Genome-wide association study of glioma subtypes identifies specific differences in genetic susceptibility to glioblastoma and non-glioblastoma tumors.
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Authors
Melin, BS
Barnholtz-Sloan, JS
Wrensch, MR
Johansen, C
Il'yasova, D
Kinnersley, B
Ostrom, QT
Labreche, K
Chen, Y
Armstrong, G
Liu, Y
Eckel-Passow, JE
Decker, PA
Labussière, M
Idbaih, A
Hoang-Xuan, K
Di Stefano, A-L
Mokhtari, K
Delattre, J-Y
Broderick, P
Galan, P
Gousias, K
Schramm, J
Schoemaker, MJ
Fleming, SJ
Herms, S
Heilmann, S
Nöthen, MM
Wichmann, H-E
Schreiber, S
Swerdlow, A
Lathrop, M
Simon, M
Sanson, M
Andersson, U
Rajaraman, P
Chanock, S
Linet, M
Wang, Z
Yeager, M
GliomaScan Consortium,
Wiencke, JK
Hansen, H
McCoy, L
Rice, T
Kosel, ML
Sicotte, H
Amos, CI
Bernstein, JL
Davis, F
Lachance, D
Lau, C
Merrell, RT
Shildkraut, J
Ali-Osman, F
Sadetzki, S
Scheurer, M
Shete, S
Lai, RK
Claus, EB
Olson, SH
Jenkins, RB
Houlston, RS
Bondy, ML
Barnholtz-Sloan, JS
Wrensch, MR
Johansen, C
Il'yasova, D
Kinnersley, B
Ostrom, QT
Labreche, K
Chen, Y
Armstrong, G
Liu, Y
Eckel-Passow, JE
Decker, PA
Labussière, M
Idbaih, A
Hoang-Xuan, K
Di Stefano, A-L
Mokhtari, K
Delattre, J-Y
Broderick, P
Galan, P
Gousias, K
Schramm, J
Schoemaker, MJ
Fleming, SJ
Herms, S
Heilmann, S
Nöthen, MM
Wichmann, H-E
Schreiber, S
Swerdlow, A
Lathrop, M
Simon, M
Sanson, M
Andersson, U
Rajaraman, P
Chanock, S
Linet, M
Wang, Z
Yeager, M
GliomaScan Consortium,
Wiencke, JK
Hansen, H
McCoy, L
Rice, T
Kosel, ML
Sicotte, H
Amos, CI
Bernstein, JL
Davis, F
Lachance, D
Lau, C
Merrell, RT
Shildkraut, J
Ali-Osman, F
Sadetzki, S
Scheurer, M
Shete, S
Lai, RK
Claus, EB
Olson, SH
Jenkins, RB
Houlston, RS
Bondy, ML
Document Type
Journal Article
Date
2017-05-01
Date Accepted
2017-03-01
Abstract
Genome-wide association studies (GWAS) have transformed our understanding of glioma susceptibility, but individual studies have had limited power to identify risk loci. We performed a meta-analysis of existing GWAS and two new GWAS, which totaled 12,496 cases and 18,190 controls. We identified five new loci for glioblastoma (GBM) at 1p31.3 (rs12752552; P = 2.04 × 10-9, odds ratio (OR) = 1.22), 11q14.1 (rs11233250; P = 9.95 × 10-10, OR = 1.24), 16p13.3 (rs2562152; P = 1.93 × 10-8, OR = 1.21), 16q12.1 (rs10852606; P = 1.29 × 10-11, OR = 1.18) and 22q13.1 (rs2235573; P = 1.76 × 10-10, OR = 1.15), as well as eight loci for non-GBM tumors at 1q32.1 (rs4252707; P = 3.34 × 10-9, OR = 1.19), 1q44 (rs12076373; P = 2.63 × 10-10, OR = 1.23), 2q33.3 (rs7572263; P = 2.18 × 10-10, OR = 1.20), 3p14.1 (rs11706832; P = 7.66 × 10-9, OR = 1.15), 10q24.33 (rs11598018; P = 3.39 × 10-8, OR = 1.14), 11q21 (rs7107785; P = 3.87 × 10-10, OR = 1.16), 14q12 (rs10131032; P = 5.07 × 10-11, OR = 1.33) and 16p13.3 (rs3751667; P = 2.61 × 10-9, OR = 1.18). These data substantiate that genetic susceptibility to GBM and non-GBM tumors are highly distinct, which likely reflects different etiology.
Citation
Nature genetics, 2017, 49 (5), pp. 789 - 794
DOI
Source Title
Publisher
NATURE PORTFOLIO
ISSN
1061-4036
eISSN
1546-1718
Research Team
Aetiological Epidemiology
Cancer Genomics
Cancer Genomics