Research Article

Contribution of catechol-O-methyltransferase Val158Met polymorphism to endometrial cancer risk in postmenopausal women: a meta-analysis

Published: December 10, 2013
Genet. Mol. Res. 12 (4) : 6442-6453 DOI: 10.4238/2013.December.10.5

Abstract

Catechol-O-methyltransferase (COMT) is a critical enzyme to detoxify the carcinogenic catechol estrogen and the Val158Met polymorphism of COMT could influence its enzymatic activity. Recent epidemiological studies have investigated the correlation of COMT Val158Met polymorphism with endometrial cancer risk; however, the results are inconsistent. To better evaluate the role of COMT Val158Met in endometrial carcinogenesis, we performed this meta-analysis, considering menopausal status, study quality, ethnicity, and source of controls. Eight eligible studies including 5109 subjects were collected from PubMed, CNKI, and Chinese Biomedicine Database (updated until September 21, 2012). Although no obvious associations were detected between COMT Val158Met and endometrial cancer susceptibility in the pooled analysis, we noted significantly decreased endometrial cancer risk for Val/Met versus Val/Val, and Met/Met + Val/Met versus Val/Val genetic models in the postmenopausal female (OR = 0.795, 95%CI = 0.656-0.962, P = 0.019; and OR = 0.819, 95%CI = 0.683-0.983, P = 0.032; respectively), and similar results existed in high-quality studies (OR = 0.835, 95%CI = 0.726-0.961, P = 0.012; and OR = 0.853, 95%CI = 0.747-0.974, P = 0.019; respectively). However, no evidence of association was noted in different ethnic groups and sources of controls. In conclusion, our results suggested that the COMT Val/Val genotype might act as a potential endometrial cancer risk factor in postmenopausal women. Further studies are needed to investigate the interactions between COMT Val158Met polymorphism and endometrial cancer in a specific population.

Catechol-O-methyltransferase (COMT) is a critical enzyme to detoxify the carcinogenic catechol estrogen and the Val158Met polymorphism of COMT could influence its enzymatic activity. Recent epidemiological studies have investigated the correlation of COMT Val158Met polymorphism with endometrial cancer risk; however, the results are inconsistent. To better evaluate the role of COMT Val158Met in endometrial carcinogenesis, we performed this meta-analysis, considering menopausal status, study quality, ethnicity, and source of controls. Eight eligible studies including 5109 subjects were collected from PubMed, CNKI, and Chinese Biomedicine Database (updated until September 21, 2012). Although no obvious associations were detected between COMT Val158Met and endometrial cancer susceptibility in the pooled analysis, we noted significantly decreased endometrial cancer risk for Val/Met versus Val/Val, and Met/Met + Val/Met versus Val/Val genetic models in the postmenopausal female (OR = 0.795, 95%CI = 0.656-0.962, P = 0.019; and OR = 0.819, 95%CI = 0.683-0.983, P = 0.032; respectively), and similar results existed in high-quality studies (OR = 0.835, 95%CI = 0.726-0.961, P = 0.012; and OR = 0.853, 95%CI = 0.747-0.974, P = 0.019; respectively). However, no evidence of association was noted in different ethnic groups and sources of controls. In conclusion, our results suggested that the COMT Val/Val genotype might act as a potential endometrial cancer risk factor in postmenopausal women. Further studies are needed to investigate the interactions between COMT Val158Met polymorphism and endometrial cancer in a specific population.