SynthesisPloS one2019
Evaluation of 12 GWAS-drawn SNPs as biomarkers of rheumatoid arthritis response to TNF inhibitors. A potential SNP association with response to etanercept.
Synthesis in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- The effect of tumor necrosis factor-alpha on rheumatoid arthritis-related pain: overview of evidence and mechanistic pathways.Croatian medical journal · 2026Review
- Novel variants in ARID1B, SPSB1, and RAET1-AS shape genetic susceptibility and protection in systemic lupus erythematosus and lupus nephritis.Journal of translational autoimmunity · 2025Article
- Review
- The Association Between Genetics and Response to Treatment with Biologics in Patients with Psoriasis.International journal of molecular sciences · 2025Article
- Towards Personalized Medicine in Rheumatoid Arthritis.Open access rheumatology : research and reviews · 2024Review
- DNA Methylation Signatures of Response to Conventional Synthetic and Biologic Disease-Modifying Antirheumatic Drugs (DMARDs) in Rheumatoid Arthritis.Biomedicines · 2023Review
- Novel DNA methylome biomarkers associated with adalimumab response in rheumatoid arthritis patients.Frontiers in immunology · 2023Article
- -Omic Approaches and Treatment Response in Rheumatoid Arthritis.Pharmaceutics · 2022Review
- Association Study of Anticitrullinated Peptide Antibody Status with Clinical Manifestations and SNPs in Patients Affected with Rheumatoid Arthritis: A Pilot Study.Disease markers · 2022Article
- A genome-wide screen for variants influencing certolizumab pegol response in a moderate to severe rheumatoid arthritis population.PloS one · 2022Article
- Pharmacogenetics of Drug Therapies in Rheumatoid Arthritis.Methods in molecular biology (Clifton, N.J.) · 2022Article
- A Molecular Signature Response Classifier to Predict Inadequate Response to Tumor Necrosis Factor-α Inhibitors: The NETWORK-004 Prospective Observational Study.Rheumatology and therapy · 2021Article
- Multi-omics approach to precision medicine for immune-mediated diseases.Inflammation and regeneration · 2021Review
- Deciphering the association of intronic single nucleotide polymorphisms of crystallin gene family with congenital cataract.Indian journal of ophthalmology · 2021Article
- Potential clinical biomarkers in rheumatoid arthritis with an omic approach.Auto- immunity highlights · 2021Review
- Review
- Toward Overcoming Treatment Failure in Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Genetic Polymorphisms Associated with Rheumatoid Arthritis Development and Antirheumatic Therapy Response.International journal of molecular sciences · 2020Review
- The Potential Role of Genomic Medicine in the Therapeutic Management of Rheumatoid Arthritis.Journal of clinical medicine · 2019Review
Corrections and comments
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Authors and funding
27 authors at 17 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Research in rheumatoid arthritis (RA) is increasingly focused on the discovery of biomarkers that could enable personalized treatments. The genetic biomarkers associated with the response to TNF inhibitors (TNFi) are among the most studied. They include 12 SNPs exhibiting promising results in the three largest genome-wide association studies (GWAS). However, they still require further validation. With this aim, we assessed their association with response to TNFi in a replication study, and a meta-analysis summarizing all non-redundant data. The replication involved 755 patients with RA that were treated for the first time with a biologic drug, which was either infliximab (n = 397), etanercept (n = 155) or adalimumab (n = 203). Their DNA samples were successfully genotyped with a single-base extension multiplex method. Lamentably, none of the 12 SNPs was associated with response to the TNFi in the replication study (p > 0.05). However, a drug-stratified exploratory analysis revealed a significant association of the NUBPL rs2378945 SNP with a poor response to etanercept (B = -0.50, 95% CI = -0.82, -0.17, p = 0.003). In addition, the meta-analysis reinforced the previous association of three SNPs: rs2378945, rs12142623, and rs4651370. In contrast, five of the remaining SNPs were less associated than before, and the other four SNPs were no longer associated with the response to treatment. In summary, our results highlight the complexity of the pharmacogenetics of TNFi in RA showing that it could involve a drug-specific component and clarifying the status of the 12 GWAS-drawn SNPs.
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