Genome-wide search for rheumatoid arthritis susceptibility loci
Author Information
Author(s): Bell Jordana Tzenova, Heather J Cordell, Mariza de Andrade, Marie-Claude Babron, Christopher W Bartlett, Joseph Beyene, Heike Bickeböller, Robert Culverhouse, Adrienne Cupples, E Warwick Daw, Josée Dupuis, Catherine T Falk, Saurabh Ghosh, Katrina A Goddard, Ellen L Goode, Elizabeth R Hauser, Lisa J Martin, Maria Martinez, Kari E North, Nancy L Saccone, Silke Schmidt, William Tapper, Duncan Thomas, David Tritchler, Veronica J Vieland, Ellen M Wijsman, Marsha A Wilcox, John S Witte, Qiong Yang, Andreas Ziegler, Laura Almasy, Jean W MacCluer
Primary Institution: Wellcome Trust Centre for Human Genetics, University of Oxford
Hypothesis
The study aims to identify pairs of loci that jointly contribute to rheumatoid arthritis susceptibility.
Conclusion
The study found evidence for multi-locus interactions in rheumatoid arthritis, particularly involving the major susceptibility locus at 6p21.
Supporting Evidence
- An epistatic interaction was identified between loci 6p21 and 16p12.
- Significant two-locus effects were observed for region 6p21 in combination with other loci.
- The study utilized a large sample of families affected by rheumatoid arthritis.
Takeaway
Scientists looked at genes to see how they work together to cause rheumatoid arthritis, and they found important interactions between certain genes.
Methodology
A two-dimensional non-parametric linkage scan was performed using 380 autosomal microsatellite markers in families affected by rheumatoid arthritis.
Limitations
The results should be interpreted with caution due to the reduced evidence for linkage at some loci when SNP data was included.
Participant Demographics
Families recruited by the North American Rheumatoid Arthritis Consortium, including affected sibling pairs.
Statistical Information
P-Value
0.011
Statistical Significance
p<0.05
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