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GWAS Study

Common variants at 6p21.1 are associated with large artery atherosclerotic stroke.

Holliday EG, Maguire JM, Evans TJ et al.

22941190 PubMed ID
GWAS Study Type
56816 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

HE
Holliday EG
MJ
Maguire JM
ET
Evans TJ
KS
Koblar SA
JJ
Jannes J
SJ
Sturm JW
HG
Hankey GJ
BR
Baker R
GJ
Golledge J
PM
Parsons MW
MR
Malik R
MM
McEvoy M
BE
Biros E
LM
Lewis MD
LL
Lincz LF
PR
Peel R
OC
Oldmeadow C
SW
Smith W
MP
Moscato P
BS
Barlera S
BS
Bevan S
BJ
Bis JC
BE
Boerwinkle E
BG
Boncoraglio GB
BT
Brott TG
BR
Brown RD
CY
Cheng YC
CJ
Cole JW
CI
Cotlarciuc I
DW
Devan WJ
FM
Fornage M
FK
Furie KL
GS
Grétarsdóttir S
GA
Gschwendtner A
IM
Ikram MA
LW
Longstreth WT
MJ
Meschia JF
MB
Mitchell BD
MT
Mosley TH
NM
Nalls MA
PE
Parati EA
PB
Psaty BM
SP
Sharma P
SK
Stefansson K
TG
Thorleifsson G
TU
Thorsteinsdottir U
TM
Traylor M
VB
Verhaaren BF
WK
Wiggins KL
WB
Worrall BB
SC
Sudlow C
RP
Rothwell PM
FM
Farrall M
DM
Dichgans M
RJ
Rosand J
MH
Markus HS
SR
Scott RJ
LC
Levi C
AJ
Attia J
Chapter II

Abstract

Summary of the research findings

Genome-wide association studies (GWAS) have not consistently detected replicable genetic risk factors for ischemic stroke, potentially due to etiological heterogeneity of this trait. We performed GWAS of ischemic stroke and a major ischemic stroke subtype (large artery atherosclerosis, LAA) using 1,162 ischemic stroke cases (including 421 LAA cases) and 1,244 population controls from Australia. Evidence for a genetic influence on ischemic stroke risk was detected, but this influence was higher and more significant for the LAA subtype. We identified a new LAA susceptibility locus on chromosome 6p21.1 (rs556621: odds ratio (OR)=1.62, P=3.9×10(-8)) and replicated this association in 1,715 LAA cases and 52,695 population controls from 10 independent population cohorts (meta-analysis replication OR=1.15, P=3.9×10(-4); discovery and replication combined OR=1.21, P=4.7×10(-8)). This study identifies a genetic risk locus for LAA and shows how analyzing etiological subtypes may better identify genetic risk alleles for ischemic stroke.

421 European ancestry large artery atherosclerosis cases, 741 European ancestry ischemic stroke cases, 1,244 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

56816
Total Participants
GWAS
Study Type
Yes
Replicated
1,715 European ancestry large artery atherosclerosis cases, 9,552 European ancestry ischemic stroke cases, 52,695 European ancestry controls
Replication Participants
European
Ancestry
U.S., Iceland, Netherlands, Germany, U.K., Australia
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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Analysis In Progress

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