Title |
Lack of replication of interactions between polymorphisms in rheumatoid arthritis susceptibility: case–control study
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Published in |
Arthritis Research & Therapy, September 2014
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DOI | 10.1186/s13075-014-0436-x |
Pubmed ID | |
Authors |
Aida Ferreiro-Iglesias, Manuel Calaza, Eva Perez-Pampin, Francisco J Lopez Longo, Jose L Marenco, Francisco J Blanco, Javier Narvaez, Federico Navarro, Juan D Cañete, Arturo R de la Serna, Isidoro Gonzalez-Alvaro, Gabriel Herrero-Beaumont, Jose L Pablos, Alejandro Balsa, Benjamin Fernandez-Gutierrez, Rafael Caliz, Juan J Gomez-Reino, Antonio Gonzalez |
Abstract |
Approximately 100 loci have been definitively associated with rheumatoid arthritis (RA) susceptibility. However, they explain only a fraction of RA heritability. Interactions between polymorphisms could explain part of the remaining heritability. Multiple interactions have been reported, but only the shared epitope (SE) × protein tyrosine phosphatase nonreceptor type 22 (PTPN22) interaction has been replicated convincingly. Two recent studies deserve attention because of their quality, including their replication in a second sample collection. In one of them, researchers identified interactions between PTPN22 and seven single-nucleotide polymorphisms (SNPs). The other showed interactions between the SE and the null genotype of glutathione S-transferase Mu 1 (GSTM1) in the anti-cyclic citrullinated peptide-positive (anti-CCP+) patients. In the present study, we aimed to replicate association with RA susceptibility of interactions described in these two high-quality studies. |
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Geographical breakdown
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Unknown | 20 | 87% |
Demographic breakdown
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Unknown | 8 | 35% |