Evidence map›Paper›PMID 22210660›Full record

ArticleRheumatology (Oxford, England)2012

Genetic association study of NF-κB genes in UK Caucasian adult and juvenile onset idiopathic inflammatory myopathy.

Hector Chinoy, Charles K-C Li, Hazel Platt, Noreen Fertig, Hemlata Varsani, Harsha Gunawardena, Zoe Betteridge, Chester V Oddis, Neil J McHugh, Lucy R Wedderburn and 3 more

Open access · greenAbstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 3 pooled it
1.6field-weighted citation impact, top 17% 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

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

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Genetics in inclusion body myositis.Current opinion in rheumatology · 2017
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Update in juvenile myositis.Current opinion in rheumatology · 2013
    Review
  16. Review
  17. T cells in myositis.Arthritis research & therapy · 2012
    Review
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

13 authors at 8 institutions in 3 countries.

Hector ChinoyThe University of Manchester Rheumatic Diseases Centre, Hope Hospital, Salford M6 8HD, UK.
Charles K-C Li
Hazel Platt
Noreen Fertig
Hemlata Varsani
Harsha Gunawardena
Zoe Betteridge
Chester V Oddis
Neil J McHugh
Lucy R Wedderburn
William E R Ollier
Robert G Cooper
UK Adult Onset Myositis Immunogenetic Consortium and UK Juvenile Dermatomyositis Research Group
Royal National Hospital for Rheumatic Diseases · GBRoyal Surrey County Hospital · GBUniversity of Pittsburgh · USInstitute of Child Health · INManchester Academic Health Science Centre · GBSalford Royal NHS Foundation Trust · GBUniversity College London · GBUniversity of Manchester · GB

Funding

Arthritis Research UK 18474Medical Research Council G0100594Medical Research Council G0600237Medical Research Council G0900753Medical Research Council G0901461
6 · The paper itself

Abstract

objectiveTreatment-resistant muscle wasting is an increasingly recognized problem in idiopathic inflammatory myopathy (IIM). TNF-α is thought to induce muscle catabolism via activation of nuclear factor-kappa B (NF-κB). Several genes share homology with the NF-κB family of proteins. This study investigated the role of NF-κB-related genes in disease susceptibility in UK Caucasian IIM.

methodsData from 362 IIM cases [274 adults, 49 (±14.0) years, 72% female; 88 juveniles, 6 (±3.6) years, 73% female) were compared with 307 randomly selected Caucasian controls. DNA was genotyped for 63 single nucleotide polymorphisms (SNPs) from NF-κB-related genes. Data were stratified by IIM subgroup/serotype.

resultsA significant allele association was observed in the overall IIM group vs controls for the IKBL-62T allele (rs2071592, odds ratio 1.5, 95% CI 1.21, 1.89, corrected P = 0.0086), which strengthened after stratification by anti-Jo-1 or -PM-Scl antibodies. Genotype analysis revealed an increase for the AT genotype in cases under a dominant model. No other SNP was associated in the overall IIM group. Strong pairwise linkage disequilibrium was noted between IKBL-62T, TNF-308A and HLA-B*08 (D' = 1). Using multivariate regression, the IKBL-62T IIM association was lost after adjustment for TNF-308A or HLA-B*08.

conclusionAn association was noted between IKBL-62T and IIM, with increased risk noted in anti-Jo-1- and -PM-Scl antibody-positive patients. However, the IKBL-62T association is dependent on TNF-308A and HLA-B*08, due to strong shared linkage disequilibrium between these alleles. After adjustment of the 8.1 HLA haplotype, NF-κB genes therefore do not independently confer susceptibility in IIM.

Indexed as

Genetic Predisposition to DiseaseAdaptor Proteins, Signal TransducingAdolescentAdultAgedAllelesFemaleGenetic Association StudiesGenotypeHaplotypesHistocompatibility Antigens Class IIHumansMaleMiddle AgedMyositisNF-kappa BAdaptor Proteins, Signal TransducingHistocompatibility Antigens Class IINF-kappa BNFKBIL1 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID22210660
PMCPMC3327167
OpenAlexW2163659251

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Registered trials

None linked

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.