Interaction between maternal 5,10-methylenetetrahydrofolate reductase C677T and methionine synthase A2756G gene variants to increase the risk of fetal neural tube defects in a Shanxi Han population / 中华医学杂志(英文版)
Chinese Medical Journal
;
(24): 865-869, 2013.
Article
in English
| WPRIM
| ID: wpr-342482
ABSTRACT
<p><b>BACKGROUND</b>The 5,10-methylenetetrahydrofolate reductase (MTHFR) and methionine synthase (MS) are attractive candidates for screening for risk of neural tube defects (NTDs). The aim of the current study was to investigate maternal MTHFR and MS polymorphisms and the interaction between them and their influence on children with NTDs in the Shanxi Province of northern China.</p><p><b>METHODS</b>Fifty-one mothers who previously had children with NTDs constituted the case group and 51 age-matched mothers with children that were unaffected by any birth defects constituted the control group. All subjects were genotyped for MTHFR C677T and MS A2756G polymorphisms. SPSS 11.5 software package was used for all analyses.</p><p><b>RESULTS</b>There was a significant difference for MTHFR genotype distribution for one site (C677T) between the case and control groups. The T allele frequencies were significantly higher in the case group than in the control group (55.9% vs. 35.3%, P < 0.05). A lack of association was observed for the MS A2756G polymorphism. There was an interaction between the maternal MTHFR C677T genotype and MS A2756G genotype.</p><p><b>CONCLUSION</b>Genetic interaction between MTHFR and MS genes raises the probability of neural tube defects.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Polymorphism, Genetic
/
5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase
/
China
/
Epidemiology
/
Genetic Predisposition to Disease
/
Methylenetetrahydrofolate Reductase (NADPH2)
/
Gene Frequency
/
Genetics
/
Genotype
/
Neural Tube Defects
Type of study:
Etiology study
Limits:
Female
/
Humans
Country/Region as subject:
Asia
Language:
English
Journal:
Chinese Medical Journal
Year:
2013
Type:
Article
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