Evidence map›Paper›PMID 11309689›Full record

ArticleAmerican journal of human genetics2001

Transmission/disequilibrium test meets measured haplotype analysis: family-based association analysis guided by evolution of haplotypes.

H Seltman, K Roeder, B Devlin

Abstract read
In one paragraph

Article in American journal of human genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
–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

31 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  15. Structures and Assumptions: Strategies to Harness Gene × Gene and Gene × Environment Interactions in GWAS.Statistical science : a review journal of the Institute of Mathematical Statistics · 2009
    Article
  16. HLA class I alleles tag HLA-DRB1*1501 haplotypes for differential risk in multiple sclerosis susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  17. Review
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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

3 authors.

H SeltmanDepartment of Statistics, Carnegie Mellon University, Pittsburgh, PA, USA.
K Roeder
B Devlin

Funding

Genetics Association in Schizophrenia and Other DisordersR37MH057881 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DEVLIN, BERNIE · 2013 to 2022
$5.4M
GENETIC ASSOCIATION IN SCHIZOPHRENIA AND OTHER DISORDERSR01MH057881 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DEVLIN, BERNIE · 1998 to 2012
$4.8M
SUBSTANCE ABUSE AND THE DOPAMINE SYSTEM GENESR01DA011922 · NIDA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI VANYUKOV, MICHAEL M · 2000 to 2004
$2.6M
NIDA NIH HHS DA11922NIDA NIH HHS R01 DA011922NIMH NIH HHS MH57881NIMH NIH HHS R01 MH057881NIMH NIH HHS R37 MH057881
6 · The paper itself

Abstract

Family data teamed with the transmission/disequilibrium test (TDT), which simultaneously evaluates linkage and association, is a powerful means of detecting disease-liability alleles. To increase the information provided by the test, various researchers have proposed TDT-based methods for haplotype transmission. Haplotypes indeed produce more-definitive transmissions than do the alleles comprising them, and this tends to increase power. However, the larger number of haplotypes, relative to alleles at individual loci, tends to decrease power, because of the additional degrees of freedom required for the test. An optimal strategy would focus the test on particular haplotypes or groups of haplotypes. In this report we develop such an approach by combining the theory of TDT with that of measured haplotype analysis (MHA). MHA uses the evolutionary relationships among haplotypes to produce a limited set of hypothesis tests and to increase the interpretability of these tests. The theory of our approach, called the "evolutionary tree" (ET)-TDT, is developed for two cases: when haplotype transmission is certain and when it is not. Simulations show the ET-TDT can be more powerful than other proposed methods under reasonable conditions. More importantly, our results show that, when multiple polymorphisms are found within the gene, the ET-TDT can be useful for determining which polymorphisms affect liability.

Indexed as

PhylogenyAllelesChromosome MappingComputer SimulationGenetic Predisposition to DiseaseHaplotypesHumansLikelihood FunctionsLinkage DisequilibriumPolymorphism, Genetic

Identifiers

PMID11309689
PMCPMC1226105

What OpenQuestion holds

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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.