Evidence map›Paper›PMID 22303403›Full record

ArticleFrontiers in genetics2011

Six Degrees of Epistasis: Statistical Network Models for GWAS.

B A McKinney, Nicholas M Pajewski

Abstract read
In one paragraph

Article in Frontiers in genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. STatistical Inference Relief (STIR) feature selection.Bioinformatics (Oxford, England) · 2019
    Article
  7. Article
  8. Evolutionary footprint of epistasis.PLoS computational biology · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Detecting epistasis in human complex traits.Nature reviews. Genetics · 2014
    Review
  14. Spurious transcription factor binding: non-functional or genetically redundant?BioEssays : news and reviews in molecular, cellular and developmental biology · 2014
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  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.

B A McKinneyDepartment of Mathematics, Tandy School of Computer Science, University of Tulsa Tulsa, OK, USA.
Nicholas M Pajewski

Funding

Cytokine Signaling Network Response to Smallpox VaccineK25AI064625 · NIAID · VANDERBILT UNIVERSITY · PI MCKINNEY, BRETT · 2006 to 2010
$534k
Machine Learning Analysis of Genetic Modulators of Vaccine Immune ResponseR56AI080932 · NIAID · UNIVERSITY OF TULSA · PI MCKINNEY, BRETT · 2009 to 2009
$346k
NIAID NIH HHS K25 AI064625NIAID NIH HHS R56 AI080932
6 · The paper itself

Abstract

There is growing evidence that much more of the genome than previously thought is required to explain the heritability of complex phenotypes. Recent studies have demonstrated that numerous common variants from across the genome explain portions of genetic variability, spawning various avenues of research directed at explaining the remaining heritability. This polygenic structure is also the motivation for the growing application of pathway and gene set enrichment techniques, which have yielded promising results. These findings suggest that the coordination of genes in pathways that are known to occur at the gene regulatory level also can be detected at the population level. Although genes in these networks interact in complex ways, most population studies have focused on the additive contribution of common variants and the potential of rare variants to explain additional variation. In this brief review, we discuss the potential to explain additional genetic variation through the agglomeration of multiple gene-gene interactions as well as main effects of common variants in terms of a network paradigm. Just as is the case for single-locus contributions, we expect each gene-gene interaction edge in the network to have a small effect, but these effects may be reinforced through hubs and other connectivity structures in the network. We discuss some of the opportunities and challenges of network methods for analyzing genome-wide association studies (GWAS) such as the study of hubs and motifs, and integrating other types of variation and environmental interactions. Such network approaches may unveil hidden variation in GWAS, improve understanding of mechanisms of disease, and possibly fit into a network paradigm of evolutionary genetics.

Indexed as

epistasis networkgenetic association interaction networkmissing heritability

Identifiers

PMID22303403
PMCPMC3261632

What OpenQuestion holds

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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.