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dc.contributor.authorOstrom, QT
dc.contributor.authorColeman, W
dc.contributor.authorHuang, W
dc.contributor.authorRubin, JB
dc.contributor.authorLathia, JD
dc.contributor.authorBerens, ME
dc.contributor.authorSpeyer, G
dc.contributor.authorLiao, P
dc.contributor.authorWrensch, MR
dc.contributor.authorEckel-Passow, JE
dc.contributor.authorArmstrong, G
dc.contributor.authorRice, T
dc.contributor.authorWiencke, JK
dc.contributor.authorMcCoy, LS
dc.contributor.authorHansen, HM
dc.contributor.authorAmos, CI
dc.contributor.authorBernstein, JL
dc.contributor.authorClaus, EB
dc.contributor.authorHoulston, RS
dc.contributor.authorIl'yasova, D
dc.contributor.authorJenkins, RB
dc.contributor.authorJohansen, C
dc.contributor.authorLachance, DH
dc.contributor.authorLai, RK
dc.contributor.authorMerrell, RT
dc.contributor.authorOlson, SH
dc.contributor.authorSadetzki, S
dc.contributor.authorSchildkraut, JM
dc.contributor.authorShete, S
dc.contributor.authorAndersson, U
dc.contributor.authorRajaraman, P
dc.contributor.authorChanock, SJ
dc.contributor.authorLinet, MS
dc.contributor.authorWang, Z
dc.contributor.authorYeager, M
dc.contributor.authorGliomaScan consortium
dc.contributor.authorMelin, B
dc.contributor.authorBondy, ML
dc.contributor.authorBarnholtz-Sloan, JS
dc.date.accessioned2020-10-26T12:29:17Z
dc.date.issued2019-01
dc.identifier.citationNeuro-oncology, 2019, 21 (1), pp. 71 - 82
dc.identifier.issn1522-8517
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/4198
dc.identifier.eissn1523-5866
dc.identifier.doi10.1093/neuonc/noy135
dc.description.abstractBackground To date, genome-wide association studies (GWAS) have identified 25 risk variants for glioma, explaining 30% of heritable risk. Most histologies occur with significantly higher incidence in males, and this difference is not explained by currently known risk factors. A previous GWAS identified sex-specific glioma risk variants, and this analysis aims to further elucidate risk variation by sex using gene- and pathway-based approaches.Methods Results from the Glioma International Case-Control Study were used as a testing set, and results from 3 GWAS were combined via meta-analysis and used as a validation set. Using summary statistics for nominally significant autosomal SNPs (P < 0.01 in a previous meta-analysis) and nominally significant X-chromosome SNPs (P < 0.01), 3 algorithms (Pascal, BimBam, and GATES) were used to generate gene scores, and Pascal was used to generate pathway scores. Results were considered statistically significant in the discovery set when P < 3.3 × 10-6 and in the validation set when P < 0.001 in 2 of 3 algorithms.Results Twenty-five genes within 5 regions and 19 genes within 6 regions reached statistical significance in at least 2 of 3 algorithms in males and females, respectively. EGFR was significantly associated with all glioma and glioblastoma in males only and a female-specific association in TERT, all of which remained nominally significant after conditioning on known risk loci. There were nominal associations with the BioCarta telomeres pathway in both males and females.Conclusions These results provide additional evidence that there may be differences by sex in genetic risk for glioma. Additional analyses may further elucidate the biological processes through which this risk is conferred.
dc.formatPrint
dc.format.extent71 - 82
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://www.rioxx.net/licenses/all-rights-reserved
dc.subjectGliomaScan consortium
dc.subjectHumans
dc.subjectGlioma
dc.subjectGenetic Predisposition to Disease
dc.subjectTelomerase
dc.subjectPrognosis
dc.subjectSurvival Rate
dc.subjectRisk Factors
dc.subjectCase-Control Studies
dc.subjectFollow-Up Studies
dc.subjectSignal Transduction
dc.subjectSex Characteristics
dc.subjectGenotype
dc.subjectPolymorphism, Single Nucleotide
dc.subjectModels, Genetic
dc.subjectFemale
dc.subjectMale
dc.subjectGenome-Wide Association Study
dc.subjectErbB Receptors
dc.subjectBiomarkers, Tumor
dc.titleSex-specific gene and pathway modeling of inherited glioma risk.
dc.typeJournal Article
dcterms.dateAccepted2018-08-14
rioxxterms.versionofrecord10.1093/neuonc/noy135
rioxxterms.licenseref.urihttps://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2019-01
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfNeuro-oncology
pubs.issue1
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.volume21
pubs.embargo.termsNot known
icr.researchteamCancer Genomicsen_US
dc.contributor.icrauthorHoulston, Richarden


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