dc.contributor.author | Takahashi, H | |
dc.contributor.author | Cornish, AJ | |
dc.contributor.author | Sud, A | |
dc.contributor.author | Law, PJ | |
dc.contributor.author | Kinnersley, B | |
dc.contributor.author | Ostrom, QT | |
dc.contributor.author | Labreche, K | |
dc.contributor.author | Eckel-Passow, JE | |
dc.contributor.author | Armstrong, GN | |
dc.contributor.author | Claus, EB | |
dc.contributor.author | Il'yasova, D | |
dc.contributor.author | Schildkraut, J | |
dc.contributor.author | Barnholtz-Sloan, JS | |
dc.contributor.author | Olson, SH | |
dc.contributor.author | Bernstein, JL | |
dc.contributor.author | Lai, RK | |
dc.contributor.author | Schoemaker, MJ | |
dc.contributor.author | Simon, M | |
dc.contributor.author | Hoffmann, P | |
dc.contributor.author | Nöthen, MM | |
dc.contributor.author | Jöckel, K-H | |
dc.contributor.author | Chanock, S | |
dc.contributor.author | Rajaraman, P | |
dc.contributor.author | Johansen, C | |
dc.contributor.author | Jenkins, RB | |
dc.contributor.author | Melin, BS | |
dc.contributor.author | Wrensch, MR | |
dc.contributor.author | Sanson, M | |
dc.contributor.author | Bondy, ML | |
dc.contributor.author | Turnbull, C | |
dc.contributor.author | Houlston, RS | |
dc.date.accessioned | 2018-02-12T11:07:33Z | |
dc.date.issued | 2018-02-05 | |
dc.identifier.citation | Scientific reports, 2018, 8 (1), pp. 2339 - ? | |
dc.identifier.issn | 2045-2322 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/1045 | |
dc.identifier.eissn | 2045-2322 | |
dc.identifier.doi | 10.1038/s41598-018-20844-w | |
dc.description.abstract | To 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.format | Electronic | |
dc.format.extent | 2339 - ? | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | NATURE PUBLISHING GROUP | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | |
dc.subject | Humans | |
dc.subject | Glioma | |
dc.subject | Brain Neoplasms | |
dc.subject | Genetic Predisposition to Disease | |
dc.subject | Vitamin D | |
dc.subject | Polymorphism, Single Nucleotide | |
dc.subject | Genetic Variation | |
dc.subject | Mendelian Randomization Analysis | |
dc.title | Mendelian randomisation study of the relationship between vitamin D and risk of glioma. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2018-01-24 | |
rioxxterms.versionofrecord | 10.1038/s41598-018-20844-w | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by/4.0 | |
rioxxterms.licenseref.startdate | 2018-02-05 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Scientific reports | |
pubs.issue | 1 | |
pubs.notes | No 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-status | Published | |
pubs.volume | 8 | |
pubs.embargo.terms | No embargo | |
icr.researchteam | Aetiological Epidemiology | |
icr.researchteam | Cancer Genomics | |
dc.contributor.icrauthor | Cornish, Alexander | |
dc.contributor.icrauthor | Sud, Amit | |
dc.contributor.icrauthor | Law, Philip | |
dc.contributor.icrauthor | Kinnersley, Benjamin | |
dc.contributor.icrauthor | Schoemaker, Minouk | |
dc.contributor.icrauthor | Turnbull, Clare | |
dc.contributor.icrauthor | Houlston, Richard | |