ArticleAmerican journal of human genetics2002
A statistical method for identification of polymorphisms that explain a linkage result.
Article in American journal of human genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- G-STRATEGY: Optimal Selection of Individuals for Sequencing in Genetic Association Studies.Genetic epidemiology · 2016Article
- Complex pedigrees in the sequencing era: to track transmissions or decorrelate?Genetic epidemiology · 2014Article
- Combined linkage and family-based association analysis improves candidate gene detection in Genetic Analysis Workshop 18 simulation data.BMC proceedings · 2014Article
- Variants in CPT1A, FADS1, and FADS2 are Associated with Higher Levels of Estimated Plasma and Erythrocyte Delta-5 Desaturases in Alaskan Eskimos.Frontiers in genetics · 2012Article
- A method to detect single-nucleotide polymorphisms accounting for a linkage signal using covariate-based affected relative pair linkage analysis.BMC proceedings · 2011Article
- Family-based designs for genome-wide association studies.Nature reviews. Genetics · 2011Review
- Evidence that multiple genetic variants of MC4R play a functional role in the regulation of energy expenditure and appetite in Hispanic children.The American journal of clinical nutrition · 2010Article
- Evaluation of approaches to identify associated SNPs that explain the linkage evidence in nuclear families with affected siblings.Human heredity · 2010Article
- Common and rare variants of DAOA in bipolar disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2009Article
- A composite-likelihood approach for identifying polymorphisms that are potentially directly associated with disease.European journal of human genetics : EJHG · 2009Article
- Genome-wide association studies: implications for multiethnic samples.Human molecular genetics · 2008Review
- Does APOE explain the linkage of Alzheimer's disease to chromosome 19q13?American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2008Article
- Exploring causality via identification of SNPs or haplotypes responsible for a linkage signal.Genetic epidemiology · 2007Article
- Case-control association testing with related individuals: a more powerful quasi-likelihood score test.American journal of human genetics · 2007Article
- Residual linkage: why do linkage peaks not disappear after an association study?Human genetics · 2007Article
- No evidence for multiple loci affecting rheumatoid arthritis risk on chromosome 6p21.BMC proceedings · 2007Article
- A new score statistic to test for association given linkage in affected sibling pair-control designs.BMC proceedings · 2007Article
- Joint linkage and association analysis for identification of potentially causal polymorphisms in GAW15 data.BMC proceedings · 2007Article
- The linkage and association of the gene encoding upstream stimulatory factor 1 with type 2 diabetes and metabolic syndrome in the Chinese population.Diabetologia · 2005Article
- Joint modeling of linkage and association: identifying SNPs responsible for a linkage signal.American journal of human genetics · 2005Article
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Authors and funding
3 authors.
Funding
Abstract
Suppose that many polymorphic sites have been identified and genotyped in a region showing strong linkage with a trait. A key question of interest is which site (or combination of sites) in the region influences susceptibility to the trait. We have developed a novel statistical approach to this problem, in the context of qualitative-trait mapping, in which we use linkage data to identify the polymorphic sites whose genotypes could fully explain the observed linkage to the region. The information provided by this analysis is different from that provided by tests of either linkage or association. Our approach is based on the observation that if a particular site is the only site in the region that influences the trait, then-conditional on the genotypes at that site for the affected relatives-there should be no unexplained oversharing in the region among affected individuals. We focus on the affected sib-pair study design and develop test statistics that are variations on the usual allele-sharing methods used in linkage studies. We perform hypothesis tests and derive a confidence set for the true causal polymorphic site, under the assumption that there is only one site in the region influencing the trait. Our method is appropriate under a very general model for how the site influences the trait, including epistasis with unlinked loci, correlated environmental effects within families, and gene-environment interaction. We extend our method to larger sibships and apply it to an NIDDM1 data set.
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