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dc.contributor.authorTakahashi, H
dc.contributor.authorCornish, AJ
dc.contributor.authorSud, A
dc.contributor.authorLaw, PJ
dc.contributor.authorKinnersley, B
dc.contributor.authorOstrom, QT
dc.contributor.authorLabreche, K
dc.contributor.authorEckel-Passow, JE
dc.contributor.authorArmstrong, GN
dc.contributor.authorClaus, EB
dc.contributor.authorIl'yasova, D
dc.contributor.authorSchildkraut, J
dc.contributor.authorBarnholtz-Sloan, JS
dc.contributor.authorOlson, SH
dc.contributor.authorBernstein, JL
dc.contributor.authorLai, RK
dc.contributor.authorSchoemaker, MJ
dc.contributor.authorSimon, M
dc.contributor.authorHoffmann, P
dc.contributor.authorNöthen, MM
dc.contributor.authorJöckel, K-H
dc.contributor.authorChanock, S
dc.contributor.authorRajaraman, P
dc.contributor.authorJohansen, C
dc.contributor.authorJenkins, RB
dc.contributor.authorMelin, BS
dc.contributor.authorWrensch, MR
dc.contributor.authorSanson, M
dc.contributor.authorBondy, ML
dc.contributor.authorTurnbull, C
dc.contributor.authorHoulston, RS
dc.date.accessioned2018-02-12T11:07:33Z
dc.date.issued2018-02-05
dc.identifier.citationScientific reports, 2018, 8 (1), pp. 2339 - ?
dc.identifier.issn2045-2322
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1045
dc.identifier.eissn2045-2322
dc.identifier.doi10.1038/s41598-018-20844-w
dc.description.abstractTo examine for a causal relationship between vitamin D and glioma risk we performed an analysis of genetic variants associated with serum 25-hydroxyvitamin D (25(OH)D) levels using Mendelian randomisation (MR), an approach unaffected by biases from confounding. Two-sample MR was undertaken using genome-wide association study data. Single nucleotide polymorphisms (SNPs) associated with 25(OH)D levels were used as instrumental variables (IVs). We calculated MR estimates for the odds ratio (OR) for 25(OH)D levels with glioma using SNP-glioma estimates from 12,488 cases and 18,169 controls, using inverse-variance weighted (IVW) and maximum likelihood estimation (MLE) methods. A non-significant association between 25(OH)D levels and glioma risk was shown using both the IVW (OR = 1.21, 95% confidence interval [CI] = 0.90-1.62, P = 0.201) and MLE (OR = 1.20, 95% CI = 0.98-1.48, P = 0.083) methods. In an exploratory analysis of tumour subtype, an inverse relationship between 25(OH)D levels and glioblastoma (GBM) risk was identified using the MLE method (OR = 0.62, 95% CI = 0.43-0.89, P = 0.010), but not the IVW method (OR = 0.62, 95% CI = 0.37-1.04, P = 0.070). No statistically significant association was shown between 25(OH)D levels and non-GBM glioma. Our results do not provide evidence for a causal relationship between 25(OH)D levels and all forms of glioma risk. More evidence is required to explore the relationship between 25(OH)D levels and risk of GBM.
dc.formatElectronic
dc.format.extent2339 - ?
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectHumans
dc.subjectGlioma
dc.subjectBrain Neoplasms
dc.subjectGenetic Predisposition to Disease
dc.subjectVitamin D
dc.subjectPolymorphism, Single Nucleotide
dc.subjectGenetic Variation
dc.subjectMendelian Randomization Analysis
dc.titleMendelian randomisation study of the relationship between vitamin D and risk of glioma.
dc.typeJournal Article
dcterms.dateAccepted2018-01-24
rioxxterms.versionofrecord10.1038/s41598-018-20844-w
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2018-02-05
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfScientific reports
pubs.issue1
pubs.notesNo embargo
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Aetiological Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Aetiological Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Cancer Genomics
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Aetiological Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Aetiological Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Cancer Genomics
pubs.publication-statusPublished
pubs.volume8
pubs.embargo.termsNo embargo
icr.researchteamAetiological Epidemiologyen_US
icr.researchteamCancer Genomicsen_US
dc.contributor.icrauthorCornish, Alexanderen
dc.contributor.icrauthorSchoemaker, Minouken
dc.contributor.icrauthorSud, Amiten
dc.contributor.icrauthorLaw, Philipen
dc.contributor.icrauthorKinnersley, Benjaminen
dc.contributor.icrauthorHoulston, Richarden
dc.contributor.icrauthorTurnbull, Clareen


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