TY - JOUR
T1 - Large-Scale Gene-Centric Analysis Identifies Novel Variants for Coronary Artery Disease
AU - Butterworth, Adam S.
AU - Braund, Peter S.
AU - Farrall, Martin
AU - Hardwick, Robert J.
AU - Saleheen, Danish
AU - Peden, John F
AU - Soranzo, Nicole
AU - Chambers, John C.
AU - Sivapalaratnam, Suthesh
AU - Kleber, Marcus E.
AU - Keating, Brendan
AU - Qasim, Atif
AU - Klopp, Norman
AU - Erdmann, Jeanette
AU - Assimes, Themistocles L.
AU - Ball, Stephen G.
AU - Balmforth, Anthony J
AU - Barnes, Timothy A.
AU - Basart, Hanneke
AU - Baumert, Jens
AU - Bezzina, Connie R
AU - Boerwinkle, Eric
AU - Boehm, Bernhard O.
AU - Brocheton, Jessy
AU - Bugert, Peter
AU - Cambien, Francois
AU - Clarke, Robert
AU - Codd, Veryan
AU - Collins, Rory
AU - Couper, David
AU - Cupples, L. Adrienne
AU - de Jong, Jonas S.
AU - Diemert, Patrick
AU - Ejebe, Kenechi
AU - Elbers, Clara C.
AU - Elliott, Paul
AU - Fornage, Myriam
AU - Franzosi, Maria Grazia
AU - Frossard, Philippe
AU - Garner, Stephen
AU - Goel, Anuj
AU - Goodall, Alison H.
AU - Hengstenberg, Christian
AU - Hunt, Sarah E.
AU - Kastelein, John J. P.
AU - Klungel, Olaf H.
AU - Klueter, Harald
AU - Koch, Kerstin
AU - Koenig, Inke R.
AU - BC 50K CAD Consortium
AU - Gorgels, Antonius
PY - 2011/9
Y1 - 2011/9
N2 - Coronary artery disease (CAD) has a significant genetic contribution that is incompletely characterized. To complement genome-wide association (GWA) studies, we conducted a large and systematic candidate gene study of CAD susceptibility, including analysis of many uncommon and functional variants. We examined 49,094 genetic variants in ?2,100 genes of cardiovascular relevance, using a customised gene array in 15,596 CAD cases and 34,992 controls (11,202 cases and 30,733 controls of European descent; 4,394 cases and 4,259 controls of South Asian origin). We attempted to replicate putative novel associations in an additional 17,121 CAD cases and 40,473 controls. Potential mechanisms through which the novel variants could affect CAD risk were explored through association tests with vascular risk factors and gene expression. We confirmed associations of several previously known CAD susceptibility loci (eg, 9p21.3:p
AB - Coronary artery disease (CAD) has a significant genetic contribution that is incompletely characterized. To complement genome-wide association (GWA) studies, we conducted a large and systematic candidate gene study of CAD susceptibility, including analysis of many uncommon and functional variants. We examined 49,094 genetic variants in ?2,100 genes of cardiovascular relevance, using a customised gene array in 15,596 CAD cases and 34,992 controls (11,202 cases and 30,733 controls of European descent; 4,394 cases and 4,259 controls of South Asian origin). We attempted to replicate putative novel associations in an additional 17,121 CAD cases and 40,473 controls. Potential mechanisms through which the novel variants could affect CAD risk were explored through association tests with vascular risk factors and gene expression. We confirmed associations of several previously known CAD susceptibility loci (eg, 9p21.3:p
U2 - 10.1371/journal.pgen.1002260
DO - 10.1371/journal.pgen.1002260
M3 - Article
VL - 7
JO - Plos Genetics
JF - Plos Genetics
SN - 1553-7390
IS - 9
M1 - e1002260
ER -