Evidence map›Paper›PMID 31145509›Full record

ArticleGenetic epidemiology2019

A comparison of two workflows for regulome and transcriptome-based prioritization of genetic variants associated with myocardial mass.

Elisabetta Manduchi, Daiane Hemerich, Jessica van Setten, Vinicius Tragante, Magdalena Harakalova, Jiayi Pei, Scott M Williams, Pim van der Harst, Folkert W Asselbergs, Jason H Moore

Abstract readComparative Study
In one paragraph

Article in Genetic epidemiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

10 authors.

Elisabetta ManduchiDepartment of Biostatistics, Epidemiology, & Informatics, University of Pennsylvania, Philadelphia, Pennsylvania.ORCID 0000-0002-4110-3714
Daiane HemerichDepartment of Cardiology, Division Heart & Lungs, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-7929-8107
Jessica van SettenDepartment of Cardiology, Division Heart & Lungs, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-4934-7510
Vinicius TraganteDepartment of Cardiology, Division Heart & Lungs, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-8223-8957
Magdalena HarakalovaDepartment of Cardiology, Division Heart & Lungs, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Jiayi PeiDepartment of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Scott M WilliamsDepartment of Population and Quantitative Health Sciences, Case Western Reserve University, Ohio.ORCID 0000-0002-4835-9544
Pim van der HarstDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Folkert W AsselbergsDepartment of Cardiology, Division Heart & Lungs, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-1692-8669
Jason H MooreDepartment of Biostatistics, Epidemiology, & Informatics, University of Pennsylvania, Philadelphia, Pennsylvania.ORCID 0000-0002-5015-1099

Funding

Bioinformatics Strategies for Genome-Wide Association StudiesR01LM010098 · NLM · UNIVERSITY OF PENNSYLVANIA · PI MOORE, JASON H., WILLIAMS, SCOTT MATTHEW · 2009 to 2023
$5.1M
NLM NIH HHS R01 LM010098
6 · The paper itself

Abstract

A typical task arising from main effect analyses in a Genome Wide Association Study (GWAS) is to identify single nucleotide polymorphisms (SNPs), in linkage disequilibrium with the observed signals, that are likely causal variants and the affected genes. The affected genes may not be those closest to associating SNPs. Functional genomics data from relevant tissues are believed to be helpful in selecting likely causal SNPs and interpreting implicated biological mechanisms, ultimately facilitating prevention and treatment in the case of a disease trait. These data are typically used post GWAS analyses to fine-map the statistically significant signals identified agnostically by testing all SNPs and applying a multiple testing correction. The number of tested SNPs is typically in the millions, so the multiple testing burden is high. Motivated by this, in this study we investigated an alternative workflow, which consists in utilizing the available functional genomics data as a first step to reduce the number of SNPs tested for association. We analyzed GWAS on electrocardiographic QRS duration using these two workflows. The alternative workflow identified more SNPs, including some residing in loci not discovered with the typical workflow. Moreover, the latter are corroborated by other reports on QRS duration. This indicates the potential value of incorporating functional genomics information at the onset in GWAS analyses.

Indexed as

Gene Expression RegulationGenome-Wide Association StudyPolymorphism, Single NucleotideTranscriptomeCardiomyopathiesHumansLinkage DisequilibriumPhenotypePromoter Regions, GeneticWorkflowfunctional genomicsGWASleft ventricular massSNP preselection

Identifiers

PMID31145509
PMCPMC6687530

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.