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GWAS Study

Identification of novel genetic markers associated with clinical phenotypes of systemic sclerosis through a genome-wide association strategy.

Gorlova O, Martin JE, Rueda B et al.

21779181 PubMed ID
GWAS Study Type
14853 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

GO
Gorlova O
MJ
Martin JE
RB
Rueda B
KB
Koeleman BP
YJ
Ying J
TM
Teruel M
DL
Diaz-Gallo LM
BJ
Broen JC
VM
Vonk MC
SC
Simeon CP
AB
Alizadeh BZ
CM
Coenen MJ
VA
Voskuyl AE
SA
Schuerwegh AJ
VR
van Riel PL
VM
Vanthuyne M
V'
van 't Slot R
IA
Italiaander A
OR
Ophoff RA
HN
Hunzelmann N
FV
Fonollosa V
ON
Ortego-Centeno N
GM
González-Gay MA
GF
García-Hernández FJ
GM
González-Escribano MF
AP
Airo P
VL
van Laar J
WJ
Worthington J
HR
Hesselstrand R
SV
Smith V
DK
de Keyser F
HF
Houssiau F
CM
Chee MM
MR
Madhok R
SP
Shiels PG
WR
Westhovens R
KA
Kreuter A
DB
de Baere E
WT
Witte T
PL
Padyukov L
NA
Nordin A
SR
Scorza R
LC
Lunardi C
LB
Lie BA
HA
Hoffmann-Vold AM
PO
Palm O
GD
García de la Peña P
CP
Carreira P
VJ
Varga J
HM
Hinchcliff M
LA
Lee AT
GP
Gourh P
AC
Amos CI
WF
Wigley FM
HL
Hummers LK
NJ
Nelson JL
RG
Riemekasten G
HA
Herrick A
BL
Beretta L
FC
Fonseca C
DC
Denton CP
GP
Gregersen PK
AS
Agarwal S
AS
Assassi S
TF
Tan FK
AF
Arnett FC
RT
Radstake TR
MM
Mayes MD
MJ
Martin J
Chapter II

Abstract

Summary of the research findings

The aim of this study was to determine, through a genome-wide association study (GWAS), the genetic components contributing to different clinical sub-phenotypes of systemic sclerosis (SSc). We considered limited (lcSSc) and diffuse (dcSSc) cutaneous involvement, and the relationships with presence of the SSc-specific auto-antibodies, anti-centromere (ACA), and anti-topoisomerase I (ATA). Four GWAS cohorts, comprising 2,296 SSc patients and 5,171 healthy controls, were meta-analyzed looking for associations in the selected subgroups. Eighteen polymorphisms were further tested in nine independent cohorts comprising an additional 3,175 SSc patients and 4,971 controls. Conditional analysis for associated SNPs in the HLA region was performed to explore their independent association in antibody subgroups. Overall analysis showed that non-HLA polymorphism rs11642873 in IRF8 gene to be associated at GWAS level with lcSSc (P = 2.32×10(-12), OR = 0.75). Also, rs12540874 in GRB10 gene (P = 1.27 × 10(-6), OR = 1.15) and rs11047102 in SOX5 gene (P = 1.39×10(-7), OR = 1.36) showed a suggestive association with lcSSc and ACA subgroups respectively. In the HLA region, we observed highly associated allelic combinations in the HLA-DQB1 locus with ACA (P = 1.79×10(-61), OR = 2.48), in the HLA-DPA1/B1 loci with ATA (P = 4.57×10(-76), OR = 8.84), and in NOTCH4 with ACA P = 8.84×10(-21), OR = 0.55) and ATA (P = 1.14×10(-8), OR = 0.54). We have identified three new non-HLA genes (IRF8, GRB10, and SOX5) associated with SSc clinical and auto-antibody subgroups. Within the HLA region, HLA-DQB1, HLA-DPA1/B1, and NOTCH4 associations with SSc are likely confined to specific auto-antibodies. These data emphasize the differential genetic components of subphenotypes of SSc.

2,296 European ancestry cases, 5,172 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

14853
Total Participants
GWAS
Study Type
Yes
Replicated
3,175 European ancestry cases, 4,210 European ancestry controls
Replication Participants
European
Ancestry
Sweden, U.S., Italy, Netherlands, Belgium, Germany, U.K., Spain, Norway
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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