Research Article

Meta-analysis of microsomal epoxide hydrolase gene polymorphism and the risk of breast carcinoma

Published: April 27, 2015
Genet. Mol. Res. 14 (2) : 4133-4141 DOI: 10.4238/2015.April.27.28

Abstract

Carcinogenesis of breast carcinoma is very complicated. Previous studies have suggested conflicting results regarding the association between Tyr113His and His139Arg microsomal epoxide hydrolase (mEH) gene polymorphisms and risk of breast carcinoma. We conducted a meta-analysis to examine the relationship between these polymorphisms and breast carcinoma risk. We searched the PubMed, EMBASE, and Google Scholar databases to identify relevant studies. After extracting relevant data, the association between mEH polymorphisms and susceptibility to breast carcinoma was examined by meta-analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the strength of the association. Seven studies were identified that included 6357 cases and 8090 controls. The mEH His-allele was not associated with the risk of breast carcinoma based on the allelic contrast model (OR = 0.99, 95%CI = 0.94-1.04, P = 0.58), dominant genetic model (OR = 1.14, 95%CI = 0.88-1.48, P = 0.33), or recessive genetic model (OR = 1.03, 95%CI = 0.96-1.10, P = 0.43). Similarly, the mEH Arg-allele was not associated with breast carcinoma risk based on the allelic contrast model (OR = 0.97, 95%CI = 0.91-1.04, P = 0.44), dominant genetic model (OR = 1.01, 95%CI = 0.84-1.21, P = 0.94), or recessive genetic model (OR = 1.04, 95%CI = 0.96-1.12, P = 0.35). Subgroup analysis based on ethnicity showed no association between the polymorphisms and risk of breast carcinoma. Thus, the Tyr113His and His139Arg mEH polymorphisms may not be risk factors for breast carcinoma.

Carcinogenesis of breast carcinoma is very complicated. Previous studies have suggested conflicting results regarding the association between Tyr113His and His139Arg microsomal epoxide hydrolase (mEH) gene polymorphisms and risk of breast carcinoma. We conducted a meta-analysis to examine the relationship between these polymorphisms and breast carcinoma risk. We searched the PubMed, EMBASE, and Google Scholar databases to identify relevant studies. After extracting relevant data, the association between mEH polymorphisms and susceptibility to breast carcinoma was examined by meta-analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the strength of the association. Seven studies were identified that included 6357 cases and 8090 controls. The mEH His-allele was not associated with the risk of breast carcinoma based on the allelic contrast model (OR = 0.99, 95%CI = 0.94-1.04, P = 0.58), dominant genetic model (OR = 1.14, 95%CI = 0.88-1.48, P = 0.33), or recessive genetic model (OR = 1.03, 95%CI = 0.96-1.10, P = 0.43). Similarly, the mEH Arg-allele was not associated with breast carcinoma risk based on the allelic contrast model (OR = 0.97, 95%CI = 0.91-1.04, P = 0.44), dominant genetic model (OR = 1.01, 95%CI = 0.84-1.21, P = 0.94), or recessive genetic model (OR = 1.04, 95%CI = 0.96-1.12, P = 0.35). Subgroup analysis based on ethnicity showed no association between the polymorphisms and risk of breast carcinoma. Thus, the Tyr113His and His139Arg mEH polymorphisms may not be risk factors for breast carcinoma.