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Folate pathway gene polymorphisms, maternal folic acid use, and risk of childhood acute lymphoblastic leukemia.

Identifieur interne : 003130 ( PubMed/Corpus ); précédent : 003129; suivant : 003131

Folate pathway gene polymorphisms, maternal folic acid use, and risk of childhood acute lymphoblastic leukemia.

Auteurs : Elizabeth Milne ; Kathryn R. Greenop ; Rodney J. Scott ; Michelle Haber ; Murray D. Norris ; John Attia ; Sarra E. Jamieson ; Margaret Miller ; Carol Bower ; Helen D. Bailey ; Somer Dawson ; Geoffrey B. Mccowage ; Nicholas H. De Klerk ; Frank M. Van Bockxmeer ; Bruce K. Armstrong

Source :

RBID : pubmed:25395472

English descriptors

Abstract

Several studies suggest that maternal folic acid supplementation before or during pregnancy protects against childhood acute lymphoblastic leukemia (ALL). We investigated associations between ALL risk and folate pathway gene polymorphisms, and their modification by maternal folic acid supplements, in a population-based case-control study (2003-2007).

DOI: 10.1158/1055-9965.EPI-14-0680
PubMed: 25395472

Links to Exploration step

pubmed:25395472

Le document en format XML

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<term>Child, Preschool</term>
<term>Dietary Supplements (analysis)</term>
<term>Female</term>
<term>Folic Acid (genetics)</term>
<term>Genetic Predisposition to Disease</term>
<term>Humans</term>
<term>Infant</term>
<term>Infant, Newborn</term>
<term>Polymorphism, Genetic</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (etiology)</term>
<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma (genetics)</term>
<term>Pregnancy</term>
<term>Risk Factors</term>
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<term>Folic Acid</term>
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<term>Dietary Supplements</term>
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<term>Precursor Cell Lymphoblastic Leukemia-Lymphoma</term>
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<term>Child</term>
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<term>Female</term>
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<div type="abstract" xml:lang="en">Several studies suggest that maternal folic acid supplementation before or during pregnancy protects against childhood acute lymphoblastic leukemia (ALL). We investigated associations between ALL risk and folate pathway gene polymorphisms, and their modification by maternal folic acid supplements, in a population-based case-control study (2003-2007).</div>
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<DateCreated>
<Year>2015</Year>
<Month>01</Month>
<Day>14</Day>
</DateCreated>
<DateCompleted>
<Year>2015</Year>
<Month>09</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised>
<Year>2015</Year>
<Month>01</Month>
<Day>14</Day>
</DateRevised>
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<ISSN IssnType="Electronic">1538-7755</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>24</Volume>
<Issue>1</Issue>
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<Year>2015</Year>
<Month>Jan</Month>
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<Title>Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology</Title>
<ISOAbbreviation>Cancer Epidemiol. Biomarkers Prev.</ISOAbbreviation>
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<ArticleTitle>Folate pathway gene polymorphisms, maternal folic acid use, and risk of childhood acute lymphoblastic leukemia.</ArticleTitle>
<Pagination>
<MedlinePgn>48-56</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1158/1055-9965.EPI-14-0680</ELocationID>
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<AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Several studies suggest that maternal folic acid supplementation before or during pregnancy protects against childhood acute lymphoblastic leukemia (ALL). We investigated associations between ALL risk and folate pathway gene polymorphisms, and their modification by maternal folic acid supplements, in a population-based case-control study (2003-2007).</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">All Australian pediatric oncology centers provided cases; controls were recruited by national random digit dialing. Data from 392 cases and 535 controls were included. Seven folate pathway gene polymorphisms (MTHFR 677C>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.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="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.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="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.</AbstractText>
<AbstractText Label="IMPACT" NlmCategory="CONCLUSIONS">Folate pathway polymorphisms may be related to risk of childhood ALL, but larger studies are needed for conclusive results.</AbstractText>
<CopyrightInformation>©2014 American Association for Cancer Research.</CopyrightInformation>
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<ForeName>Elizabeth</ForeName>
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</AffiliationInfo>
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</AffiliationInfo>
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</AffiliationInfo>
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<Affiliation>Telethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.</Affiliation>
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<Affiliation>Telethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia. Section of Environment and Radiation, International Agency for Research on Cancer, Lyon, France.</Affiliation>
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<LastName>Dawson</LastName>
<ForeName>Somer</ForeName>
<Initials>S</Initials>
<AffiliationInfo>
<Affiliation>Telethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.</Affiliation>
</AffiliationInfo>
</Author>
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<Affiliation>Oncology Unit, The Children's Hospital at Westmead, Sydney, Australia.</Affiliation>
</AffiliationInfo>
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<ForeName>Nicholas H</ForeName>
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<AffiliationInfo>
<Affiliation>Telethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>van Bockxmeer</LastName>
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<Initials>FM</Initials>
<AffiliationInfo>
<Affiliation>Department of Clinical Biochemistry, Royal Perth Hospital and the School of Surgery, University of Western Australia, Perth, Western Australia, Australia.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Armstrong</LastName>
<ForeName>Bruce K</ForeName>
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<AffiliationInfo>
<Affiliation>Sax Institute, Haymarket, New South Wales, Australia. Sydney School of Public Health, University of Sydney, Sydney, New South Wales, Australia.</Affiliation>
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