Evidence map›Paper›PMID 2896152›Full record

ReviewHuman genetics1988

DNA polymorphism and the study of disease associations.

D N Cooper, J F Clayton

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Gene environment interaction.Journal of epidemiology and community health · 1996
    Review
  5. Article
  6. Article
  7. Genetics of osteoporosis.Calcified tissue international · 1994
    Article
  8. Article
  9. Article
  10. Article
  11. Dissecting the genetic contribution to coronary heart disease.American journal of human genetics · 1991
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Effective testing of gene-disease associations.American journal of human genetics · 1990
    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

2 authors.

D N CooperHaematology Department, King's College Hospital School of Medicine and Dentistry, London, UK.
J F Clayton

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recombinant DNA approaches to disease analysis may be as applicable to studies of disease association as they are to the analysis and diagnosis of single-gene defects. Population and/or family association analyses, using restriction fragment length polymorphisms around candidate genes as markers, have been employed to study conditions such as atherosclerosis and disease with an HLA-association. Progress made to date in disease-association studies using recombinant DNA methodology is reviewed, the rationale behind such studies is examined and associated problems and pitfalls discussed.

Indexed as

Polymorphism, GeneticPolymorphism, Restriction Fragment LengthAllelesArteriosclerosisDisease SusceptibilityDNADNA, RecombinantEthics, MedicalGene FrequencyGenetic Diseases, InbornGenetic LinkageGenetic MarkersGenetic Predisposition to DiseaseHLA AntigensHumansModels, GeneticDNADNA, RecombinantGenetic MarkersHLA Antigens

Identifiers

PMID2896152

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.