论文部分内容阅读
AIM:To summarize the relationship between p.Tyr113His and p.His139Arg polymorphisms in microsomal epoxide hydrolase(EPHX1)and risk for esophageal cancer(EC).METHODS:The MEDLINE/PubMed and EMBASE databases were searched for studies of the association between EPHX1 polymorphisms and EC risk that were published from the database inception date to April2013.A total of seven case-control studies,including seven on p.Tyr113His(cases,n=1118;controls,n=1823)and six on p.His139Arg(cases,n=861;controls,n=1571),were included in the meta-analysis.After data extraction by two investigators working independently,the meta-analyses were carried out with STATA 11.0 software.Pooled odds ratios and 95%CI were calculated using a fixed-effects model or a random-effects model,as appropriate.RESULTS:The pooled EPHX1 p.Tyr113His polymorphism data showed no significant association with EC in any of the genetic models(OR=1.00,95%CI:0.70-1.48 for Tyr/His vs Tyr/Tyr;OR=1.10,95%CI:0.77-1.57 for His/His vs Tyr/Tyr;OR=1.06,95%CI:0.75-1.49 for a dominant model;OR=1.09,95%CI:0.89-1.34 for a recessive model).Similar results were obtained from the p.His139Arg polymorphism analysis(Arg/His vs His/His:OR=1.02,95%CI:0.84-1.23;Arg/Arg vs His/His:OR=0.96,95%CI:0.60-1.54;OR=1.03,95%CI:0.78-1.37 for the dominant model;OR=0.97,95%CI:0.61-1.56 for the recessive model).Subgroup analyses for ethnicity,subtype of EC,and source of controls(population-based or hospital-based)showed trends that were consistent with the pooled analysis(reported above),with no significant associations found.CONCLUSION:This meta-analysis suggests that the p.Tyr113His and p.His139Arg polymorphisms in EPHX1may not be associated with EC development.
AIM: To summarize the relationship between p. Tyr113His and p. His139 Arg polymorphisms in microsomal epoxide hydrolase (EPHX1) and risk for esophageal cancer (EC). METHODS: The MEDLINE / PubMed and EMBASE databases were searched for studies of the association between EPHX1 polymorphisms and EC risk that were published from the database inception date to April 2013. A total of seven case-control studies, including seven on p. Tyr113 His (cases, n = 1118; controls, n = 1823) and six on p. His139 Arg , n = 861; controls, n = 1571) were included in the meta-analysis. After data extraction by two investigators working independently, the meta-analyzes were carried out with STATA 11.0 software. Pooled odds ratios and 95% CI were calculated using a fixed-effects model or a random-effects model, as appropriate .RESULTS: The pooled EPHX1 p.Tyr113His polymorphism data showed no significant association with EC in any of the the genetic models (OR = 1.00, 95% CI: 0.70-1.48 for Tyr / His vs Tyr / Tyr; OR = 1.10, 95% CI: 0.77-1.57 for His / His vs Tyr / Tyr; OR = 1.06, 95% CI: 0.75-1.49 for a dominant model; OR = 1.09, 95% CI: 0.89-1.34 for a recessive model). Similar results were obtained from the p.His 139 Arg polymorphism analysis (Arg / His vs His /His:OR=1.02,95%CI:0.84-1.23;Arg/Arg vs His / His: OR = 0.96, 95% CI: 0.60-1.54; OR = 1.03, 95% CI: 0.78-1.37 for the dominant model ; OR = 0.97, 95% CI: 0.61-1.56 for the recessive model. Subgroup analyzes for ethnicity, subtype of EC, and source of controls (population-based or hospital-based) showed trends that were consistent with the pooled analysis ( reported above), with no significant associations found. CONCLUSION: This meta-analysis suggests that the p. Tyr113 His and p. His139 Arg polymorphisms in EPHX1 may not be associated with EC development.