Evidence map›Paper›PMID 22922440›Full record

ArticleAmerican journal of epidemiology2012

Detecting and exploiting etiologic heterogeneity in epidemiologic studies.

Colin B Begg, Emily C Zabor

Abstract read
In one paragraph

Article in American journal of epidemiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Can We Interpret Analyses of Etiologic Heterogeneity When Molecular Markers Are Used to Classify Tumors?Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
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  20. Molecular pathological epidemiology of epigenetics: emerging integrative science to analyze environment, host, and disease.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2013
    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

2 authors.

Colin B BeggDepartment of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. beggc@mskcc.org
Emily C Zabor

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Statistical Strategies for Establishing Etiologic Heterogeneity of TumorsR01CA163251 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI BEGG, COLIN B · 2012 to 2015
$1.5M
Estimating Cancer Risks of Rare Genetic VariantsR01CA131010 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI BEGG, COLIN B, CAPANU, MARINELA · 2008 to 2010
$944k
NCI NIH HHS CA131010NCI NIH HHS CA163251NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA131010NCI NIH HHS R01 CA163251
6 · The paper itself

Abstract

Contemporary searches for new risk factors frequently involve genome-wide explorations of very large numbers of candidate risk variants. Given that diseases can often be classified into subtypes that possess evidence of etiologic heterogeneity, the question arises as to whether or not a search for new risk factors would be improved by looking separately within subtypes. Etiologic risk heterogeneity inevitably increases the signal in at least one of the subtypes, but this advantage may be offset by smaller sample sizes and the increased chances of false discovery. In this article, the authors show that only a relatively modest degree of etiologic heterogeneity is necessary for the subtyping strategies to have improved statistical power. In practice, effective exploitation of etiologic heterogeneity requires strong evidence that the subtypes selected are likely to exhibit substantial heterogeneity. Further, defining the subtypes that demonstrate the most heterogeneous profiles is important for optimizing the search for new risk factors. The concepts are illustrated by using data from a breast cancer study in which results are available separately for estrogen receptor-positive (ER+) and -negative (ER-) tumors.

Indexed as

CausalityData Interpretation, StatisticalEpidemiologic Research DesignRiskBiomarkers, TumorBreast NeoplasmsCase-Control StudiesFemaleGenome-Wide Association StudyHumansOdds RatioPolymorphism, Single NucleotideReceptors, EstrogenRisk FactorsBiomarkers, TumorReceptors, Estrogen

Identifiers

PMID22922440
PMCPMC3530356

What OpenQuestion holds

Textmetadata
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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.