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.
Genome-wide association study of glioma subtypes identifies specific differences in genetic susceptibility to glioblastoma and non-glioblastoma tumors.
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