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dc.contributor.authorSaunders, CN
dc.contributor.authorCornish, AJ
dc.contributor.authorKinnersley, B
dc.contributor.authorLaw, PJ
dc.contributor.authorHoulston, RS
dc.contributor.authorCollaborators
dc.date.accessioned2020-10-20T11:05:32Z
dc.date.issued2021-01
dc.identifier.citationBritish journal of cancer, 2021, 124 (2), pp. 447 - 454
dc.identifier.issn0007-0920
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/4177
dc.identifier.eissn1532-1827
dc.identifier.doi10.1038/s41416-020-01083-1
dc.description.abstractBackground The aetiology of glioma is poorly understood. Summary data from genome-wide association studies (GWAS) can be used in a Mendelian randomisation (MR) phenome-wide association study (PheWAS) to search for glioma risk factors.Methods We performed an MR-PheWAS analysing 316 phenotypes, proxied by 8387 genetic variants, and summary genetic data from a GWAS of 12,488 glioma cases and 18,169 controls. Causal effects were estimated under a random-effects inverse-variance-weighted (IVW-RE) model, with robust adjusted profile score (MR-RAPS), weighted median and mode-based estimates computed to assess the robustness of findings. Odds ratios per one standard deviation increase in each phenotype were calculated for all glioma, glioblastoma (GBM) and non-GBM tumours.Results No significant associations (P < 1.58 × 10 -4 ) were observed between phenotypes and glioma under the IVW-RE model. Suggestive associations (1.58 × 10 -4  < P < 0.05) were observed between leukocyte telomere length (LTL) with all glioma (OR SD  = 3.91, P = 9.24 × 10 -3 ) and GBM (OR SD  = 4.86, P = 3.23 × 10 -2 ), but the association was primarily driven by the TERT variant rs2736100. Serum low-density lipoprotein cholesterol and plasma HbA1C showed suggestive associations with glioma (OR SD  = 1.11, P = 1.39 × 10 -2 and OR SD  = 1.28, P = 1.73 × 10 -2 , respectively), both associations being reliant on single genetic variants.Conclusions Our study provides further insight into the aetiological basis of glioma for which published data have been mixed.
dc.formatPrint-Electronic
dc.format.extent447 - 454
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectCollaborators
dc.titleSearching for causal relationships of glioma: a phenome-wide Mendelian randomisation study.
dc.typeJournal Article
dcterms.dateAccepted2020-09-04
rioxxterms.versionofrecord10.1038/s41416-020-01083-1
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2021-01
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfBritish journal of cancer
pubs.issue2
pubs.notesNot known
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/Genetics and 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/Genetics and Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Cancer Genomics
pubs.publication-statusPublished
pubs.volume124
pubs.embargo.termsNot known
icr.researchteamCancer Genomicsen_US
dc.contributor.icrauthorSaunders, Charlesen
dc.contributor.icrauthorKinnersley, Benjaminen
dc.contributor.icrauthorHoulston, Richarden


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