American Association for Cancer Research
Browse
10559965epi141248-sup-140660_1_supp_2876163_nkb49b.docx (44.03 kB)

Supplemental Tables 1-9 from Folate Pathway Gene Polymorphisms and Risk of Childhood Brain Tumors: Results from an Australian Case–Control Study

Download (44.03 kB)
journal contribution
posted on 2023-03-31, 13:43 authored by Kathryn R. Greenop, Rodney J. Scott, John Attia, Carol Bower, Nicholas H. de Klerk, Murray D. Norris, Michelle Haber, Sarra E. Jamieson, Frank M. van Bockxmeer, Nicholas G. Gottardo, Lesley J. Ashton, Bruce K. Armstrong, Elizabeth Milne

Supplemental Tables 1-9. Supplemental Table S1: Tests for deviation from Hardy-Weinberg Equilibrium using parental genotypes. Supplemental Table S2: Folate pathway genotype and the risk of CBT with only cases also available for case-parent trio analysis (N=246). Supplemental Table S3: Folate pathway genotype and the risk of CBT with adjustment only for matching variables. Supplemental Table S4: Folate pathway genotype and the risk of CBT where child has 3 or more European grandparents. Supplemental Table S5: Folate-pathway genotype and the risk of CBT (excluding FTA samples). Supplemental Table S6: Child's folate pathway genotype and risk of CBT by tumor subtype. Supplemental Table S7: Maternal folate pathway genotype and risk of CBT by tumor subtype. Supplemental Table S8: Paternal folate pathway genotype and risk of CBT by tumor subtype. Supplemental Table S9: Child's folate pathway genotype and risk of CBT by sex of the child.

History

ARTICLE ABSTRACT

Background: Recent research suggests that maternal folic acid supplementation is associated with a reduced risk of childhood brain tumors (CBT); polymorphisms in folate pathway genes could modify this association or directly influence CBT risk.Methods: Associations between risk of CBT and folate pathway polymorphisms were investigated in a population-based case–control study in Australia (2005–2010). Cases were recruited through all Australian pediatric oncology centers and controls by national random digit dialing. Data were available from 321 cases and 552 controls. Six polymorphisms were genotyped in children and parents (MTHFR 677C>T, MTHFR 1298A>C, MTRR 66A>G, MTR 2756A>G, MTR 5049C>A, and CBS 2199 T>C). Maternal folic acid use was ascertained via questionnaire. ORs were estimated using unconditional logistic regression. Case–parent trio analyses were also undertaken.Results: There was weak evidence of a reduced risk of CBT for the MTRR 66GG genotype in the child or father: ORs 0.71 [95% confidence interval (CI), 0.48–1.07]; 0.54 (95% CI, 0.34–0.87), respectively. Maternal prepregnancy folic acid supplementation showed a stronger negative association with CBT risk where the child, mother, or father had the MTRR 66GG genotype (Pinteraction = 0.07, 0.10, and 0.18, respectively).Conclusions: Evidence for an association between folate pathway genotypes and CBT is limited in this study. There was possible protection by the MTRR 66GG genotype, particularly when combined with maternal prepregnancy folic acid supplementation; these results are novel and require replication.Impact: The possible interaction between folic acid supplementation and MTRR 66A>G, if confirmed, would strengthen evidence for prepregnancy folate protection against CBT. Cancer Epidemiol Biomarkers Prev; 24(6); 931–7. ©2015 AACR.

Usage metrics

    Cancer Epidemiology, Biomarkers & Prevention

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC