Meta-Analysis
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World J Gastroenterol. May 7, 2014; 20(17): 5124-5130
Published online May 7, 2014. doi: 10.3748/wjg.v20.i17.5124
Association between esophageal cancer risk and EPHX1 polymorphisms: A meta-analysis
Qin-Tao Li, Wei Kang, Man Wang, Jun Yang, Yang Zuo, Wei Zhang, Dan-Ke Su
Qin-Tao Li, Wei Kang, Man Wang, Jun Yang, Yang Zuo, Wei Zhang, Dan-Ke Su, Radiology Department, Tumor Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Author contributions: Li QT, Kang W and Wang M contributed equally to this work; Su DK designed the meta-analysis; Li QT and Kang W performed the literature search and data extraction; Yang J, Zuo Y and Zhang W performed the data analysis; Li QT, Kang W and Wang M wrote the manuscript.
Correspondence to: Dan-Ke Su, MD, Radiology Department, Tumor Hospital of Guangxi Medical University, 71 Hedi Road, Nanning 530021, Guangxi Zhuang Autonomous Region,China. sudanke@hotmail.com
Telephone: +86-771-5334950  Fax: +86-771-5334950
Received: September 17, 2013
Revised: January 8, 2014
Accepted: February 17, 2014
Published online: May 7, 2014
Processing time: 232 Days and 10 Hours
Abstract

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 April 2013. 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 EPHX1 may not be associated with EC development.

Keywords: Esophageal cancer; Squamous cell carcinoma; Adenocarcinoma; EPHX1; Polymorphism; Meta-analysis

Core tip: A meta-analysis was performed to determine if the p.Tyr113His and p.His139Arg polymorphisms in microsomal epoxide hydrolase (EPHX1) are associated with an increased risk for esophageal cancer (EC). A total of seven studies of the association between EC risk and the EPHX1 polymorphisms (p.Tyr113His in seven and p.His139Arg in six) were included in the analysis. No significant association was found in any of the genetic models for the p.Tyr113His polymorphism in EPHX1 and EC. Similar results were obtained from the p.His139Arg polymorphism analysis. Subgroup analyses for ethnicity, subtype of EC, and source of controls also showed no significant association of EPHX1 polymorphisms with EC risk.