Evidence map›Paper›PMID 39749473›Full record

ArticleGenetic epidemiology2025

Bayesian Effect Size Ranking to Prioritise Genetic Risk Variants in Common Diseases for Follow-Up Studies.

Daniel J M Crouch, Jamie R J Inshaw, Catherine C Robertson, Esther Ng, Jia-Yuan Zhang, Wei-Min Chen, Suna Onengut-Gumuscu, Antony J Cutler, Carlo Sidore, Francesco Cucca and 4 more

Abstract read
In one paragraph

Article in Genetic epidemiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

14 authors.

Daniel J M CrouchJDRF/Wellcome Diabetes and Inflammation Laboratory, Nuffield Department of Medicine, Centre for Human Genetics, NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.ORCID http://orcid.org/0000-0003-4122-9648
Jamie R J InshawJDRF/Wellcome Diabetes and Inflammation Laboratory, Nuffield Department of Medicine, Centre for Human Genetics, NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Catherine C RobertsonCenter for Public Health Genomics, University of Virginia, Charlottesville, Virginia, USA.
Esther NgJDRF/Wellcome Diabetes and Inflammation Laboratory, Nuffield Department of Medicine, Centre for Human Genetics, NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Jia-Yuan ZhangJDRF/Wellcome Diabetes and Inflammation Laboratory, Nuffield Department of Medicine, Centre for Human Genetics, NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Wei-Min ChenCenter for Public Health Genomics, University of Virginia, Charlottesville, Virginia, USA.
Suna Onengut-GumuscuCenter for Public Health Genomics, University of Virginia, Charlottesville, Virginia, USA.
Antony J CutlerJDRF/Wellcome Diabetes and Inflammation Laboratory, Nuffield Department of Medicine, Centre for Human Genetics, NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Carlo SidoreInstitute for Research in Genetics and Biomedicine (IRGB), Sardinia, Italy.
Francesco CuccaInstitute for Research in Genetics and Biomedicine (IRGB), Sardinia, Italy.
Flemming PociotDepartment of Pediatrics, Herlev University Hospital, Copenhagen, Denmark.
Patrick ConcannonDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, Florida, USA.
Stephen S RichCenter for Public Health Genomics, University of Virginia, Charlottesville, Virginia, USA.ORCID http://orcid.org/0000-0003-3872-7793
John A ToddJDRF/Wellcome Diabetes and Inflammation Laboratory, Nuffield Department of Medicine, Centre for Human Genetics, NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.

Funding

Type 1 Diabetes Genetics ConsortiumU01DK062418 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RICH, STEPHEN S. · 2002 to 2007
$59.8M
Systematic identification of functional T1D-associated non-coding SNPs using genetic, transcriptomic and epigenetic methodsDP3DK111906 · NIDDK · UNIVERSITY OF VIRGINIA · PI RICH, STEPHEN S. · 2016 to 2016
$4.0M
Transdisciplinary Big Data Science Training at UVaT32LM012416 · NLM · UNIVERSITY OF VIRGINIA · PI BROWN, DONALD E, LOUGHRAN, THOMAS P. · 2016 to 2020
$1.3M
NIDDK NIH HHS DP3 DK111906NIDDK NIH HHS U01 DK062418NLM NIH HHS T32 LM012416This work was funded by JDRF grants 9-2011-253, 5-SRA-2015-130-A-N and 4-SRA-2017-473-A-N, and Wellcome grants 091157/Z/10/Z and 107212/Z/15/Z, to the Diabetes and Inflammation Laboratory, University of Oxford, Fondazione di Sardegna grant U1301.2015/AI.1157.BE to Francesco Cucca, NIDDK grants U01 DK062418 and DP3 DK111906 and US National Library of Medicine grant T32 LM012416.Wellcome Trust
6 · The paper itself

Abstract

Biological datasets often consist of thousands or millions of variables, e.g. genetic variants or biomarkers, and when sample sizes are large it is common to find many associated with an outcome of interest, for example, disease risk in a GWAS, at high levels of statistical significance, but with very small effects. The False Discovery Rate (FDR) is used to identify effects of interest based on ranking variables according to their statistical significance. Here, we develop a complementary measure to the FDR, the priorityFDR, that ranks variables by a combination of effect size and significance, allowing further prioritisation among a set of variables that pass a significance or FDR threshold. Applying to the largest GWAS of type 1 diabetes to date (15,573 cases and 158,408 controls), we identified 26 independent genetic associations, including two newly-reported loci, with qualitatively lower priorityFDRs than the remaining 175 signals. We detected putatively causal type 1 diabetes risk genes using Mendelian Randomisation, and found that these were located disproportionately close to low priorityFDR signals (p = 0.005), as were genes in the IL-2 pathway (p = 0.003). Selecting variables on both effect size and significance can lead to improved prioritisation for mechanistic follow-up studies from genetic and other large biological datasets.

Indexed as

Bayes TheoremDiabetes Mellitus, Type 1Genetic Predisposition to DiseaseGenome-Wide Association StudyMendelian Randomization AnalysisPolymorphism, Single NucleotideFollow-Up StudiesGenetic VariationHumanseffect sizeempirical Bayesfalse discovery rateGWASsignificance

Identifiers

PMID39749473
PMCPMC11696485

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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.