dc.contributor.author | Atkins, I | |
dc.contributor.author | Kinnersley, B | |
dc.contributor.author | Ostrom, QT | |
dc.contributor.author | Labreche, K | |
dc.contributor.author | Il'yasova, D | |
dc.contributor.author | Armstrong, GN | |
dc.contributor.author | Eckel-Passow, JE | |
dc.contributor.author | Schoemaker, MJ | |
dc.contributor.author | Nöthen, MM | |
dc.contributor.author | Barnholtz-Sloan, JS | |
dc.contributor.author | Swerdlow, AJ | |
dc.contributor.author | Simon, M | |
dc.contributor.author | Rajaraman, P | |
dc.contributor.author | Chanock, SJ | |
dc.contributor.author | Shildkraut, J | |
dc.contributor.author | Bernstein, JL | |
dc.contributor.author | Hoffmann, P | |
dc.contributor.author | Jöckel, K-H | |
dc.contributor.author | Lai, RK | |
dc.contributor.author | Claus, EB | |
dc.contributor.author | Olson, SH | |
dc.contributor.author | Johansen, C | |
dc.contributor.author | Wrensch, MR | |
dc.contributor.author | Melin, B | |
dc.contributor.author | Jenkins, RB | |
dc.contributor.author | Sanson, M | |
dc.contributor.author | Bondy, ML | |
dc.contributor.author | Houlston, RS | |
dc.date.accessioned | 2019-02-04T10:17:20Z | |
dc.date.issued | 2019-04-15 | |
dc.identifier.citation | Cancer research, 2019, 79 (8), pp. 2065 - 2071 | |
dc.identifier.issn | 0008-5472 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/3040 | |
dc.identifier.eissn | 1538-7445 | |
dc.identifier.doi | 10.1158/0008-5472.can-18-2888 | |
dc.description.abstract | Genome-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.format | Print-Electronic | |
dc.format.extent | 2065 - 2071 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | AMER ASSOC CANCER RESEARCH | |
dc.rights.uri | https://www.rioxx.net/licenses/under-embargo-all-rights-reserved | |
dc.subject | Humans | |
dc.subject | Glioma | |
dc.subject | Genetic Predisposition to Disease | |
dc.subject | Prognosis | |
dc.subject | Case-Control Studies | |
dc.subject | Gene Expression Regulation, Neoplastic | |
dc.subject | Genotype | |
dc.subject | Polymorphism, Single Nucleotide | |
dc.subject | Quantitative Trait Loci | |
dc.subject | Genome-Wide Association Study | |
dc.subject | Transcriptome | |
dc.subject | Biomarkers, Tumor | |
dc.title | Transcriptome-Wide Association Study Identifies New Candidate Susceptibility Genes for Glioma. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2019-01-24 | |
rioxxterms.versionofrecord | 10.1158/0008-5472.can-18-2888 | |
rioxxterms.licenseref.uri | https://www.rioxx.net/licenses/under-embargo-all-rights-reserved | |
rioxxterms.licenseref.startdate | 2019-04 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Cancer research | |
pubs.issue | 8 | |
pubs.notes | Not 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-status | Published | |
pubs.volume | 79 | |
pubs.embargo.terms | Not known | |
icr.researchteam | Aetiological Epidemiology | |
icr.researchteam | Cancer Genomics | |
dc.contributor.icrauthor | Kinnersley, Benjamin | |
dc.contributor.icrauthor | Schoemaker, Minouk | |
dc.contributor.icrauthor | Swerdlow, Anthony | |
dc.contributor.icrauthor | Houlston, Richard | |