TY - JOUR
T1 - Chromosome 7p11.2 (EGFR) variation influences glioma risk
AU - Sanson, Marc
AU - Hosking, Fay J.
AU - Shete, Sanjay
AU - Zelenika, Diana
AU - Dobbins, Sara E.
AU - Ma, Yussanne
AU - Enciso-Mora, Victor
AU - Idbaih, Ahmed
AU - Delattre, Jean Yves
AU - Hoang-Xuan, Khe
AU - Marie, Yannick
AU - Boisselier, Blandine
AU - Carpentier, Catherine
AU - Wang, Xiao Wei
AU - Di Stefano, Anna Luisa
AU - Labussière, Marianne
AU - Gousias, Konstantinos
AU - Schramm, Johannes
AU - Boland, Anne
AU - Lechner, Doris
AU - Gut, Ivo
AU - Armstrong, Georgina
AU - Liu, Yanhong
AU - Yu, Robert
AU - Lau, Ching
AU - Di Bernardo, Maria Chiara
AU - Robertson, Lindsay B.
AU - Muir, Kenneth
AU - Hepworth, Sarah
AU - Swerdlow, Anthony
AU - Schoemaker, Minouk J.
AU - Wichmann, H. Erich
AU - Müller, Martina
AU - Schreiber, Stefan
AU - Franke, Andre
AU - Moebus, Susanne
AU - Eisele, Lewin
AU - Försti, Asta
AU - Hemminki, Kari
AU - Lathrop, Mark
AU - Bondy, Melissa
AU - Houlston, Richard S.
AU - Simon, Matthias
N1 - Funding Information:
In the UK, funding was provided by the Wellcome Trust and Cancer Research UK (C1298/A8362 supported by the Bobby Moore Fund) and the DJ Fielding Medical Research Trust. The UK INTERPHONE study was supported by the European Union Fifth Framework Program ‘Quality of life and Management of Living Resources’ (QLK4-CT-1999-01563) and the International Union against Cancer (UICC). The UICC received funds from the Mobile Manufacturers’ Forum and GSM Association. Provision of funds via the UICC was governed by agreements that guaranteed INTERPHONE’s scientific independence (http://www.iarc.fr/ENG/Units/RCAd.html). The UK centers were also supported by the Mobile Telecommunications and Health Research (MTHR) Programme and the Northern UK Centre was supported by the Health and Safety Executive, Department of Health and Safety Executive and the UK Network Operators. In the US, funding was provided by NIH grants 5R01(CA119215&5R01 CA070917). Support was also obtained from the American Brain Tumor Association and the National Brain Tumor Society. In France, funding was provided by the Délégation à la Recherche Clinique (MUL03012), the Association pour la Recherche sur les Tumeurs Cérébrales (ARTC), the Institut National du Cancer (INCa;PL046) and the French Ministry of Higher Education and Research. In Germany, funding was provided to M.S. and J.S. by the Deutsche Forschungsgemeinschaft (Si552,Schr285), the Deutsche Krebshilfe (70-2385-Wi2,70-3163-Wi3,10-6262) and BONFOR. Funding for the WTCCC was provided by the Wellcome Trust (076113&085475). The KORA Augsburg studies are supported by grants from the German Federal Ministry of Education and Research (BMBF) and were mainly financed by the Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg. This work was financed by the German National Genome Research Network (NGFN) and supported within the Munich Center of Health Sciences (MC Health) as part of LMUinnovativ.
PY - 2011/7
Y1 - 2011/7
N2 - While gliomas are the most common primary brain tumors, their etiology is largely unknown. To identify novel risk loci for glioma, we conducted genome-wide association (GWA) analysis of two case-control series from France and Germany (2269 cases and 2500 controls). Pooling these data with previously reported UK and US GWA studies provided data on 4147 glioma cases and 7435 controls genotyped for 424 460 common tagging single-nucleotide polymorphisms. Using these data, we demonstrate two statistically inde- pendent associations between glioma and rs11979158 and rs2252586, at 7p11.2 which encompasses the EGFR gene (population-corrected statistics, Pc = 7.72 × 10-8 and 2.09 × 10-8, respectively). Both associ- ations were independent of tumor subtype, and were independent of EGFR amplification, p16INK4a deletion and IDH1 mutation status in tumors; compatible with driver effects of the variants on glioma development. These findings show that variation in 7p11.2 is a determinant of inherited glioma risk.
AB - While gliomas are the most common primary brain tumors, their etiology is largely unknown. To identify novel risk loci for glioma, we conducted genome-wide association (GWA) analysis of two case-control series from France and Germany (2269 cases and 2500 controls). Pooling these data with previously reported UK and US GWA studies provided data on 4147 glioma cases and 7435 controls genotyped for 424 460 common tagging single-nucleotide polymorphisms. Using these data, we demonstrate two statistically inde- pendent associations between glioma and rs11979158 and rs2252586, at 7p11.2 which encompasses the EGFR gene (population-corrected statistics, Pc = 7.72 × 10-8 and 2.09 × 10-8, respectively). Both associ- ations were independent of tumor subtype, and were independent of EGFR amplification, p16INK4a deletion and IDH1 mutation status in tumors; compatible with driver effects of the variants on glioma development. These findings show that variation in 7p11.2 is a determinant of inherited glioma risk.
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U2 - 10.1093/hmg/ddr192
DO - 10.1093/hmg/ddr192
M3 - Article
C2 - 21531791
AN - SCOPUS:79959793196
SN - 0964-6906
VL - 20
SP - 2897
EP - 2904
JO - Human molecular genetics
JF - Human molecular genetics
IS - 14
M1 - ddr192
ER -