1.
Association of Intake Folate and Related Gene Polymorphisms with Breast Cancer.
Chen, X, Ahamada, H, Zhang, T, Bai, Z, Wang, C
Journal of nutritional science and vitaminology. 2019;(6):459-469
Abstract
Breast cancer is one of the most common malignancies in women worldwide and is associated with a variety of risk factors. Folate and vitamin B12 are key elements of the one-carbon metabolism pathway where methylenetetrahydrofolate reductase (MTHFR) plays a significant role. Though many molecular and epidemiological studies have been performed to explore the relationship between intake folate, vitamin B12, MTHFR gene polymorphism and breast cancer risk, there is no consensus to date. By reviewing the relevant literatures and summarizing the potential effect of dietary folate intake on MTHFR genes polymorphism and breast cancer risk, we conclude that MTHFR C677T gene polymorphism is associated with breast cancer risk among Asian, but not Caucasians, and the MTHFR A1298C gene polymorphism is not a susceptibility factor of breast cancers. Concomitant low activity of MTHFR enzyme resulted from C677T gene polymorphism and low dietary folate intake is associated with increased breast cancer risk.
2.
The protective effect of methylenetetrahydrofolate reductase C677T polymorphism against prostate cancer risk: Evidence from 23 case-control studies.
Guo, S, Jiang, X, Chen, X, Chen, L, Li, X, Jia, Y
Gene. 2015;(1):90-5
Abstract
Genetic polymorphisms of methylenetetrahydrofolate reductase (MTHFR) were considered to have some influence on both folate metabolism and cancer risk. Previous studies on the relation between MTHFR C677T polymorphism and prostate cancer (PCa) risk remained controversial. To derive a more precise estimation of the relationship, we carried out an update comprehensive meta-analysis to assess the associations of the MTHFR C677T polymorphism with the susceptibility of PCa. Twenty-three trials with a total of 24,024 participants on the MTHFR C677T polymorphism that met inclusion criteria were analyzed in the current study. Overall, no statistical relationship was found with any MTHFR C677T genetic model associated with susceptibility to PCa (TT versus CC, OR=0.83, 95% CI 0.68-1.02, P=0.07; CT versus CC, OR=0.95, 95% CI 0.85-1.07, P=0.43; Dominant, OR=0.93, 95% CI 0.83-1.03, P=0.17; Recessive, OR=0.84, 95% CI 0.70-1.02, P=0.09.). Nevertheless, subgroup analysis found a reduced PCa risk associated with polymorphism in Asian population (TT versus CC, CT versus CC, dominant and recessive model). Moreover, the protective effect of polymorphism against PCa risk was also shown upon hospital-based studies (TT versus CC, and recessive model). When benign prostate hyperplasia was chosen as controls, both TT versus CC and recessive model showed significant difference. In addition, the protective effect of homozygote TT against high aggressive PCa was proved to have significant difference. Taken together, the existing evidence indicates the homozygote TT of MTHFR C677T should be viewed as a protective factor against PCa risk for clinical practice with the consideration of different gene background, study design as well as specific controls.
3.
Association between MTHFR 677C>T polymorphism and risk of gliomas: evidence from a meta-analysis.
Lu, Q, Dai, D, Zhao, W, Wang, L, Yue, Z, Chen, X, Han, G, Hao, B, Yang, P, Deng, A, et al
Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine. 2013;(5):2801-7
Abstract
Folate metabolism plays an important role in carcinogenesis. Methylenetetrahydrofolate reductase (MTHFR) 677C>T polymorphism is a genetic alteration in an enzyme involved in folate metabolism, but its effect on risk of gliomas is still uncertain. To shed some light on these contradictory results from previous studies, we performed a meta-analysis of published data investigating the association between MTHFR 677C>T polymorphism and risk of gliomas. PubMed, Embase, and Web of Science databases were searched for eligible case-control studies. Odds ratios (ORs) and 95 % confidence intervals (CIs) were used to assess the strength of this association. Ten individual case-control studies from six publications with a total of 1,786 cases and 2,076 controls were included into this meta-analysis. There was no obvious heterogeneity under all comparison models of this meta-analysis. Meta-analysis of those ten studies showed that there was no obvious association between MTHFR 677C>T polymorphism and risk of gliomas under all five genetic models (for T versus C, OR = 1.00, 95 % CI 0.90-1.12, P OR = 0.959; for TT versus CC, OR = 1.02, 95 % CI 0.82-1.27, P OR = 0.870; for CT versus CC, OR = 1.02, 95 % CI 0.89-1.18, P OR = 0.733; for TT+CT versus CC, OR = 1.02, 95 % CI 0.90-1.16, P OR = 0.781; for TT versus CT+CC, OR = 0.99, 95 % CI 0.81-1.21, P OR = 0.902). There was also no obvious association between MTHFR 677C>T polymorphism and risk of gliomas in the sensitivity and subgroup analyses of Caucasians. There was no risk of publication bias in this meta-analysis. The evidence from our meta-analysis supports that there is no association between MTHFR 677C>T polymorphism and risk of gliomas.