Abstract

Abstract A role for folate in the etiology of childhood acute lymphoblastic leukemia (ALL) has long been suspected due to folate's dual role in control of DNA methylation as well as maintenance of DNA synthesis. Case-control studies examining self-reported maternal folate intake and supplementation during pregnancy have been inconclusive. Furthermore, while studies of children's own folate metabolism and transport genes have identified potential disease loci, the results have been mixed on the whole. A child's exposure to folate in utero is modulated by a number of factors, including maternal intake/supplementation, maternal genes, and child's genes. Therefore, we examined the role of folate in childhood ALL risk more directly by utilizing a quantitative microbiologic assay to measure newborn red blood cell folate levels in archived dried bloodspots collected at birth from 319 incident cases and 413 matched population-based controls who enrolled in the Northern California Childhood Leukemia Study between 1995 and 2002. After adjustment for income, race/ethnicity, gender, and age, we found no difference in newborn folate levels between cases and controls overall (971 vs. 968 nmol/L, p=0.94). In addition, no differences between cases and controls were observed after stratification by birth year to account for the start of folate fortification of grain products in the US (1982-1994: 953 vs. 952 nmol/L, p=0.98; 1995-1998: 1018 vs. 975 nmol/L, p=0.34; and 1999-2002: 878 vs. 990 nmol/L, p=0.23). Children whose mothers reported pre-pregnancy supplement use had somewhat higher newborn folate levels overall, but we observed no case-control differences in folate levels after stratification by supplement use. Our results do not support an association between folate levels at birth and risk of childhood ALL. However, our results do not rule out a role for folate exposures after birth. Future epidemiologic studies of childhood ALL should pay particular attention to post-natal folate exposures. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 676. doi:1538-7445.AM2012-676

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