Evidence map›Paper›PMID 8751869›Full record

ArticleAmerican journal of human genetics1996

Genetic variability in the tumor necrosis factor-lymphotoxin region influences susceptibility to rheumatoid arthritis.

B Mulcahy, F Waldron-Lynch, M F McDermott, C Adams, C I Amos, D K Zhu, R H Ward, D O Clegg, F Shanahan, M G Molloy and 1 more

Open access · greenAbstract readMulticenter Study
In one paragraph

Article in American journal of human genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 174 citations in OpenAlex.

  1. Article
  2. Pharmacogenetics of Drug Therapies in Rheumatoid Arthritis.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  3. Review
  4. The role of polymorphism ofPostepy dermatologii i alergologii · 2016
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Rheumatoid arthritis genetics: 2009 update.Current rheumatology reports · 2009
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

11 authors at 5 institutions in 3 countries.

B MulcahyMicrobiology Department, University College, Cork, Ireland.
F Waldron-Lynch
M F McDermott
C Adams
C I Amos
D K Zhu
R H Ward
D O Clegg
F Shanahan
M G Molloy
F O'Gara
University College Cork · IEThe University of Texas MD Anderson Cancer Center · USCenter for Rheumatology · USRoyal London Hospital · GBUniversity of Oxford · GB

Funding

GENETIC EPIDEMIOLOGY OF RHEUMATOID ARTHRITIS IN UTAHR01AR040057 · NIAMS · UNIVERSITY OF UTAH · PI WARD, RICHARD H · 1989 to 1991
–
NIAMS NIH HHS AR40057PHS HHS R01G52607
6 · The paper itself

Abstract

The major histocompatibility complex class III tumor necrosis factor-lymphotoxin (TNF-LT) region (6p21.3) was investigated as a possible susceptibility locus for rheumatoid arthritis (RA). Inheritance of five TNF microsatellite markers was determined in 50 multiplex families. Overall, 47 different haplotypes were observed. One of these, the TNF a6, b5, c1, d3, e3 (H1) haplotype, was present in 35.3% of affected, but in only 20.5% of unaffected, individuals (P < .005). This haplotype accounted for 21.5% of the parental haplotypes transmitted to affected offspring and only 7.3% not transmitted to affected offspring (P = .0003). The TNF a6 and TNF c1 alleles were individually associated with RA (P = .0005 and .0008, respectively), as were the HLA-DRB1 "shared epitope" (SE) (P = .0001) and HLA-DRB1*0401 (P = .0018). Both univariate and bivariate conditional logistic regression analysis showed significant effects of TNF c1 and SE in increasing risk to RA (P < .001). Stratification by the presence of SE indicated an independent effect of the TNFc1 allele (P = .0003) and the HLA A1, B8, DR3 extended haplotype (always TNFa2, b3, c1, d1, e3) (P = .0027) in SE heterozygotes, while the H1 haplotype was associated with RA in SE homozygotes (P = .0018). The TNF-LT region appears to influence susceptibility to RA, distinct from HLA-DR.

Indexed as

Arthritis, RheumatoidDisease SusceptibilityFemaleGenetic MarkersGenetic VariationGenotypeHaplotypesHLA-B AntigensHLA-DR AntigensHumansLinkage DisequilibriumLymphotoxin-alphaMajor Histocompatibility ComplexMaleMicrosatellite RepeatsTumor Necrosis Factor-alphaGenetic MarkersHLA-B AntigensHLA-DR AntigensLymphotoxin-alphaTumor Necrosis Factor-alpha

Identifiers

PMID8751869
PMCPMC1914921
OpenAlexW2113723054

What OpenQuestion holds

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Read underepoch 390

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.