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dc.contributor.authorAtkins, I
dc.contributor.authorKinnersley, B
dc.contributor.authorOstrom, QT
dc.contributor.authorLabreche, K
dc.contributor.authorIl'yasova, D
dc.contributor.authorArmstrong, GN
dc.contributor.authorEckel-Passow, JE
dc.contributor.authorSchoemaker, MJ
dc.contributor.authorNöthen, MM
dc.contributor.authorBarnholtz-Sloan, JS
dc.contributor.authorSwerdlow, AJ
dc.contributor.authorSimon, M
dc.contributor.authorRajaraman, P
dc.contributor.authorChanock, SJ
dc.contributor.authorShildkraut, J
dc.contributor.authorBernstein, JL
dc.contributor.authorHoffmann, P
dc.contributor.authorJöckel, K-H
dc.contributor.authorLai, RK
dc.contributor.authorClaus, EB
dc.contributor.authorOlson, SH
dc.contributor.authorJohansen, C
dc.contributor.authorWrensch, MR
dc.contributor.authorMelin, B
dc.contributor.authorJenkins, RB
dc.contributor.authorSanson, M
dc.contributor.authorBondy, ML
dc.contributor.authorHoulston, RS
dc.date.accessioned2019-02-04T10:17:20Z
dc.date.issued2019-04
dc.identifier.citationCancer research, 2019, 79 (8), pp. 2065 - 2071
dc.identifier.issn0008-5472
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3040
dc.identifier.eissn1538-7445
dc.identifier.doi10.1158/0008-5472.can-18-2888
dc.description.abstractGenome-wide association studies (GWAS) have so far identified 25 loci associated with glioma risk, with most showing specificity for either glioblastoma (GBM) or non-GBM tumors. The majority of these GWAS susceptibility variants reside in noncoding regions and the causal genes underlying the associations are largely unknown. Here we performed a transcriptome-wide association study to search for novel risk loci and candidate causal genes at known GWAS loci using Genotype-Tissue Expression Project (GTEx) data to predict cis -predicted gene expression in relation to GBM and non-GBM risk in conjunction with GWAS summary statistics on 12,488 glioma cases (6,183 GBM and 5,820 non-GBM) and 18,169 controls. Imposing a Bonferroni-corrected significance level of P < 5.69 × 10 -6 , we identified 31 genes, including GALNT6 at 12q13.33, as a candidate novel risk locus for GBM (mean Z = 4.43; P = 5.68 × 10 -6 ). GALNT6 resides at least 55 Mb away from any previously identified glioma risk variant, while all other 30 significantly associated genes were located within 1 Mb of known GWAS-identified loci and were not significant after conditioning on the known GWAS-identified variants. These data identify a novel locus ( GALNT6 at 12q13.33) and 30 genes at 12 known glioma risk loci associated with glioma risk, providing further insights into glioma tumorigenesis. SIGNIFICANCE: This study identifies new genes associated with glioma risk, increasing understanding of how these tumors develop.
dc.formatPrint-Electronic
dc.format.extent2065 - 2071
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://www.rioxx.net/licenses/under-embargo-all-rights-reserved
dc.subjectHumans
dc.subjectGlioma
dc.subjectGenetic Predisposition to Disease
dc.subjectPrognosis
dc.subjectCase-Control Studies
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectGenotype
dc.subjectPolymorphism, Single Nucleotide
dc.subjectQuantitative Trait Loci
dc.subjectGenome-Wide Association Study
dc.subjectTranscriptome
dc.subjectBiomarkers, Tumor
dc.titleTranscriptome-Wide Association Study Identifies New Candidate Susceptibility Genes for Glioma.
dc.typeJournal Article
dcterms.dateAccepted2019-01-24
rioxxterms.versionofrecord10.1158/0008-5472.can-18-2888
rioxxterms.licenseref.urihttps://www.rioxx.net/licenses/under-embargo-all-rights-reserved
rioxxterms.licenseref.startdate2019-04
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfCancer research
pubs.issue8
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/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.volume79
pubs.embargo.termsNot known
icr.researchteamAetiological Epidemiologyen_US
icr.researchteamCancer Genomicsen_US
dc.contributor.icrauthorKinnersley, Benjaminen
dc.contributor.icrauthorSchoemaker, Minouken
dc.contributor.icrauthorHoulston, Richarden
dc.contributor.icrauthorSwerdlow, Anthonyen


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