Evidence map›Paper›PMID 26771711›Full record

ReviewCell cycle (Georgetown, Tex.)2016

Reducing GWAS Complexity.

Dennis J Hazelett, David V Conti, Ying Han, Ali Amin Al Olama, Doug Easton, Rosalind A Eeles, Zsofia Kote-Jarai, Christopher A Haiman, Gerhard A Coetzee

Abstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. ArXiv · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

9 authors.

Dennis J Hazeletta Bioinformatics and Computational Biology Research Center, Biomedical Sciences, Cedars-Sinai Medical Center , Los Angeles , CA , USA.
David V Contib Departments of Preventive Medicine and Urology , USC/Norris Cancer Center , USA.
Ying Hanb Departments of Preventive Medicine and Urology , USC/Norris Cancer Center , USA.
Ali Amin Al Olamac Division of Genetics & Epidemiology, Centre of Cancer Genetic Epidemiology, University of Cambridge , Cambridge , UK.
Doug Eastonc Division of Genetics & Epidemiology, Centre of Cancer Genetic Epidemiology, University of Cambridge , Cambridge , UK.
Rosalind A Eelesd The Institute of Cancer Research & Royal Marsden NHS Foundation Trust , London , UK.
Zsofia Kote-Jaraid The Institute of Cancer Research & Royal Marsden NHS Foundation Trust , London , UK.
Christopher A Haimanb Departments of Preventive Medicine and Urology , USC/Norris Cancer Center , USA.
Gerhard A Coetzeeb Departments of Preventive Medicine and Urology , USC/Norris Cancer Center , USA.

Funding

Prostate Cancer Risk EnhancersR01CA136924 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI COETZEE, GERHARD A, FARNHAM, PEGGY J · 2010 to 2019
$5.4M
Breast Cancer Risk EnhancersR01CA190182 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI COETZEE, GERHARD A · 2015 to 2019
$2.1M
Cancer Research UK 16563Cancer Research UK 17528NCI NIH HHS R01 CA136924NCI NIH HHS R01 CA190182
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have revealed numerous genomic 'hits' associated with complex phenotypes. In most cases these hits, along with surrogate genetic variation as measure by numerous single nucleotide polymorphisms (SNPs) that are in linkage disequilibrium, are not in coding genes making assignment of functionality or causality intractable. Here we propose that fine-mapping along with the matching of risk SNPs at chromatin biofeatures lessen this complexity by reducing the number of candidate functional/causal SNPs. For example, we show here that only on average 2 SNPs per prostate cancer risk locus are likely candidates for functionality/causality; we further propose that this manageable number should be taken forward in mechanistic studies. The candidate SNPs can be looked up for each prostate cancer risk region in 2 recent publications in 2015 (1,2) from our groups.

Indexed as

AnimalsGenetic Predisposition to DiseaseGenome, HumanGenome-Wide Association StudyHumansLinkage DisequilibriumPolymorphism, Single NucleotideCancerchromatinenhancerfine-mappingGWASnon-coding DNASNP

Identifiers

PMID26771711
PMCPMC4825730

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.