2, which is subsequently metabolized to various biologically active metabolites, such as prostacyclin and thromboxane A2 [1] Both PTGS1 and PTGS2 catalyze the same committed step in prostanoid biosynthesis with similar efficiencies, they are encoded by distinct genes located on different chromosomes, and they substantially differ in their expression pattern [1]. 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; those studies have produced mixed results. 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
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