@article{3153019,
    title = "Variants of the MTHFR gene and susceptibility to acute lymphoblastic
leukemia in children: A synthesis of genetic association studies",
    author = "Zintzaras, Elias and Doxani, Chrysoula and Rodopoulou, Paraskevi and and Bakalos, Georgios and Ziogas, Dimitris C. and Ziakas, Panayiotis and and Voulgarelis, Michael",
    journal = "Cancer Epidemiology and Prevention Biomarkers",
    year = "2012",
    volume = "36",
    number = "2",
    pages = "169-176",
    publisher = "Elsevier Sci Ltd, Exeter, United Kingdom",
    doi = "10.1016/j.canep.2011.10.002",
    keywords = "Acute lymphoblastic leukemia; ALL; MTHFR; C677T; A1298C; Genetic
association; Gene; Polymorphism; Risk; Susceptibility; Meta-analysis",
    abstract = "Background: Acute lymphoblastic leukemia (ALL) is a complex disease with
genetic background. The genetic association studies (GAS) that
investigated the association between ALL and the MTHFR C677T and A1298C
gene variants have produced contradictory or inconclusive results.
Materials and methods: In order to decrease the uncertainty of estimated
genetic risk effects, a meticulous meta-analysis of published GAS
related the variants in the MTFHR gene with susceptibility to ALL was
conducted. The risk effects were estimated based on the odds ratio (OR)
of the allele contrast and the generalized odds ratio (ORG). Cumulative
and recursive cumulative meta-analyses were also performed.
Results: The analysis showed marginal significant association for the
C677T variant, overall [OR = 0.91 (0.82-1.00) and ORG = 0.89
(0.79-1.01)], and in Whites [OR = 0.88 (0.77-0.99) and ORG = 0.85
(0.73-0.99)]. The A1298C variant produced non-significant results. For
both variants, the cumulative meta-analysis did not show a trend of
association as evidence accumulates and the recursive cumulative
meta-analysis indicated lack of sufficient evidence for denying or
claiming an association. Conclusion: The current evidence is not
sufficient to draw definite conclusions regarding the association of
MTHFR variants and development of ALL. (C) 2011 Elsevier Ltd. All rights
reserved."
}