Jing Cui, Eli A Stahl, Saedis Saevarsdottir, Corinne Miceli, Dorothee Diogo, Gosia Trynka, Towfique Raj, Maša Umiċeviċ Mirkov, Helena Canhao, Katsunori Ikari, Chikashi Terao, Yukinori Okada, Sara Wedrén, Johan Askling, Hisashi Yamanaka, Shigeki Momohara, Atsuo Taniguchi, Koichiro Ohmura, Fumihiko Matsuda, Tsuneyo Mimori, Namrata Gupta, Manik Kuchroo, Ann W Morgan, John D Isaacs, Anthony G Wilson, Kimme L Hyrich, Marieke Herenius, Marieke E Doorenspleet, Paul-Peter Tak, J Bart A Crusius, Irene E van der Horst-Bruinsma, Gert Jan Wolbink, Piet L C M van Riel, Mart van de Laar, Henk-Jan Guchelaar, Nancy A Shadick, Cornelia F Allaart, Tom W J Huizinga, Rene E M Toes, Robert P Kimberly, S Louis Bridges, Lindsey A Criswell, Larry W Moreland, João Eurico Fonseca, Niek de Vries, Barbara E Stranger, Philip L De Jager, Soumya Raychaudhuri, Michael E Weinblatt, Peter K Gregersen, Xavier Mariette, Anne Barton, Leonid Padyukov, Marieke J H Coenen, Elizabeth W Karlson, Robert M Plenge
Anti-tumor necrosis factor alpha (anti-TNF) biologic therapy is a widely used treatment for rheumatoid arthritis (RA). It is unknown why some RA patients fail to respond adequately to anti-TNF therapy, which limits the development of clinical biomarkers to predict response or new drugs to target refractory cases. To understand the biological basis of response to anti-TNF therapy, we conducted a genome-wide association study (GWAS) meta-analysis of more than 2 million common variants in 2,706 RA patients from 13 different collections...
March 2013: PLoS Genetics