Browse by author
Lookup NU author(s): Professor Heather Cordell, Professor John IsaacsORCiD
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
The introduction of tumour necrosis factor antagonists (anti-TNF) has greatly improved the treatment of rheumatoid arthritis, however, a significant proportion of patients fail to respond to therapy. We hypothesized that variants spanning the type 2 TNF receptor (TNFR2) and the TNF cleavage enzyme (TACE) genes contribute towards the observed variation in patient response (defined as the absolute change in 28- joint count disease activity score). Twenty-nine single nucleotide polymorphisms (SNPs) were genotyped in a large cohort of patients (n = 602) and analysed by multivariate linear regression. Three SNPs (rs520916, rs652625, rs597519) mapping upstream of TNFR2 showed borderline evidence for association (P < 0.1) across the complete cohort and, more so, in the etanercept-treated subgroup. However, the evidence of association was neither replicated in an independent cohort (n = 377) nor strengthened after combined analysis (n = 979). We conclude that common SNPs spanning the TNFR2 and TNF cleavage enzyme (TACE) genes do not have a major effect on the response to anti-TNF therapy in rheumatoid arthritis patients. Pharmacogenetics and Genomics 20: 338-341 (c) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
Author(s): Potter C, Gibbons LJ, Bowes JD, Cordell HJ, Hyrich K, Isaacs JD, Morgan AW, Wilson AG, Barton A, Biol Rheumatoid Arthrit Genetics Group
Publication type: Article
Publication status: Published
Journal: Pharmacogenetics and Genomics
Year: 2010
Volume: 20
Issue: 5
Pages: 338-341
Print publication date: 01/05/2010
ISSN (print): 1744-6872
ISSN (electronic): 1744-6880
Publisher: Lippincott Williams & Wilkins
URL: http://dx.doi.org/10.1097/FPC.0b013e32833878d7
DOI: 10.1097/FPC.0b013e32833878d7
Altmetrics provided by Altmetric