Evidence map›Paper›PMID 20640184›Full record

ArticleStatistical science : a review journal of the Institute of Mathematical Statistics2009

Structures and Assumptions: Strategies to Harness Gene × Gene and Gene × Environment Interactions in GWAS.

Charles Kooperberg, Michael Leblanc, James Y Dai, Indika Rajapakse

Open access · bronzeAbstract read
In one paragraph

Article in Statistical science : a review journal of the Institute of Mathematical Statistics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Boosting predictions of treatment success.Proceedings of the National Academy of Sciences of the United States of America · 2010
    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

4 authors at 1 institution in 1 country.

Charles KooperbergFred Hutchinson Cancer Research Center Division of Public Health Sciences.
Michael Leblanc
James Y Dai
Indika Rajapakse
Fred Hutch Cancer Center · US

Funding

Interdisciplinary Tranining in Cancer ResearchT32CA080416 · NCI · UNIVERSITY OF WASHINGTON · PI STODDARD, BARRY L. · 1998 to 2023
$9.7M
Use of Biomarkers in Diagnosis, Prognosis, Risk Prediction and Early Detection ofP01CA053996 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HSU, LI · 1991 to 2015
$9.4M
STATISTICAL METHODS FOR CLINICAL STUDIESR01CA090998 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI LEBLANC, MICHAEL L. · 2001 to 2011
$2.2M
Adaptive Function Estimation for Genomic DataR01CA074841 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KOOPERBERG, CHARLES L · 2003 to 2006
$1.1M
Dissecting complex traits with diverse resourcesU01CA125489 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KOOPERBERG, CHARLES L · 2006 to 2008
$807k
NCI NIH HHS P01 CA053996NCI NIH HHS R01 CA074841NCI NIH HHS R01 CA090998NCI NIH HHS T32 CA080416NCI NIH HHS U01 CA125489
6 · The paper itself

Abstract

Genome-wide association studies, in which as many as a million single nucleotide polymorphisms (SNP) are measured on several thousand samples, are quickly becoming a common type of study for identifying genetic factors associated with many phenotypes. There is a strong assumption that interactions between SNPs or genes and interactions between genes and environmental factors substantially contribute to the genetic risk of a disease. Identification of such interactions could potentially lead to increased understanding about disease mechanisms; drug × gene interactions could have profound applications for personalized medicine; strong interaction effects could be beneficial for risk prediction models. In this paper we provide an overview of different approaches to model interactions, emphasizing approaches that make specific use of the structure of genetic data, and those that make specific modeling assumptions that may (or may not) be reasonable to make. We conclude that to identify interactions it is often necessary to do some selection of SNPs, for example, based on prior hypothesis or marginal significance, but that to identify SNPs that are marginally associated with a disease it may also be useful to consider larger numbers of interactions.

Identifiers

PMID20640184
PMCPMC2904990
OpenAlexW2062437660

What OpenQuestion holds

Textmetadata
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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.