Evidence map›Paper›PMID 16909384›Full record

ArticleAmerican journal of human genetics2006

The value of molecular haplotypes in a family-based linkage study.

E M Gillanders, J V Pearson, A J M Sorant, J M Trent, J R O'Connell, J E Bailey-Wilson

Abstract read
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Article in American journal of human genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

E M GillandersInherited Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Baltimore, MD 21224, USA. lgilland@mail.nih.gov
J V Pearson
A J M Sorant
J M Trent
J R O'Connell
J E Bailey-Wilson

Funding

Development of statistical genetics methodologyZIAHG000153 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BAILEY-WILSON, JOAN ELLEN · 2009 to 2022
$5.0M
Development of Statistical Genetics MethodologyZ01HG000153 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BAILEY-WILSON, JOAN ELLEN · 1999 to 2008
$616k
6 · The paper itself

Abstract

Novel methods that could improve the power of conventional methods of gene discovery for complex diseases should be investigated. In a simulation study, we aimed to investigate the value of molecular haplotypes in the context of a family-based linkage study. The term "haplotype" (or "haploid genotype") refers to syntenic alleles inherited on a single chromosome, and we use the term "molecular haplotype" to refer to haplotypes that have been determined directly by use of a molecular technique such as long-range allele-specific polymerase chain reaction. In our study, we simulated genotype and phenotype data and then compared the powers of analyzing these data under the assumptions that various levels of information from molecular haplotypes were available. (This information was available because of the simulation procedure.) Several conclusions can be drawn. First, as expected, when genetic homogeneity is expected or when marker data are complete, it is not efficient to generate molecular haplotyping information. However, with levels of heterogeneity and missing data patterns typical of complex diseases, we observed a 23%-77% relative increase in the power to detect linkage in the presence of heterogeneity with heterogeneity LOD scores >3.0 when all individuals are molecularly haplotyped (compared with the power when only standard genotypes are used). Furthermore, our simulations indicate that most of the increase in power can be achieved by molecularly haplotyping a single individual in each family, thereby making molecular haplotyping a valuable strategy for increasing the power of gene mapping studies of complex diseases. Maximization of power, given an existing family set, can be particularly important for late-onset, often-fatal diseases such as cancer, for which informative families are difficult to collect.

Indexed as

Computer SimulationGenetic LinkageGenetic Predisposition to DiseaseGenetic TestingGenotypeHaplotypesHumansPedigreeSoftware

Identifiers

PMID16909384
PMCPMC1559540

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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.