Genome-wide association study of glioma and meta-analysis

Preetha Rajaraman; Beatrice S. Melin; Zhaoming Wang; Roberta McKean-Cowdin; Dominique S. Michaud; Sophia S. Wang; Melissa Bondy; Richard Houlston; Robert B. Jenkins; Margaret Wrensch; Meredith Yeager; Anders Ahlbom; Demetrius Albanes; Ulrika Andersson; Laura E.Beane Freeman; Julie E. Buring; Mary Ann Butler; Melissa Braganza; Tania Carreon; Maria Feychting; Sarah J. Fleming; Susan M. Gapstur; J. Michael Gaziano; Graham G. Giles; Goran Hallmans; Roger Henriksson; Judith Hoffman-Bolton; Peter D. Inskip; Christoffer Johansen; Cari M. Kitahara; Mark Lathrop; Chenwei Liu; Loic Le Marchand; Martha S. Linet; Stefan Lonn; Ulrike Peters; Mark P. Purdue; Nathaniel Rothman; Avima M. Ruder; Marc Sanson; Howard D. Sesso; Gianluca Severi; Gianluca Shu; Matthias Simon; Meir Stampfer; Victoria L. Stevens; Kala Visvanathan; Emily White; Alicja Wolk; Anne Zeleniuch-Jacquotte; Wei Zheng; Paul Decker; Victor Enciso-Mora; Brooke Fridley; Yu Tang Gao; Matthew Kosel; Daniel H. Lachance; Ching Lau; Terri Rice; Anthony Swerdlow; Joseph L. Wiemels; John K. Wiencke; Sanjay Shete; Yong Bing Xiang; Yuanyuan Xiao; Robert N. Hoover; Joseph F. Fraumeni; Nilanjan Chatterjee; Patricia Hartge; Stephen J. Chanock

doi:10.1007/s00439-012-1212-0

Genome-wide association study of glioma and meta-analysis

Preetha Rajaraman, Beatrice S. Melin, Zhaoming Wang, Roberta McKean-Cowdin, Dominique S. Michaud, Sophia S. Wang, Melissa Bondy, Richard Houlston, Robert B. Jenkins, Margaret Wrensch, Meredith Yeager, Anders Ahlbom, Demetrius Albanes, Ulrika Andersson, Laura E.Beane Freeman, Julie E. Buring, Mary Ann Butler, Melissa Braganza, Tania Carreon, Maria FeychtingSarah J. Fleming, Susan M. Gapstur, J. Michael Gaziano, Graham G. Giles, Goran Hallmans, Roger Henriksson, Judith Hoffman-Bolton, Peter D. Inskip, Christoffer Johansen, Cari M. Kitahara, Mark Lathrop, Chenwei Liu, Loic Le Marchand, Martha S. Linet, Stefan Lonn, Ulrike Peters, Mark P. Purdue, Nathaniel Rothman, Avima M. Ruder, Marc Sanson, Howard D. Sesso, Gianluca Severi, Gianluca Shu, Matthias Simon, Meir Stampfer, Victoria L. Stevens, Kala Visvanathan, Emily White, Alicja Wolk, Anne Zeleniuch-Jacquotte, Wei Zheng, Paul Decker, Victor Enciso-Mora, Brooke Fridley, Yu Tang Gao, Matthew Kosel, Daniel H. Lachance, Ching Lau, Terri Rice, Anthony Swerdlow, Joseph L. Wiemels, John K. Wiencke, Sanjay Shete, Yong Bing Xiang, Yuanyuan Xiao, Robert N. Hoover, Joseph F. Fraumeni, Nilanjan Chatterjee, Patricia Hartge, Stephen J. Chanock

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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.

Original language	English (US)
Pages (from-to)	1877-1888
Number of pages	12
Journal	Human genetics
Volume	131
Issue number	12
DOIs	https://doi.org/10.1007/s00439-012-1212-0
State	Published - Dec 2012

ASJC Scopus subject areas

Genetics
Genetics(clinical)

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10.1007/s00439-012-1212-0

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Rajaraman, P., Melin, B. S., Wang, Z., McKean-Cowdin, R., Michaud, D. S., Wang, S. S., Bondy, M., Houlston, R., Jenkins, R. B., Wrensch, M., Yeager, M., Ahlbom, A., Albanes, D., Andersson, U., Freeman, L. E. B., Buring, J. E., Butler, M. A., Braganza, M., Carreon, T., ... Chanock, S. J. (2012). Genome-wide association study of glioma and meta-analysis. Human genetics, 131(12), 1877-1888. https://doi.org/10.1007/s00439-012-1212-0

Rajaraman, P, Melin, BS, Wang, Z, McKean-Cowdin, R, Michaud, DS, Wang, SS, Bondy, M, Houlston, R, Jenkins, RB, Wrensch, M, Yeager, M, Ahlbom, A, Albanes, D, Andersson, U, Freeman, LEB, Buring, JE, Butler, MA, Braganza, M, Carreon, T, Feychting, M, Fleming, SJ, Gapstur, SM, Gaziano, JM, Giles, GG, Hallmans, G, Henriksson, R, Hoffman-Bolton, J, Inskip, PD, Johansen, C, Kitahara, CM, Lathrop, M, Liu, C, Marchand, LL, Linet, MS, Lonn, S, Peters, U, Purdue, MP, Rothman, N, Ruder, AM, Sanson, M, Sesso, HD, Severi, G, Shu, G, Simon, M, Stampfer, M, Stevens, VL, Visvanathan, K, White, E, Wolk, A, Zeleniuch-Jacquotte, A, Zheng, W, Decker, P, Enciso-Mora, V, Fridley, B, Gao, YT, Kosel, M, Lachance, DH, Lau, C, Rice, T, Swerdlow, A, Wiemels, JL, Wiencke, JK, Shete, S, Xiang, YB, Xiao, Y, Hoover, RN, Fraumeni, JF, Chatterjee, N, Hartge, P & Chanock, SJ 2012, 'Genome-wide association study of glioma and meta-analysis', Human genetics, vol. 131, no. 12, pp. 1877-1888. https://doi.org/10.1007/s00439-012-1212-0

@article{00bb637c1d8445b1b6e110079bf70eac,

title = "Genome-wide association study of glioma and meta-analysis",

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.",

author = "Preetha Rajaraman and Melin, {Beatrice S.} and Zhaoming Wang and Roberta McKean-Cowdin and Michaud, {Dominique S.} and Wang, {Sophia S.} and Melissa Bondy and Richard Houlston and Jenkins, {Robert B.} and Margaret Wrensch and Meredith Yeager and Anders Ahlbom and Demetrius Albanes and Ulrika Andersson and Freeman, {Laura E.Beane} and Buring, {Julie E.} and Butler, {Mary Ann} and Melissa Braganza and Tania Carreon and Maria Feychting and Fleming, {Sarah J.} and Gapstur, {Susan M.} and Gaziano, {J. Michael} and Giles, {Graham G.} and Goran Hallmans and Roger Henriksson and Judith Hoffman-Bolton and Inskip, {Peter D.} and Christoffer Johansen and Kitahara, {Cari M.} and Mark Lathrop and Chenwei Liu and Marchand, {Loic Le} and Linet, {Martha S.} and Stefan Lonn and Ulrike Peters and Purdue, {Mark P.} and Nathaniel Rothman and Ruder, {Avima M.} and Marc Sanson and Sesso, {Howard D.} and Gianluca Severi and Gianluca Shu and Matthias Simon and Meir Stampfer and Stevens, {Victoria L.} and Kala Visvanathan and Emily White and Alicja Wolk and Anne Zeleniuch-Jacquotte and Wei Zheng and Paul Decker and Victor Enciso-Mora and Brooke Fridley and Gao, {Yu Tang} and Matthew Kosel and Lachance, {Daniel H.} and Ching Lau and Terri Rice and Anthony Swerdlow and Wiemels, {Joseph L.} and Wiencke, {John K.} and Sanjay Shete and Xiang, {Yong Bing} and Yuanyuan Xiao and Hoover, {Robert N.} and Fraumeni, {Joseph F.} and Nilanjan Chatterjee and Patricia Hartge and Chanock, {Stephen J.}",

note = "Funding Information: Acknowledgments This research was supported by intramural funds from the NCI, NIH, Department of Health and Human Services, and has been funded in whole or in part with federal funds from the NCI, NIH, under contract N01-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US government. We are indebted to the scientific and field efforts of Michelle Brotzman (Westat), Laurie Burdette, Peter Hui (IMS), Annelie Landgren, Leah Mechanic, Lisa Newman (RTI), Aurelie Vogt, Tim Sheehy, Mitchel Berger, Susan Chang, Mike Prados, Tarik Tihan, Ivan Smirnov, and Lucie McCoy.",

year = "2012",

month = dec,

doi = "10.1007/s00439-012-1212-0",

language = "English (US)",

volume = "131",

pages = "1877--1888",

journal = "Human genetics",

issn = "0340-6717",

publisher = "Springer Verlag",

number = "12",

}

TY - JOUR

T1 - Genome-wide association study of glioma and meta-analysis

AU - Rajaraman, Preetha

AU - Melin, Beatrice S.

AU - Wang, Zhaoming

AU - McKean-Cowdin, Roberta

AU - Michaud, Dominique S.

AU - Wang, Sophia S.

AU - Bondy, Melissa

AU - Houlston, Richard

AU - Jenkins, Robert B.

AU - Wrensch, Margaret

AU - Yeager, Meredith

AU - Ahlbom, Anders

AU - Albanes, Demetrius

AU - Andersson, Ulrika

AU - Freeman, Laura E.Beane

AU - Buring, Julie E.

AU - Butler, Mary Ann

AU - Braganza, Melissa

AU - Carreon, Tania

AU - Feychting, Maria

AU - Fleming, Sarah J.

AU - Gapstur, Susan M.

AU - Gaziano, J. Michael

AU - Giles, Graham G.

AU - Hallmans, Goran

AU - Henriksson, Roger

AU - Hoffman-Bolton, Judith

AU - Inskip, Peter D.

AU - Johansen, Christoffer

AU - Kitahara, Cari M.

AU - Lathrop, Mark

AU - Liu, Chenwei

AU - Marchand, Loic Le

AU - Linet, Martha S.

AU - Lonn, Stefan

AU - Peters, Ulrike

AU - Purdue, Mark P.

AU - Rothman, Nathaniel

AU - Ruder, Avima M.

AU - Sanson, Marc

AU - Sesso, Howard D.

AU - Severi, Gianluca

AU - Shu, Gianluca

AU - Simon, Matthias

AU - Stampfer, Meir

AU - Stevens, Victoria L.

AU - Visvanathan, Kala

AU - White, Emily

AU - Wolk, Alicja

AU - Zeleniuch-Jacquotte, Anne

AU - Zheng, Wei

AU - Decker, Paul

AU - Enciso-Mora, Victor

AU - Fridley, Brooke

AU - Gao, Yu Tang

AU - Kosel, Matthew

AU - Lachance, Daniel H.

AU - Lau, Ching

AU - Rice, Terri

AU - Swerdlow, Anthony

AU - Wiemels, Joseph L.

AU - Wiencke, John K.

AU - Shete, Sanjay

AU - Xiang, Yong Bing

AU - Xiao, Yuanyuan

AU - Hoover, Robert N.

AU - Fraumeni, Joseph F.

AU - Chatterjee, Nilanjan

AU - Hartge, Patricia

AU - Chanock, Stephen J.

N1 - Funding Information: Acknowledgments This research was supported by intramural funds from the NCI, NIH, Department of Health and Human Services, and has been funded in whole or in part with federal funds from the NCI, NIH, under contract N01-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US government. We are indebted to the scientific and field efforts of Michelle Brotzman (Westat), Laurie Burdette, Peter Hui (IMS), Annelie Landgren, Leah Mechanic, Lisa Newman (RTI), Aurelie Vogt, Tim Sheehy, Mitchel Berger, Susan Chang, Mike Prados, Tarik Tihan, Ivan Smirnov, and Lucie McCoy.

PY - 2012/12

Y1 - 2012/12

N2 - 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.

AB - 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.

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U2 - 10.1007/s00439-012-1212-0

DO - 10.1007/s00439-012-1212-0

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AN - SCOPUS:84870988159

SN - 0340-6717

VL - 131

SP - 1877

EP - 1888

JO - Human genetics

JF - Human genetics

IS - 12

ER -

Genome-wide association study of glioma and meta-analysis

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