https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Confirmation of childhood acute lymphoblastic leukemia variants, ARID5B and IKZF1, and interaction with parental environmental exposures https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16807 -9), and IKZF1 rs1110701 (OR 1.69, CI 1.42–2.02, p = 7.26 x 10-9). There was evidence of gene-environment interaction for risk genotype at IKZF1, whereby an apparently stronger genetic effect was observed if the mother took folic acid or if the father did not smoke prior to pregnancy (respective interaction P-values: 0.04, 0.05). There were no interactions of risk genotypes with age or sex (P-values >0.2). Our results evidence that interaction of genetic variants and environmental exposures may further alter risk of childhood ALL however, investigation in a larger population is required. If interaction of folic acid supplementation and IKZF1 variants holds, it may be useful to quantify folate levels prior to initiating use of folic acid supplements.]]> Wed 11 Apr 2018 16:52:33 AEST ]]> Exposure to pesticides and the risk of childhood brain tumors https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19876 Tue 09 Jun 2020 09:48:40 AEST ]]> Exposure to professional pest control treatments and the risk of childhood acute lymphoblastic leukemia https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13263 Sat 24 Mar 2018 08:15:58 AEDT ]]> Maternal dietary intake of folate and vitamins B6 and B12 during pregnancy and the risk of childhood acute lymphoblastic leukemia https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21473 Sat 24 Mar 2018 08:03:41 AEDT ]]> Parental alcohol consumption and risk of childhood acute lymphoblastic leukemia and brain tumors https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17308 Sat 24 Mar 2018 08:01:48 AEDT ]]> Parental smoking and risk of childhood brain tumors https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18434 Sat 24 Mar 2018 07:59:46 AEDT ]]> Maternal use of folic acid and other supplements and risk of childhood brain tumors https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21562 Sat 24 Mar 2018 07:59:02 AEDT ]]> Parental prenatal smoking and risk of childhood acute lymphoblastic leukemia https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21565 Sat 24 Mar 2018 07:59:01 AEDT ]]> Exposure to household painting and floor treatments, and parental occupational paint exposure and risk of childhood brain tumors: results from an Australian case-control study https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20586 Sat 24 Mar 2018 07:55:35 AEDT ]]> Maternal dietary intake of folate and vitamins B6 and B12 during pregnancy and risk of childhood brain tumors https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21121 Sat 24 Mar 2018 07:54:00 AEDT ]]> Childhood folate, B6, B12, and food group intake and the risk of childhood brain tumors: results from an Australian case-control study https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27963 Sat 24 Mar 2018 07:38:45 AEDT ]]> Folate pathway gene polymorphisms and risk of childhood brain tumors: results from an Australian case-control study https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27952 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.]]> Sat 24 Mar 2018 07:38:45 AEDT ]]> Folate pathway gene polymorphisms, maternal folic acid use, and risk of childhood acute lymphoblastic leukemia https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26915 T, MTHFR 1298A>C, MTRR 66A>G, MTR 2756 A>G, MTR 5049 C>A, CBS 844 Ins68, and CBS 2199 T>C) were genotyped in children and their parents. Information on prepregnancy maternal folic acid supplement use was collected. ORs were estimated with unconditional logistic regression adjusted for frequency-matched variables and potential confounders. Case-parent trios were also analyzed. Results: There was some evidence of a reduced risk of ALL among children who had, or whose father had, the MTRR 66GG genotype: ORs 0.60 [95% confidence interval (CI) 0.39-0.91] and 0.64 (95% CI, 0.40-1.03), respectively. The ORs for paternal MTHFR 677CT and TT genotypes were 1.41 (95% CI, 1.02-1.93) and 1.81 (95% CI, 1.06-3.07). ORs varied little by maternal folic acid supplementation. Conclusions: Some folate pathway gene polymorphisms in the child or a parent may influence ALL risk. While biologically plausible, underlying mechanisms for these associations need further elucidation. Impact: Folate pathway polymorphisms may be related to risk of childhood ALL, but larger studies are needed for conclusive results.]]> Sat 24 Mar 2018 07:23:34 AEDT ]]>