Evidence map›Paper›PMID 27698401›Full record

ArticleThe pharmacogenomics journal2018

Confirmation of an IRAK3 polymorphism as a genetic marker predicting response to anti-TNF treatment in rheumatoid arthritis.

J Sode, U Vogel, S Bank, P S Andersen, M L Hetland, H Locht, N H H Heegaard, V Andersen

Abstract read
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In one paragraph

Article in The pharmacogenomics journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 3 syntheses or guidelines pooled it, 30 citations in OpenAlex.

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  11. Pharmacogenetics of Drug Therapies in Rheumatoid Arthritis.Methods in molecular biology (Clifton, N.J.) · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 6 institutions in 1 country.

J SodeDepartment of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark.ORCID 0000-0002-2718-9320
U VogelNational Research Centre for the Working Environment, Copenhagen, Denmark.
S BankDepartment of Medicine, Viborg Regional Hospital, Viborg, Denmark.
P S AndersenDepartment of Microbiology and Infection Control, Statens Serum Institut, Copenhagen, Denmark.
M L HetlandThe DANBIO Registry, Copenhagen Center for Arthritis Research, Center for Rheumatology and Spine Diseases, Centre for Head and Orthopaedics, Rigshospitalet, Glostrup, Denmark.
H LochtDepartment of Rheumatology, Frederiksberg Hospital, Frederiksberg, Denmark.
N H H HeegaardDepartment of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark.
V AndersenInstitute of Regional Health Research-Center Sønderjylland, University of Southern Denmark, Odense, Denmark.
Statens Serum Institut · DKAarhus University · DKFrederiksberg Hospital · DKNational Research Centre for the Working Environment · DKUniversity of Copenhagen · DKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several genetic variants in Toll-like receptor (TLR) and nuclear factor (NF)-κB signalling pathways have been reported associated with responsiveness to tumour necrosis factor inhibitor (anti-TNF) treatment in rheumatoid arthritis (RA). The present study was undertaken to replicate these findings. In a retrospective case-case study including 1007 Danish anti-TNF-treated RA patients, we genotyped 7 previously reported associated single-nucleotide polymorphisms (SNPs) in these pathways. Furthermore, 5 SNPs previously reported by our group were genotyped in a subcohort (N=469). Primary analyses validated the IRAK3 rs11541076 variant as associated (odds ratio (OR)=1.33, 95% confidence interval (CI): 1.00-1.77, P-value=0.047) with a positive treatment response (EULAR (European League Against Rheumatism) good/moderate vs none response at 4±2 months), and found the NLRP3 rs461266 variant associated (OR=0.75, 95% CI: 0.60-0.94, P=0.014) with a negative treatment response. Meta-analyses combining data from previous studies suggested smaller effect sizes of associations between variant alleles of CHUK rs11591741, NFKBIB rs3136645 and rs9403 and a negative treatment response. In conclusion, this study validates rs11541076 in IRAK3, a negative regulator of TLR signalling, as a predictor of anti-TNF treatment response, and suggests true positive associations of previously reported SNPs within genes encoding activators/inhibitors of NF-κB (CHUK, MYD88, NFKBIB, and NLRP3).

Indexed as

AllelesAntirheumatic AgentsArthritis, RheumatoidCase-Control StudiesFemaleGenetic MarkersGenotypeHumansInterleukin-1 Receptor-Associated KinasesMaleMiddle AgedPolymorphism, Single NucleotideRetrospective StudiesTumor Necrosis Factor-alphaAntirheumatic AgentsGenetic MarkersInterleukin-1 Receptor-Associated KinasesIRAK3 protein, humanTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID27698401
OpenAlexW2527906820

What OpenQuestion holds

Textmetadata
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.