Genome-wide Association Study of Glioma and Meta-Analysis
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Author
Rajaraman, Preetha
Melin, Beatrice
Wang, Zhaoming
McKean-Cowdin, Roberta
Michaud, Dominique
Wang, Sophia
Bondy, Melissa
Houlston, Richard
Jenkins, Robert
Wrensch, Margaret
Yeager, Meredith
Ahlbom, Anders
Albanes, Demetrius
Andersson, Ulrika
Freeman, Laura E. Beane
Buring, Julie
Butler, Mary Ann
Braganza, Melissa
Carreon, Tania
Feychting, Maria
Fleming, Sarah
Gapstur, Susan
Gaziano, J. Michael
Giles, Graham
Hallmans, Goran
Henriksson, Roger
Hoffman-Bolton, Judith
Inskip, Peter
Johansen, Christoffer
Kitahara, Cari
Lathrop, Mark
Liu, Chenwei
Le Marchand, Loic
Linet, Martha
Lonn, Stefan
Peters, Ulrike
Purdue, Mark
Rothman, Nathaniel
Ruder, Avima
Sanson, Marc
Sesso, Howard
Severi, Gianluca
Shu, Xiao-Ou
Simon, Matthias
Stevens, Victoria
Visvanathan, Kala
White, Emily
Wolk, Alicja
Zeleniuch-Jacquotte, Anne
Zheng, Wei
Decker, Paul
Enciso-Mora, Victor
Fridley, Brooke
Gao, Yu-Tang
Kosel, Matt
Lachance, Dan
Lau, Ching
Rice, Terri
Swerdlow, Anthony
Wiemels, Joe
Wiencke, John
Shete, Sanjay
Xiang, Yong-Bing
Xiao, Yuanyuan
Hoover, Robert
Fraumeni, Joseph Jr.
Chatterjee, Nilanjan
Hartge, Patricia
Chanock, Stephen
Published Version
https://doi.org/10.1007/s00439-012-1212-0Metadata
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Rajaraman, Preetha, Beatrice S. Melin, Zhaoming Wang, Roberta McKean-Cowdin, Dominique S. Michaud, Sophia S. Wang, Melissa Bondy, et al. 2012. “Genome-Wide Association Study of Glioma and Meta-Analysis.” Human Genetics 131 (12): 1877–88. https://doi.org/10.1007/s00439-012-1212-0.Abstract
Gliomas account for approximately 80 % of all primary malignant brain tumors and, despite improvements in clinical care over the last 20 years, remain among the most lethal tumors, underscoring the need for gaining new insights that could translate into clinical advances. Recent genome-wide association studies (GWAS) have identified seven new susceptibility regions. We conducted a new independent GWAS of glioma using 1,856 cases and 4,955 controls (from 14 cohort studies, 3 case-control studies, and 1 population-based case-only study) and found evidence of strong replication for three of the seven previously reported associations at 20q13.33 (RTEL), 5p15.33 (TERT), and 9p21.3 (CDKN2BAS), and consistent association signals for the remaining four at 7p11.2 (EGFR both loci), 8q24.21 (CCDC26) and 11q23.3 (PHLDB1). The direction and magnitude of the signal were consistent for samples from cohort and case-control studies, but the strength of the association was more pronounced for loci rs6010620 (20q,13.33; RTEL) and rs2736100 (5p15.33, TERT) in cohort studies despite the smaller number of cases in this group, likely due to relatively more higher grade tumors being captured in the cohort studies. We further examined the 85 most promising single nucleotide polymorphism (SNP) markers identified in our study in three replication sets (5,015 cases and 11,601 controls), but no new markers reached genome-wide significance. Our findings suggest that larger studies focusing on novel approaches as well as specific tumor subtypes or subgroups will be required to identify additional common susceptibility loci for glioma risk.Terms of Use
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