Abstract
Polymorphic variants of genes involved in folate metabolism are implicated in the susceptibility to meningioma and glioma, but the results from published articles are controversial and inconclusive. Therefore, we performed this meta-analysis including all studies available to evaluate the relationship between folate metabolism genetic polymorphisms and the susceptibility to meningioma and glioma in adults. We searched the literature in PubMed, EMBASE and Cochrane Central Library for relevant articles published up to August 2016. The odds ratios (ORs) and the corresponding 95% confidence intervals (95%Cls) were used to evaluate the associations of two folate metabolism genetic variants MTRR A66G (rs1801394) and MTHFR A1298C (rs1801131) with the risk of meningioma and glioma in adults. We found significant association of MTHFR A1298C (rs1801131) variant genotypes with increased incidence of meningioma and glioma in this study population (CA vs. AA: OR=1.22, P<0.001; CA+CC vs. AA: OR=1.18, P=0.002). Moreover, we found that MTRR A66G (rs1801394) variant genotypes was associated with increased risk of meningioma and glioma (G vs. A: OR=1.11, P=0.020; GG vs. AA+AG: OR=1.17, P=0.043; GG vs. AA: OR=1.22, P=0.023). In conclusion, our meta-analysis suggests that two folate metabolism genetic variants MTRR A66G (rs1801394) and MTHFR A1298C (rs1801131) contribute to genetic susceptibility to meningioma and glioma in adults.
Highlights
Based on the GLOBOCAN2012 investigations, approximately 14.1 million new cancer cases and 8.2 million deaths were reported worldwide [1]
We found that MTRR A66G variant genotypes was associated with increased risk of meningioma and glioma (G vs. A: odds ratios (ORs)=1.11, P=0.020; GG vs. AA+AG: OR=1.17, P=0.043; GG vs. AA: OR=1.22, P=0.023)
Our meta-analysis suggests that two folate metabolism genetic variants MTRR A66G and Methylenetetrahydrofolate reductase (MTHFR) A1298C contribute to genetic susceptibility to meningioma and glioma in adults
Summary
Based on the GLOBOCAN2012 investigations, approximately 14.1 million new cancer cases and 8.2 million deaths were reported worldwide [1]. The overall incidence of brain tumor is estimated at 3.5 case per 100,000 persons, and glioma and meningioma are the most common types of primary brain tumors, accounting for approximately 50% and 20%, respectively [2, 3]. Primary brain tumors mostly occur in familial aggregation, indicating important role of genetic variants in the pathogenesis of brain tumor [4]. Folate metabolism plays an important role in carcinogenesis, due to its involvement in DNA synthesis, methylation and repair. Folate metabolism regulates nucleotide synthesis and DNA methylation via a complex pathway involving at least 30 different enzymes [5]. Individual genetic variation www.impactjournals.com/oncotarget in these enzymes could change the general balance between DNA synthesis, methylation, and repair. Genetic polymorphisms of folate metabolism pathways have been shown to be associated with diverse tumor types, including pancreatic cancer [6], cervical intraepithelial neoplasia [7], breast cancer [8] and acute leukemia [9,10,11]
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