Evidence map›Paper›PMID 18588573›Full record

ArticleTissue antigens2008

Fas promoter polymorphisms: genetic predisposition to sarcoidosis in African-Americans.

Y S Wasfi, L J Silveira, A Jonth, J E Hokanson, T Fingerlin, H Sato, C E Parsons, P Lympany, K Welsh, R M du Bois and 3 more

Open access · greenAbstract readComparative StudyMulticenter Study
In one paragraph

Article in Tissue antigens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

13 authors at 5 institutions in 2 countries.

Y S WasfiMerck Research Laboratories, Upper Gwynedd, PA, USA.
L J Silveira
A Jonth
J E Hokanson
T Fingerlin
H Sato
C E Parsons
P Lympany
K Welsh
R M du Bois
L S Newman
L A Maier
ACCESS Research Group
Genomics (United Kingdom) · GBUniversity of Colorado Denver · USUniversity of Colorado Health · USNational Jewish Health · USGwynedd Mercy University · US

Funding

ZOPOLRESTAT PHARMACOKINETICS IN DIABETICS WITH VARYING RENAL FUNCTIONM01RR000051 · NCRR · UNIVERSITY OF COLORADO DENVER · PI KOSMISKI, LISA A. · 1985 to 2008
$52.6M
ETIOLOGY OF SARCOIDOSIS A CASE CONTROL STUDY-268956075N01HR056075 · HR · CLINICAL TRIALS AND SURVEYS CORPORATION · 1995 to 2003
$369k
ETIOLOGY OF SARCOIDOSIS A CASE CONTROL STUDYN01HR056072 · HR · UNIVERSITY OF PENNSYLVANIA · PI ROSSMAN, MILTON D · 1995 to 2000
$199k
ETIOLOGY OF SARCOIDOSIS A CASE CONTROL STUDYN01HR056074 · HR · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEINBERGER, STEVEN · 1995 to 2000
$142k
CLINICAL CENTER FOR ETIOLOGY OF SARCOIDOSISN01HR056065 · HR · JOHNS HOPKINS UNIVERSITY · PI MOLLER, DAVID R · 1995 to 2000
$134k
CLINICAL CENTER FOR ETIOLOGY OF SARCOIDOSISN01HR056066 · HR · NATIONAL JEWISH HEALTH · PI NEWMAN, LEE S · 1995 to 2000
$127k
CLINICAL CENTER FOR ETIOLOGY OF SARCOIDOSISN01HR056067 · HR · HENRY FORD HEALTH SYSTEM · PI IANNUZZI, MICHAEL C · 1995 to 2000
$125k
CLINICAL CENTER FOR ETIOLOGY OF SARCOIDOSISN01HR056068 · HR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JUDSON, MARC A · 1995 to 2000
$97k
ETIOLOGY OF SARCOIDOSIS A CASE CONTROL STUDYN01HR056071 · HR · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI TEIRSTEIN, ALVIN S · 1995 to 2000
$97k
CLINICAL CENTER FOR ETIOLOGY OF SARCOIDOSISN01HR056069 · HR · UNIVERSITY OF CINCINNATI · PI BAUGHMAN, ROBERT P · 1995 to 2000
$64k
CLINICAL CENTERS FOR ETIOLOGY OF SARCOIDOSISN01HR056070 · HR · UNIVERSITY OF IOWA · PI MCLENNAN, GEOFFREY · 1995 to 2000
$62k
ETIOLOGY OF SARCOIDOSIS A CASE CONTROL STUDYN01HR056073 · HR · GEORGETOWN UNIVERSITY · PI YEAGER, HENRY · 1995 to 2000
$60k
NCRR NIH HHS M01 RR000051NCRR NIH HHS M01 RR00051NHLBI NIH HHS N01 HR056075NHLBI NIH HHS N01-HR-56065NHLBI NIH HHS N01-HR-56066NHLBI NIH HHS N01-HR-56067NHLBI NIH HHS N01-HR-56068NHLBI NIH HHS N01-HR-56069NHLBI NIH HHS N01-HR-56070NHLBI NIH HHS N01-HR-56071NHLBI NIH HHS N01-HR-56072NHLBI NIH HHS N01-HR-56073NHLBI NIH HHS N01-HR-56074NHLBI NIH HHS N01-HR-56075
6 · The paper itself

Abstract

Apoptosis may perpetuate some forms of inflammation. Of the apoptotic pathway proteins, Fas is particularly overexpressed in sarcoidosis. We hypothesized that Fas promoter single nucleotide polymorphisms (SNPs) contribute to the development and severity of sarcoidosis. Associations of known Fas promoter SNPs (-670, -690 and -1377) and deduced haplotypes with sarcoidosis and sarcoidosis severity were evaluated using matched case-control (n = 656 pairs) and case-comparison (n = 656) studies, respectively, using conditional logistic regression. Hardy-Weinberg equilibrium was confirmed for all three polymorphisms in African-Americans (AA), and for the -670 and -1377 in whites. Genotype and allele frequencies were significantly different between whites and AA. Race-stratified analysis revealed that a common haplotype, -1377G/-690T/-670G, was associated with sarcoidosis [odds ratio (OR) = 1.78, P = 0.05] only in AA. The haplotype -1377G/-690C/-670A was negatively associated with sarcoidosis (OR = 0.39, P = 0.03) only in AA. In conclusion, the consistency of these findings suggests that Fas promoter genetic variants may be related to sarcoidosis disease risk in AA.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdolescentAdultAgedAged, 80 and overBlack or African AmericanCase-Control Studiesfas ReceptorFemaleHumansIncidenceMaleMiddle AgedPromoter Regions, GeneticSarcoidosisFAS protein, humanfas Receptor

Identifiers

PMID18588573
PMCPMC3061555
OpenAlexW2047984124

What OpenQuestion holds

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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.