Methionine synthase reductase A66G polymorphism is not associated with breast cancer susceptibility - a meta-analysis.

Abstract

BACKGROUND:

Several studies have investigated the association between methionine synthase reductase (MTRR) A66G polymorphism and breast cancer risk, but controversial results were yielded. Therefore, we performed a meta-analysis to provide a more robust estimate of the effect of this polymorphism on susceptibility to breast cancer.

MATERIALS AND METHODS:

Case-control studies investigating the relationship between MTRR A66G polymorphism and breast cancer risk were included by searching PubMed, EMBASE, China National Knowledge Infrastructure and Wanfang Database. Either fixed-effects or random-effects models were applied to calculate odds ratios(ORs) and 95% confidence intervals (CIs) by RevMan5.2 software.

RESULTS:

A total of 9 studies bearing 7,097 cases and 7,710 controls were included in the meta-analysis. The results were that the combined ORs and 95%CIs of MTRR 66AG, GG, (AG+GG) genotypes were 0.98(0.91-1.05), 1.06(0.97-1.16) and 1.02(0.94-1.10), respectively with p=0.52, 0.19 and 0.65. We also performed subgroup analysis by specific ethnicity. The results of the combined analysis of MTRR 66AG, GG, (AG+GG) genotypes and breast cancer in Asian descent were Z=0.50, 0.53 and 0.21, with p all>0.05; for breast cancer in Caucasian descent, the results were Z=1.14, 1.65 and 0.43, with p all>0.05.

CONCLUSIONS:

Our findings suggested that MTRR A66G polymorphism was not associated with breast cancer susceptibility.

• Authors: Shu Hu, Hong-Chao Liu, Shou-Ming Xi
• Journal: Asian Pacific journal of cancer prevention : APJCP (Asian Pac J Cancer Prev) Vol. 15 Issue 7 Pg. 3267-71 ( 2014) ISSN: 2476-762X [Electronic] Thailand
• PMID: 24815481 (Publication Type: Journal Article, Meta-Analysis)

Chemical References

• methionine synthase reductase
• Ferredoxin-NADP Reductase

Topics

• Breast Neoplasms (genetics)
• Female
• Ferredoxin-NADP Reductase (genetics)
• Gene Frequency
• Genetic Predisposition to Disease
• Genotype
• Humans
• Polymorphism, Single Nucleotide