Tumour necrosis factor α −308G→A polymorphism is not associated with response to TNFα blockers in Caucasian patients with rheumatoid arthritis: systematic review and meta-analysis

Abstract

According to this meta-analysis, the TNFA -308 polymorphism is not a predictor of the clinical response to anti-TNF treatment in RA.

Association of Tumor Necrosis Factor-Alpha -308 G>A Polymorphism With Rheumatoid Arthritis in Two North Indian Cohorts

“…Some studies have reported a positive association of TNF-α -308 alleles with RA 3,16,31-34 while others have reported lack of association with RA. 36,[48][49][50][51][52] In conformity with the majority of previous studies, the present study failed to demonstrate any association between the TNF-α -308 G>A promoter polymorphism and RA in cohort 1. Interestingly, the comparison between RA patients who were RF positive and RF negative revealed a marginally significant difference in the allele frequencies (p=0.05, OR=2.86, 0.96-8.52 at 95% CI).…”

Tumor Necrosis Factor-α Gene Polymorphisms and Risk of Oral Cancer: Evidence from a Meta-analysis

“…In complex biologic systems, the effect of a single gene polymorphism in determining cytokine secretion may be affected by factors such as genetic and epigenetic determinants or may be minimized through interaction with environmental factors (Powell et al, 2001;Malleo et al, 2007). Most of all, both SNPs of the TNF-α gene may not be specific to oral cancer although they are associated with many inflammatory diseases (Lu et al, 2008;Pavy et al, 2010;Lee et al, 2012;).…”

Diagnostic, Prognostic and Theranostic Biomarkers for Rheumatoid Arthritis

“…There has been considerable data accumulated here, in particular with regard to single nucleotide polymorphisms (SNPs) which effect the TNF promoter such as -308G>A, and -857C>T. Reports on TNF-308G/A have indicated that a genetic predisposition toward increased TNF expression (carrying the A allele) can be associated with nonresponse to anti-TNF therapy [29][30][31][32]. These findings however have been disputed in a recent meta-analysis by Pavy et al and so the role of this SNP remains unclear [33]. In addition to studies of TNF, SNPs within other cytokine genes such as IL-10, TGF-B1, IL-1B and the IL-1 receptor antagonist IL-RA have also been examined where opposing associations as biomarkers for response and non-response are reported [34,35].…”