NDLI: Folic acid supplementation, MTHFR and MTRR polymorphisms, and the risk of childhood leukemia: the ESCALE study (SFCE)

Content Provider	Springer Nature Link
Author	Amigou, Alicia Rudant, Jérémie Orsi, Laurent Goujon Bellec, Stéphanie Leverger, Guy Baruchel, André Bertrand, Yves Nelken, Brigitte Plat, Geneviève Michel, Gérard Haouy, Stéphanie Chastagner, Pascal Ducassou, Stéphane Rialland, Xavier Hémon, Denis Clavel, Jacqueline
Copyright Year	2012
Abstract	Fetal folate deficiency may increase the risk of subsequent childhood acute leukemia (AL), since folates are required for DNA methylation, synthesis, and repair, but the literature remains scarce. This study tested the hypothesis that maternal folic acid supplementation before or during pregnancy reduces AL risk, accounting for the SNPs rs1801133 (C677T) and rs1801131 (A1298C) in MTHFR and rs1801394 (A66G) and rs1532268 (C524T) in MTRR, assumed to modify folate metabolism.The nationwide registry-based case–control study, ESCALE, carried out in 2003–2004, included 764 AL cases and 1,681 controls frequency matched with the cases on age and gender. Information on folic acid supplementation was obtained by standardized telephone interview. The genotypes were obtained using high-throughput platforms and imputation for untyped polymorphisms. Odds ratios (OR) were estimated using unconditional regression models adjusted for potential confounders.AL was significantly inversely associated with maternal folic acid supplementation before and during pregnancy (OR = 0.4; 95 % confidence interval: [0.3–0.6]). MTHFR and MTRR genetic polymorphisms were not associated with AL. However, AL was positively associated with homozygosity for any of the MTHFR polymorphisms and carriership of both MTRR variant alleles (OR = 1.6 [0.9–3.1]). No interaction was observed between MTHFR, MTRR, and maternal folate supplementation.The study findings support the hypothesis that maternal folic acid supplementation may reduce the risk of childhood AL. The findings also suggest that the genotype homozygous for any of the MTHFR variants and carrying both MTRR variants could be a risk factor for AL.
Starting Page	1265
Ending Page	1277
Page Count	13
File Format	PDF
ISSN	09575243
Journal	Cancer Causes & Control
Volume Number	23
Issue Number	8
e-ISSN	15737225
Language	English
Publisher	Springer Netherlands
Publisher Date	2012-06-16
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Childhood leukemia Folic acid Metabolism MTHFR MTRR Gene–environment interaction Hematology Oncology Epidemiology Public Health/Gesundheitswesen Biomedicine general Cancer Research
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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