Evidence map›Paper›PMID 21308764›Full record

ArticleGenetic epidemiology2011

Latent class model with familial dependence to address heterogeneity in complex diseases: adapting the approach to family-based association studies.

Alexandre Bureau, Jordie Croteau, Arafat Tayeb, Chantal Mérette, Aurélie Labbe

Abstract read
In one paragraph

Article in Genetic epidemiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Family-based association analysis of alcohol dependence criteria and severity.Alcoholism, clinical and experimental research · 2014
    Article
  5. Article
  6. Article
  7. 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

5 authors at 2 institutions in 1 country.

Alexandre BureauCentre de recherche Université Laval Robert-Giffard, Quebec City, Quebec, Canada. alexandre.bureau@msp.ulaval.ca
Jordie Croteau
Arafat Tayeb
Chantal Mérette
Aurélie Labbe
Université Laval · CAMcGill University · CA

Funding

Center for Genomic and Phenomic Studies in AutismU24MH081810 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LAJONCHERE, CLARA M · 2007 to 2011
$8.3M
CIHR 80219CIHR 80219-1CIHR NPE-80219NIMH NIH HHS 1U24MH081810NIMH NIH HHS U24 MH081810
6 · The paper itself

Abstract

Clinical diagnoses of complex diseases may often encompass multiple genetically heterogeneous disorders. One way of dissecting this heterogeneity is to apply latent class (LC) analysis to measurements related to the diagnosis, such as detailed symptoms, to define more homogeneous disease sub-types, influenced by a smaller number of genes that will thus be more easily detectable. We have previously developed a LC model allowing dependence between the latent disease class status of relatives within families. We have also proposed a strategy to incorporate the posterior probability of class membership of each subject in parametric linkage analysis, which is not directly transferable to genetic association methods. Under the framework of family-based association tests (FBAT), we now propose to make the contribution of an affected subject to the FBAT statistic proportional to his or her posterior class membership probability. Simulations showed a modest but robust power advantage compared to simply assigning each subject to his or her most probable class, and important power gains over the analysis of the disease diagnosis without LC modeling under certain scenarios. The use of LC analysis with FBAT is illustrated using autism spectrum disorder (ASD) symptoms on families from the Autism Genetics Research Exchange, where we examined eight regions previously associated to autism in this sample. The analysis using the posterior probability of membership to an LC detected an association in the JARID2 gene as significant as that for ASD (P = 3 × 10(-5)) but with a larger effect size (odds ratio = 2.17 vs. 1.55).

Indexed as

Models, GeneticChildChild Development Disorders, PervasiveDatabases, GeneticDiseaseFamilyFemaleGenetic MarkersGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansMaleModels, StatisticalMolecular EpidemiologyProbabilityGenetic Markers

Identifiers

PMID21308764
PMCPMC4000257
OpenAlexW1986007519

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.