A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease

Title: A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease
Author(s): Nikpay, M
Goel, A
Won, H-H
Hall, LM
Willenborg, C
Kanoni, S
Saleheen, D
Kyriakou, T
Nelson, CP
Hopewell, JC
Webb, TR
Zeng, L
Dehghan, A
Alver, M
Armasu, SM
Auro, K
Bjonnes, A
Chasman, DI
Chen, S
Ford, I
Franceschini, N
Gieger, C
Grace, C
Gustafsson, S
Huang, J
Hwang, S-J
Kim, YK
Kleber, ME
Lau, KW
Lu, X
Lu, Y
Lyytikainen, L-P
Mihailov, E
Morrison, AC
Pervjakova, N
Qu, L
Rose, LM
Salfati, E
Saxena, R
Scholz, M
Smith, AV
Tikkanen, E
Uitterlinden, A
Yang, X
Zhang, W
Zhao, W
De Andrade, M
De Vries, PS
Van Zuydam, NR
Anand, SS
Bertram, L
Beutner, F
Dedoussis, G
Frossard, P
Gauguier, D
Goodall, AH
Gottesman, O
Haber, M
Han, B-G
Huang, J
Jalilzadeh, S
Kessler, T
Koenig, IR
Lannfelt, L
Lieb, W
Lind, L
Lindgren, CM
Lokki, M-L
Magnusson, PK
Mallick, NH
Mehra, N
Meitinger, T
Memon, F-U-R
Morris, AP
Nieminen, MS
Pedersen, NL
Peters, A
Rallidis, LS
Rasheed, A
Samuel, M
Shah, SH
Sinisalo, J
Stirrups, KE
Trompet, S
Wang, L
Zaman, KS
Ardissino, D
Boerwinkle, E
Borecki, IB
Bottinger, EP
Buring, JE
Chambers, JC
Collins, R
Cupples, LA
Danesh, J
Demuth, I
Elosua, R
Epstein, SE
Esko, T
Feitosa, MF
Franco, OH
Franzosi, MG
Granger, CB
Gu, D
Gudnason, V
Hall, AS
Hamsten, A
Harris, TB
Hazen, SL
Hengstenberg, C
Hofman, A
Ingelsson, E
Iribarren, C
Jukema, JW
Karhunen, PJ
Kim, B-J
Kooner, JS
Kullo, IJ
Lehtimaki, T
Loos, RJF
Melander, O
Metspalu, A
Maerz, W
Palmer, CN
Perola, M
Quertermous, T
Rader, DJ
Ridker, PM
Ripatti, S
Roberts, R
Salomaa, V
Sanghera, DK
Schwartz, SM
Seedorf, U
Stewart, AF
Stott, DJ
Thiery, J
Zalloua, PA
O'Donnell, CJ
Reilly, MP
Assimes, TL
Thompson, JR
Erdmann, J
Clarke, R
Watkins, H
Kathiresan, S
McPherson, R
Deloukas, P
Schunkert, H
Samani, NJ
Farrall, M
Item Type: Journal Article
Abstract: Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largely based on genome-wide association studies (GWAS) analysis of common SNPs. Leveraging phased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of 185 thousand CAD cases and controls, interrogating 6.7 million common (MAF>0.05) as well as 2.7 million low frequency (0.005<MAF<0.05) variants. In addition to confirmation of most known CAD loci, we identified 10 novel loci, eight additive and two recessive, that contain candidate genes that newly implicate biological processes in vessel walls. We observed intra-locus allelic heterogeneity but little evidence of low frequency variants with larger effects and no evidence of synthetic association. Our analysis provides a comprehensive survey of the fine genetic architecture of CAD showing that genetic susceptibility to this common disease is largely determined by common SNPs of small effect size
Publication Date: 7-Sep-2015
Date of Acceptance: 1-Sep-2015
URI: http://hdl.handle.net/10044/1/49225
DOI: https://dx.doi.org/10.1038/ng.3396
ISSN: 1061-4036
Publisher: Nature Publishing Group
Start Page: 1121
End Page: 1130
Journal / Book Title: Nature Genetics
Volume: 47
Issue: 10
Copyright Statement: © 2015, Rights Managed by Nature Publishing Group
Copyright Statement: © 2015, Rights Managed by Nature Publishing Group
Keywords: Science & Technology
Life Sciences & Biomedicine
Genetics & Heredity
HEART-DISEASE
CARDIOVASCULAR-DISEASE
MYOCARDIAL-INFARCTION
SUSCEPTIBILITY LOCUS
GENETIC-VARIANTS
CELL-MIGRATION
IDENTIFIES 13
MICE LACKING
EXPRESSION
RISK
Coronary Artery Disease
Genome, Human
Genome-Wide Association Study
Humans
Phenotype
CARDIoGRAMplusC4D Consortium
Humans
Phenotype
Genome, Human
Coronary Artery Disease
Genome-Wide Association Study
Developmental Biology
11 Medical And Health Sciences
06 Biological Sciences
Publication Status: Published
Appears in Collections:Faculty of Medicine
Epidemiology, Public Health and Primary Care



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