Evidence map›Paper›PMID 24661571›Full record

ReviewTrends in genetics : TIG2014

Laying a solid foundation for Manhattan--'setting the functional basis for the post-GWAS era'.

Xiaoyang Zhang, Swneke D Bailey, Mathieu Lupien

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Trends in genetics : TIG, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
–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

49 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Deletion ofProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Genetic variants ofAmerican journal of cancer research · 2021
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. FOXO3 on the Road to Longevity: Lessons From SNPs and Chromatin Hubs.Computational and structural biotechnology journal · 2019
    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

3 authors.

Xiaoyang ZhangDepartment of Genetics, Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, NH, USA.
Swneke D BaileyThe Princess Margaret Cancer Centre - University Health Network, Toronto, ON, M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada.
Mathieu LupienThe Princess Margaret Cancer Centre - University Health Network, Toronto, ON, M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada; Ontario Institute for Cancer Research, Toronto, ON, Canada. Electronic address: mlupien@uhnres.utoronto.ca.

Funding

Breast and prostate cancer risk SNPs regulate FoxA1 and nuclear receptor activityR01CA155004 · NCI · UNIVERSITY HEALTH NETWORK · PI LUPIEN, MATHIEU · 2011 to 2015
$1.2M
CIHRNCI NIH HHS R01 CA155004NCI NIH HHS R01CA155004
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have identified more than 8900 genetic variants, mainly single-nucleotide polymorphisms (SNPs), associated with hundreds of human traits and diseases, which define risk-associated loci. Variants that map to coding regions can affect protein sequence, translation rate, and alternative splicing, all of which influence protein function. However, the vast majority of sequence variants map to non-coding intergenic and intronic regions, and it has been much more challenging to assess the functional nature of these variants. Recent work annotating the non-coding regions of the genome has contributed to post-GWAS studies by facilitating the identification of the functional targets of risk-associated loci. Many non-coding genetic variants within risk-associated loci alter gene expression by modulating the activity of cis-regulatory elements. We review here these recent findings, discuss their implication for the post-GWAS era, and relate their importance to the interpretation of disease-associated mutations identified through whole-genome sequencing.

Indexed as

Genome-Wide Association StudyDNA, IntergenicGenetic Predisposition to DiseaseGenetic VariationGenomeHumansOpen Reading FramesDNA, Intergeniccausal variantfunctional genomicgenetic risk variantGWASmissing heritabilitynon-coding

Identifiers

PMID24661571
PMCPMC4026049

What OpenQuestion holds

Textmetadata
LicenceTDM
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.