Evidence map›Paper›PMID 12082592›Full record

Trial reportThe pharmacogenomics journal2002

Multi-locus interactions predict risk for post-PTCA restenosis: an approach to the genetic analysis of common complex disease.

R Y L Zee, J Hoh, S Cheng, R Reynolds, M A Grow, A Silbergleit, K Walker, L Steiner, G Zangenberg, A Fernandez-Ortiz and 5 more

Open access · bronzeAbstract readClinical Trial
PubMed Publisher
In one paragraph

Trial report in The pharmacogenomics journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.5field-weighted citation impact, top 3% 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, 65 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Pathogenesis and Clinical Significance of In-Stent Restenosis in Patients with Diabetes.International journal of environmental research and public health · 2021
    Review
  6. Article
  7. Analysis of gene-gene interactions.Current protocols in human genetics · 2011
    Article
  8. Bayesian epistasis association mapping via SNP imputation.Biostatistics (Oxford, England) · 2011
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

15 authors at 4 institutions in 3 countries.

R Y L ZeeDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
J Hoh
S Cheng
R Reynolds
M A Grow
A Silbergleit
K Walker
L Steiner
G Zangenberg
A Fernandez-Ortiz
C Macaya
E Pintor
A Fernandez-Cruz
J Ott
K Lindpainter
GeneTrace Systems (United States) · USHospital Clínico San Carlos · ESHarvard University · USRockefeller University · US

Funding

GENETICS OF CEREBROVASCULAR DISEASEK04HL003138 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI LINDPAINTNER, KLAUS · 1994 to 1996
–
NHGRI NIH HHS HG00008NHLBI NIH HHS K04-HL-03138-01
6 · The paper itself

Abstract

The complexity of recognizing the potential contribution of a number of possible predictors of complex disorders is increasingly challenging with the application of large-scale single nucleotide polymorphism (SNP) typing. In the search for putative genetic factors predisposing to coronary artery restenosis following balloon angioplasty, we determined genotypes for 94 SNPs representing 62 candidate genes, in a prospectively assembled cohort of 342 cases and 437 controls. Using a customized coupled-logistic regression procedure accounting for both additive and interactive effects, we identified seven SNPs in seven genes that, together, showed a statistically significant association with restenosis incidence (P <0.0001), accounting for 11.6% of overall variance observed. Among them are candidate genes for cardiovascular pathophysiology (apolipoprotein-species and NOS), inflammatory response (TNF receptor and CD14), and cell-cycle control (p53 and p53-associated protein). Our results emphasize the need to account for complex multi-gene influences and interactions when assessing the molecular pathology of multifactorial medical entities.

Indexed as

Angioplasty, Balloon, CoronaryCardiovascular DiseasesCell CycleCohort StudiesConstriction, PathologicGenetic MarkersHumansInflammationLogistic ModelsPolymorphism, GeneticPredictive Value of TestsProspective StudiesRecurrenceRisk AssessmentGenetic Markers

Identifiers

PMID12082592
OpenAlexW2061232867

What OpenQuestion holds

Textmetadata
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.