Evidence map›Paper›PMID 24482034›Full record

ArticleGenetic epidemiology2014

A generalized genetic random field method for the genetic association analysis of sequencing data.

Ming Li, Zihuai He, Min Zhang, Xiaowei Zhan, Changshuai Wei, Robert C Elston, Qing Lu

Registry-linked trialAbstract read
In one paragraph

Article in Genetic epidemiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00556530 (Genetic Modifiers of 22q11.2 Deletion Syndrome), which is not on this map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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.

NCT00556530 recruitingnot on this mapstarted 2016, after this paper: background citation

Genetic Modifiers of 22q11.2 Deletion Syndrome

TypeobservationalSponsorAlbert Einstein College of MedicineRan2016 to 2029Enrolled1,000ConditionsDiGeorge Syndrome, 22q11.2 Deletion Syndrome
3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Article
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  11. Observational
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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

7 authors.

Ming LiDivision of Biostatistics, Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Zihuai He
Min Zhang
Xiaowei Zhan
Changshuai Wei
Robert C Elston
Qing Lu

Funding

UT Southwestern Center for Translational Medicine (UL1/KL2/TL1)UL1TR001105 · NCATS · UT SOUTHWESTERN MEDICAL CENTER · PI TOTO, ROBERT DANIEL · 2013 to 2017
$24.5M
Gene-Gene/Gene-Environment Interactions Associated with Nicotine DependenceK01DA033346 · NIDA · MICHIGAN STATE UNIVERSITY · PI LU, QING · 2013 to 2017
$833k
High-dimensional Statistical Genetic Approach for Family-based Orofacial CleftsR03DE022379 · NIDCR · MICHIGAN STATE UNIVERSITY · PI LU, QING · 2012 to 2013
$441k
Role of Mitochondrial CYP2E1 in Chemical Exposure-Driven NeurodegenerationF32ES027306 · NIEHS · DUKE UNIVERSITY · PI HARTMAN, JESSICA HELENE · 2016 to 2018
$171k
NCATS NIH HHS UL1 TR001105NIDA NIH HHS K01 DA033346NIDA NIH HHS K01DA033346NIDCR NIH HHS R03 DE022379NIDCR NIH HHS R03DE022379NIEHS NIH HHS 27306C0004
6 · The paper itself

Abstract

With the advance of high-throughput sequencing technologies, it has become feasible to investigate the influence of the entire spectrum of sequencing variations on complex human diseases. Although association studies utilizing the new sequencing technologies hold great promise to unravel novel genetic variants, especially rare genetic variants that contribute to human diseases, the statistical analysis of high-dimensional sequencing data remains a challenge. Advanced analytical methods are in great need to facilitate high-dimensional sequencing data analyses. In this article, we propose a generalized genetic random field (GGRF) method for association analyses of sequencing data. Like other similarity-based methods (e.g., SIMreg and SKAT), the new method has the advantages of avoiding the need to specify thresholds for rare variants and allowing for testing multiple variants acting in different directions and magnitude of effects. The method is built on the generalized estimating equation framework and thus accommodates a variety of disease phenotypes (e.g., quantitative and binary phenotypes). Moreover, it has a nice asymptotic property, and can be applied to small-scale sequencing data without need for small-sample adjustment. Through simulations, we demonstrate that the proposed GGRF attains an improved or comparable power over a commonly used method, SKAT, under various disease scenarios, especially when rare variants play a significant role in disease etiology. We further illustrate GGRF with an application to a real dataset from the Dallas Heart Study. By using GGRF, we were able to detect the association of two candidate genes, ANGPTL3 and ANGPTL4, with serum triglyceride.

Indexed as

Sequence Analysis, DNAAngiopoietin-Like Protein 3Angiopoietin-Like Protein 4Angiopoietin-like ProteinsAngiopoietinsDiseaseGenetic Association StudiesGenetic VariationHeartHumansModels, GeneticPhenotypeTexasTriglyceridesAngiopoietin-Like Protein 3Angiopoietin-Like Protein 4Angiopoietin-like ProteinsAngiopoietinsANGPTL3 protein, humanANGPTL4 protein, humanTriglyceridesgeneralized estimating equationrare variantssmall-scale sequencing studies

Identifiers

PMID24482034
PMCPMC5241166

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Registered trials

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.