Evidence map›Paper›PMID 20814428›Full record

ArticlePloS one2010

A general model for multilocus epistatic interactions in case-control studies.

Zhong Wang, Tian Liu, Zhenwu Lin, John Hegarty, Walter A Koltun, Rongling Wu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Zhong WangCenter for Statistical Genetics, Pennsylvania State University, Hershey, Pennsylvania, United States of America.
Tian Liu
Zhenwu Lin
John Hegarty
Walter A Koltun
Rongling Wu
Pennsylvania State University · USGenome Institute of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpistasis, i.e., the interaction of alleles at different loci, is thought to play a central role in the formation and progression of complex diseases. The complexity of disease expression should arise from a complex network of epistatic interactions involving multiple genes. METHODOLOGY: We develop a general model for testing high-order epistatic interactions for a complex disease in a case-control study. We incorporate the quantitative genetic theory of high-order epistasis into the setting of cases and controls sampled from a natural population. The new model allows the identification and testing of epistasis and its various genetic components.

conclusionsSimulation studies were used to examine the power and false positive rates of the model under different sampling strategies. The model was used to detect epistasis in a case-control study of inflammatory bowel disease, in which five SNPs at a candidate gene were typed, leading to the identification of a significant three-locus epistasis.

Indexed as

Models, GeneticAdolescentAdultAgedAged, 80 and overCase-Control StudiesComputer SimulationEpistasis, GeneticFalse Positive ReactionsGenetic LociGenotypeHumansInflammatory Bowel DiseasesMiddle AgedPolymorphism, Single NucleotideReproducibility of Results

Identifiers

PMID20814428
PMCPMC2909900
OpenAlexW2061530118

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.