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. Author manuscript; available in PMC: 2009 Oct 6.
Published in final edited form as: Nat Genet. 2008 Sep 14;40(10):1216–1223. doi: 10.1038/ng.233

Table 1.

Sample collections

Case collection Control collection Origin Antibody status Cases Controls Genotyping platform Case-control stratification
Meta-analysis North American Rheumatoid Arthritis Consortium (NARAC) New York Cancer Project, New York City North America 100% CCP+ 873 1,196 Illumina 550K Identity-by-state clustering
3,393 cases; 12,460 controls Epidemiological Investigation of Rheumatoid Arthritis (EIRA) EIRA Sweden 100% CCP+ 660 658 Illumina 317K Epidemiologically matched, identity- by-state clustering
Wellcome Trust Case Control Consortium (WTCCC) Shared controls, multiple non-autoimmune diseases United Kingdom 80% CCP+, 84% RF+ 1,860 10,606 Affymetrix 500K Geographically matched

Stage 1 replication Nurses Health Study (NHS) NHS North America 100% RF+ or CCP+ 257 411 Sequenom iPlex Epidemiologically matched
Brigham Rheumatoid Arthritis Sequential Study (BRASS) National Institutes of Mental Health (NIMH) Boston, USA 100% CCP+ 407 814 Sequenom iPlex, Affymetrix 500K Case-control matching with GWAS data
1,089 cases; 1,862 controls NARAC II New York Cancer Project, New York City North America 100% CCP+ 425 637 Sequenom iPlex Case-control matching with ancestry informative markers
NARAC III Publicly available Shared controls North America 100% CCP+ 869 1,303 Illumina 317K Case-control matching with GWAS data

Stage 2 replication Genomics Collaborative Initiative (GCI) GCI North America 100% RF+ 457 460 Kinetic PCR Epidemiologically matched
Leiden University Medical Center (LUMC) LUMC Leiden, The Netherlands 100% RF+ or CCP+ 528 540 Kinetic PCR Geographically matched
2,840 cases; 3,945 controls EIRA-II EIRA-II Sweden 100% CCP+ 435 412 Sequenom iPlex Epidemiologically matched
Genetics Network Rheumatology Amsterdam (GENRA) GENRA Amsterdam, The Netherlands 100% CCP+ 551 1,230 Sequenom iPlex Geographically matched

GWA data from three meta-analysis collections were used to identify candidate SNPs for replication. The replication set was divided into two stages: stage 1 replication (three collections) and stage 2 replication (five collections). For each collection we list the geographic origin, the source of the controls, the autoantibody status of cases, and the number of cases and controls. We also list the genotyping technology used to type SNPs of interest. Finally, we specify the strategy used to correct for case-control population stratification.