Evidence map›Paper›PMID 25735482›Full record

ArticleEuropean journal of human genetics : EJHG2015

Kullback-Leibler divergence for detection of rare haplotype common disease association.

Shili Lin

Abstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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0cells of the map it votes in
1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

1 author.

Shili LinDepartment of Statistics, The Ohio State University, Columbus, OH, USA.

Funding

Omics analysis of three-dimensional transcriptional regulationR01GM114142 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JIN, VICTOR, LIN, SHILI · 2015 to 2024
$2.7M
Identifying rare haplotype-environment interactions using Logistic Bayesian LassoR03CA171011 · NCI · UNIVERSITY OF TEXAS DALLAS · PI BISWAS, SWATI, LIN, SHILI · 2012 to 2013
$167k
NIGMS NIH HHS R01 GM114142
6 · The paper itself

Abstract

Rare haplotypes may tag rare causal variants of common diseases; hence, detection of such rare haplotypes may also contribute to our understanding of complex disease etiology. Because rare haplotypes frequently result from common single-nucleotide polymorphisms (SNPs), focusing on rare haplotypes is much more economical compared with using rare single-nucleotide variants (SNVs) from sequencing, as SNPs are available and 'free' from already amassed genome-wide studies. Further, associated haplotypes may shed light on the underlying disease causal mechanism, a feat unmatched by SNV-based collapsing methods. In recent years, data mining approaches have been adapted to detect rare haplotype association. However, as they rely on an assumed underlying disease model and require the specification of a null haplotype, results can be erroneous if such assumptions are violated. In this paper, we present a haplotype association method based on Kullback-Leibler divergence (hapKL) for case-control samples. The idea is to compare haplotype frequencies for the cases versus the controls by computing symmetrical divergence measures. An important property of such measures is that both the frequencies and logarithms of the frequencies contribute in parallel, thus balancing the contributions from rare and common, and accommodating both deleterious and protective, haplotypes. A simulation study under various scenarios shows that hapKL has well-controlled type I error rates and good power compared with existing data mining methods. Application of hapKL to age-related macular degeneration (AMD) shows a strong association of the complement factor H (CFH) gene with AMD, identifying several individual rare haplotypes with strong signals.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseComplement Factor HComputer SimulationHaplotypesHumansLinkage DisequilibriumMacular DegenerationPolymorphism, Single NucleotideRare DiseasesComplement Factor H

Identifiers

PMID25735482
PMCPMC4613467

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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.