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|Title:||Association analyses based on false discovery rate implicate new loci for coronary artery disease|
|Authors:||Nelson, Christopher P.|
Webb, Tom R.
Lai, Florence Y.
Hamby, Stephen E.
Di Angelantonio, E
UK Biobank CardioMetabolic Consortium CHD working group
Samani, Nilesh J.
|Publisher:||Nature Publishing Group|
|Citation:||Nature Genetics, 2017, 49 (9), pp. 1385-1391|
|Abstract:||Genome-wide association studies (GWAS) in coronary artery disease (CAD) had identified 66 loci at 'genome-wide significance' (P < 5 × 10(-8)) at the time of this analysis, but a much larger number of putative loci at a false discovery rate (FDR) of 5% (refs. 1,2,3,4). Here we leverage an interim release of UK Biobank (UKBB) data to evaluate the validity of the FDR approach. We tested a CAD phenotype inclusive of angina (SOFT; ncases = 10,801) as well as a stricter definition without angina (HARD; ncases = 6,482) and selected cases with the former phenotype to conduct a meta-analysis using the two most recent CAD GWAS. This approach identified 13 new loci at genome-wide significance, 12 of which were on our previous list of loci meeting the 5% FDR threshold, thus providing strong support that the remaining loci identified by FDR represent genuine signals. The 304 independent variants associated at 5% FDR in this study explain 21.2% of CAD heritability and identify 243 loci that implicate pathways in blood vessel morphogenesis as well as lipid metabolism, nitric oxide signaling and inflammation.|
|Rights:||Copyright © 2017, Nature Publishing Group. Deposited with reference to the publisher’s open access archiving policy.|
|Description:||The file associated with this record is under embargo until 6 months after publication, in accordance with the publisher's self-archiving policy. The full text may be available through the publisher links provided above.|
|Appears in Collections:||Published Articles, Dept. of Cardiovascular Sciences|
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