This article is part of the supplement: Genetic Analysis Workshop 15: Gene Expression Analysis and Approaches to Detecting Multiple Functional Loci ProceedingsData for Genetic Analysis Workshop (GAW) 15 Problem 2, genetic causes of rheumatoid arthritis and associated traitsChristopher I Amos1 1Departments of Epidemiology and Biomathematics, University of Texas, M.D. Anderson Cancer Center, 1155 Pressler Street, Unit 1340, Houston, Texas 77030, USA 2Genetics and Genomics Branch, NIAMS, NIH, 9 Memorial Drive, MSC 0908, Building 9, Room 1W108, Bethesda, Maryland 20892, USA 3Mount Sinai Hospital, SLRI, Room 656A, 600 University Avenue, Toronto, Ontario M5G 1X5 Canada 4Rowe Program of Human Genetics, Department of Medicine, 4303 Tupper Hall, University of California – Davis, Davis, California 95616, USA 5The Rosalind Russell Medical Research Center for Arthritis, Department of Medicine, Division of Rheumatology, University of California at San Francisco, California 94122, USA 6Center for Genomics and Human Genetics, North Shore-Feinstein Medical Research Institute, 350 Community Drive, Manhasset, New York 11030, USA 7Cancer Research-UK, Institute for Cancer Studies, School of Medicine and Biomedical Sciences, University of Sheffield, Beech Hill Road, Sheffield, S10 2RX, UK 8Centre for Integrated Genomic Medical Research, Stopford Building, University of Manchester, Oxford Road, Manchester, M13 9PL, UK 9GenHotel-EA 3886, University Evry-Paris 7/AP-HP, Evry-Genopole, Cedex, France 10Broad Institute of MIT and Harvard, Brigham and Women's Hospital, Division of Rheumatology, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA 11Celera Diagnostics, 1401 Harbor Bay Parkway, Alameda, California 94502, USA 12Department of Genetics, Southwest Foundation for Biomedical Research, 7620 Northwest Loop 410, San Antonio, Texas 78227, USA
BMC Proceedings 2007, 1(Suppl 1):S3
AbstractFor Genetic Analysis Workshop 15 Problem 2, we organized data from several ongoing studies designed to identify genetic and environmental risk factors for rheumatoid arthritis. Data were derived from the North American Rheumatoid Arthritis Consortium (NARAC), collaboration among Canadian researchers, the European Consortium on Rheumatoid Arthritis Families (ECRAF), and investigators from Manchester, England. All groups used a common standard for defining rheumatoid arthritis, but NARAC also further selected for a more severe phenotype in the probands. Genotyping and family structures for microsatellite-based linkage analysis were provided from all centers. In addition, all centers but ECRAF have genotyped families for linkage analysis using SNPs and these data were additionally provided. NARAC also had additional data from a dense genotyping analysis of a region of chromosome 18 and results from candidate gene studies, which were provided. Finally, smoking influences risk for rheumatoid arthritis, and data were provided from the NARAC study on this behavior as well as some additional phenotypes measuring severity. Several questions could be evaluated using the data that were provided. These include comparing linkage analysis using single-nucleotide polymorphisms versus microsatellites and identifying credible regions of linkage outside the HLA region on chromosome 6p13, which has been extensively documented; evaluating the joint effects of smoking with genetic factors; and identifying more homogenous subsets of families for whom genetic susceptibility might be stronger, so that linkage and association studies may be more efficiently conducted. |
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