Evidence map›Paper›PMID 18318786›Full record

ArticleAnnals of human genetics2008

Polymorphisms of the tumor suppressor gene LSAMP are associated with left main coronary artery disease.

L Wang, E R Hauser, S H Shah, D Seo, P Sivashanmugam, S T Exum, S G Gregory, C B Granger, J L Haines, C J H Jones and 7 more

Open access · greenAbstract readValidation Study
In one paragraph

Article in Annals of human genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
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  13. A Guide for a Cardiovascular Genomics Biorepository: the CATHGEN Experience.Journal of cardiovascular translational research · 2015
    Review
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  20. Genomics of premature atherosclerotic vascular disease.Current atherosclerosis reports · 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

17 authors at 7 institutions in 2 countries.

L WangMiami Institute of Human Genomics, University of Miami, Miami, FL 33101, USA.
E R Hauser
S H Shah
D Seo
P Sivashanmugam
S T Exum
S G Gregory
C B Granger
J L Haines
C J H Jones
D Crossman
C Haynes
W E Kraus
N J Freedman
M A Pericak-Vance
P J Goldschmidt-Clermont
J M Vance
Duke Medical Center · USUniversity of Miami · USDuke University Hospital · USCenter for Human Genetics · USUniversity of Sheffield · GBUniversity of Wales · GBVanderbilt University · US

Funding

SNP discoveryP01HL073042 · NHLBI · DUKE UNIVERSITY · PI KRAUS, WILLIAM E · 2002 to 2006
$13.5M
MULTIDISCIPLINARY HEART &VASCULAR DISEASEST32HL007101 · NHLBI · DUKE UNIVERSITY · PI FREEDMAN, NEIL J. · 1985 to 2020
$9.8M
An Integrated Genomic Approach to Alzheimer DiseaseR01AG019757 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PERICAK-VANCE, MARGARET A. · 2002 to 2006
$4.8M
GENECARD-Gene Identification in Early-Onset CADR01HL073389 · NHLBI · DUKE UNIVERSITY · PI HAUSER, ELIZABETH R · 2003 to 2007
$3.5M
Alzheimer's Disease and Gene Discovery on Chromosome 9R01AG021547 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PERICAK-VANCE, MARGARET A. · 2003 to 2007
$3.1M
Mechanisms of Arterial Wall-Mediated AtherogenesisR01HL073005 · NHLBI · DUKE UNIVERSITY · PI FREEDMAN, NEIL J. · 2005 to 2008
$1.5M
NHLBI NIH HHS HL073389NHLBI NIH HHS HL73005NHLBI NIH HHS HL73042NHLBI NIH HHS P01 HL073042NHLBI NIH HHS R01 HL073005NHLBI NIH HHS R01 HL073389NHLBI NIH HHS T32 HL007101NIA NIH HHS AG019757NIA NIH HHS AG021547NIA NIH HHS R01 AG019757NIA NIH HHS R01 AG021547
6 · The paper itself

Abstract

Previous association mapping on chromosome 3q13-21 detected evidence for association at the limbic system-associated membrane protein (LSAMP) gene in individuals with late-onset coronary artery disease (CAD). LSAMP has never been implicated in the pathogenesis of CAD. We sought to thoroughly characterize the association and the gene. Non-redundant single nucleotide polymorphisms (SNPs) across the gene were examined in an initial dataset (168 cases with late-onset CAD, 149 controls). Stratification analysis on left main CAD (N = 102) revealed stronger association, which was further validated in a validation dataset (141 cases with left main CAD, 215 controls), a third control dataset (N = 255), and a family-based dataset (N = 2954). A haplotype residing in a novel alternative transcript of the LSAMP gene was significant in all independent case-control datasets (p = 0.0001 to 0.0205) and highly significant in the joint analysis (p = 0.00004). Lower expression of the novel alternative transcript was associated with the risk haplotype (p = 0.0002) and atherosclerosis burden in human aortas (p = 0.0001). Furthermore, silencing LSAMP expression in human aortic smooth muscle cells (SMCs) substantially augmented SMC proliferation (p<0.01). Therefore, the risk conferred by the LSAMP haplotype appears to be mediated by LSAMP down-regulation, which may promote SMC proliferation in the arterial wall and progression of atherosclerosis.

Indexed as

Polymorphism, Single NucleotideAgedAge of OnsetAortaAtherosclerosisCase-Control StudiesCell Adhesion Molecules, NeuronalCells, CulturedChromosomes, Human, Pair 3Coronary Artery DiseaseDown-RegulationFemaleGene ExpressionGPI-Linked ProteinsHaplotypesHumansCell Adhesion Molecules, NeuronalGPI-Linked Proteinslimbic system-associated membrane proteinTumor Suppressor Proteins

Identifiers

PMID18318786
PMCPMC2652886
OpenAlexW2006990386

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Read underepoch 390

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.