作者
Beatrice Melin,Jill S. Barnholtz‐Sloan,Margaret Wrensch,Christoffer Johansen,Dora Il’yasova,Ben Kinnersley,Quinn T. Ostrom,Karim Labreche,Yanwen Chen,Georgina Armstrong,Yanhong Liu,Jeanette E. Eckel‐Passow,Paul A. Decker,Marianne Labussière,Ahmed Idbaïh,Khê Hoang‐Xuan,Anna Luisa Di Stefano,Karima Mokhtari,Jean‐Yves Delattre,Peter Broderick,Pilar Galán,Konstantinos Gousias,Johannes Schramm,Minouk J. Schoemaker,Sarah Fleming,Stefan Herms,Stefanie Heilmann,Markus M. Nöthen,Heinz‐Erich Wichmann,Stefan Schreiber,Anthony Swerdlow,Mark Lathrop,Matthias Simon,Marc Sanson,Ulrika Andersson,Preetha Rajaraman,Stephen J. Chanock,Martha S. Linet,Zhaoming Wang,Meredith Yeager,John K. Wiencke,Helen M. Hansen,Lucie McCoy,Terri Rice,Matthew L. Kosel,Hugues Sicotte,Christopher I. Amos,Jonine L. Bernstein,Faith E. Davis,Dan Lachance,Ching C. Lau,Ryan Merrell,Joellen Shildkraut,Francis Ali‐Osman,Siegal Sadetzki,Michael E. Scheurer,Sanjay Shete,Rose Lai,Elizabeth B. Claus,Sara H. Olson,Robert B. Jenkins,Richard S. Houlston,Melissa L. Bondy
摘要
Beatrice Melin, Richard Houlston, Melissa Bondy and colleagues report results of a large-scale genome-wide association study of glioma. They identify five new risk loci for glioblastoma and eight new risk loci for non-glioblastoma tumors, highlighting distinct genetic etiologies for these two glioma subtypes. 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.