Evidence map›Paper›PMID 19950259›Full record

ArticleArthritis and rheumatism2009

The FAS -670A>G polymorphism influences susceptibility to systemic sclerosis phenotypes.

J Broen, P Gourh, B Rueda, M Coenen, M Mayes, J Martin, F C Arnett, T R D J Radstake, European Consortium on Systemic Sclerosis Genetics

Abstract read
In one paragraph

Article in Arthritis and rheumatism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

12 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Genetics of systemic sclerosis: recent advances.Current opinion in rheumatology · 2015
    Review
  6. Article
  7. Article
  8. Article
  9. The genetics of scleroderma.Current rheumatology reports · 2011
    Review
  10. Genetic variation in the FAS gene and associations with acute lung injury.American journal of respiratory and critical care medicine · 2011
    Article
  11. Review
  12. The genetics of systemic sclerosis.Discovery medicine · 2010
    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

9 authors.

J BroenRadboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
P Gourh
B Rueda
M Coenen
M Mayes
J Martin
F C Arnett
T R D J Radstake
European Consortium on Systemic Sclerosis Genetics

Funding

Role of TGF-beta and CTGF Signaling Transgenic Mouse Models of SclerodermaP50AR054144 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TAN, FILEMON K. · 2006 to 2010
$7.7M
Two-Stage Genome-Wide Association Study in Systemic SclerosisR01AR055258 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MAYES, MAUREEN MAUREEN · 2008 to 2012
$5.9M
SCLERODERMA FAMILY REGISTRY AND DNA REPOSITORY-264002251-264002251-264002251N01AR002251 · NIAMS · WAYNE STATE UNIVERSITY · PI MAYES, MAUREEN · 2000 to 2006
$659k
NCRR NIH HHS 1-U54-RR-23417NIAMS NIH HHS 1-P50-AR-054144NIAMS NIH HHS N01 AR002251NIAMS NIH HHS N01-AR-0-2251NIAMS NIH HHS P50 AR054144NIAMS NIH HHS R01 AR055258
6 · The paper itself

Abstract

objectiveTo investigate the possible role of the FAS -670A>G functional polymorphism in the genetic predisposition to systemic sclerosis (SSc) susceptibility or clinical phenotype.

methodsA total of 2,900 SSc patients and 3,186 healthy controls were included in this study. We analyzed the genotype and allele frequencies of the FAS -670A>G polymorphism in 9 distinct ethnic cohorts, including 6 cohorts of European ancestry (a Spanish cohort of 228 SSc patients and 265 controls, a Dutch cohort of 203 SSc patients and 277 controls, a German cohort of 313 SSc patients and 247 controls, an Italian cohort of 323 SSc cases and 89 controls, a British cohort of 269 SSc patients, and a Swedish cohort of 182 patients) and 3 distinct ethnic cohorts from the US (a cohort of 1,047 white patients and 692 controls, a cohort of 159 Hispanic patients and 137 controls, and a cohort of 176 black SSc patients and 194 controls). Genotyping was performed using a TaqMan 5' allelic discrimination assay.

resultsIn the British, Italian, and American white cohorts we observed an association of the FAS -670G allele with limited cutaneous SSc (lcSSc) (odds ratios [ORs] 1.25, 1.43, and 1.18, respectively). A meta-analysis comprising all 9 cohorts revealed an association of both the FAS -670G allele (OR 1.10) and the FAS -670GG genotype (OR 1.13) with the lcSSc phenotype. In a meta-analysis including only white subjects, both the FAS -670G allele and the FAS -670GG genotype remained associated with lcSSc (allele OR 1.12; genotype OR 1.16). In addition, a recessive model of the -670GG genotype exhibited a strong association with SSc, lcSSc, and anticentromere antibody-positive lcSSc (OR 1.23, OR 1.33, and OR 1.45, respectively).

conclusionOur data show that the FAS -670A>G polymorphism plays a role in lcSSc susceptibility. A similar trend has been observed in other autoimmune diseases.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdenosinefas ReceptorFemaleGenotypeGuanosineHumansMaleMiddle AgedPhenotypePromoter Regions, GeneticScleroderma, DiffuseScleroderma, LimitedAdenosineFAS protein, humanfas ReceptorGuanosine

Identifiers

PMID19950259
PMCPMC2876716

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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.