Evidence map›Paper›PMID 10731466›Full record

ArticleAmerican journal of human genetics2000

Linkage analysis in the presence of errors IV: joint pseudomarker analysis of linkage and/or linkage disequilibrium on a mixture of pedigrees and singletons when the mode of inheritance cannot be accurately specified.

H H Göring, J D Terwilliger

Abstract read
In one paragraph

Article in American journal of human genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing 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

69 citing papers in PubMed.

  1. Trial
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  5. PeerJ · 2017
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  14. Analysis of detailed phenotype profiles reveals CHRNA5-CHRNA3-CHRNB4 gene cluster association with several nicotine dependence traits.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2012
    Article
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9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

H H GöringDepartment of Genetics and Development, Columbia University, New York, NY, USA.
J D Terwilliger

Funding

LINKAGE ANALYSIS METHODS FOR HUMAN GENE MAPPINGR01HG000008 · NHGRI · ROCKEFELLER UNIVERSITY · PI OTT, JURG · 1990 to 2004
$1.2M
NHGRI NIH HHS HG00008NHGRI NIH HHS R01 HG000008
6 · The paper itself

Abstract

There is a lot of confusion in the literature about the "differences" between "model-based" and "model-free" methods and about which approach is better suited for detection of the genes predisposing to complex multifactorial phenotypes. By starting from first principles, we demonstrate that the differences between the two approaches have more to do with study design than statistical analysis. When simple data structures are repeatedly ascertained, no assumptions about the genotype-phenotype relationship need to be made for the analysis to be powerful, since simple data structures admit only a small number of df. When more complicated and/or heterogeneous data structures are ascertained, however, the number of df in the underlying probability model is too large to have a powerful, truly "model-free" test. So-called "model-free" methods typically simplify the underlying probability model by implicitly assuming that, in some sense, all meioses connecting two affected individuals are informative for linkage with identical probability and that the affected individuals in a pedigree share as many disease-predisposing alleles as possible. By contrast, "model-based" methods add structure to the underlying parameter space by making assumptions about the genotype-phenotype relationship, making it possible to probabilistically assign disease-locus genotypes to all individuals in the data set on the basis of the observed phenotypes. In this study, we demonstrate the equivalence of these two approaches in a variety of situations and exploit this equivalence to develop more powerful and efficient likelihood-based analogues of "model-free" tests of linkage and/or linkage disequilibrium. Through the use of a "pseudomarker" locus to structure the space of observations, sib-pairs, triads, and singletons can be analyzed jointly, which will lead to tests that are more well-behaved, efficient, and powerful than traditional "model-free" tests such as the affected sib-pair, transmission/disequilibrium, haplotype relative risk, and case-control tests. Also described is an extension of this approach to large pedigrees, which, in practice, is equivalent to affected relative-pair analysis. The proposed methods are equally applicable to two-point and multipoint analysis (using complex-valued recombination fractions).

Indexed as

Models, GeneticCase-Control StudiesChromosome MappingComputer SimulationFemaleGenes, DominantGenetic Diseases, InbornGenetic MarkersGenetic Predisposition to DiseaseGenotypeHaplotypesHumansLikelihood FunctionsLinkage DisequilibriumMaleMatched-Pair AnalysisGenetic Markers

Identifiers

PMID10731466
PMCPMC1288197

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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.