Evidence mapPaperPMID 41559068Full record

ArticleNature communications2026

Preventing premature deaths through polygenic risk scores.

Melisa Chuong, Deborah Thompson, Michael E Weale, Fernando Riveros-Mckay, Nilesh J Samani, Daniel Wells, Vincent Plagnol, Gil McVean, Euan A Ashley, Peter Donnelly and 2 more

Abstract read
In one paragraph

Article in Nature communications, 2026. 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. Article
  2. 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

12 authors.

Melisa ChuongGenomics Ltd, Oxford, UK.
Deborah ThompsonGenomics Ltd, Oxford, UK.
Michael E WealeGenomics Ltd, Oxford, UK.ORCID http://orcid.org/0000-0003-4593-1186
Fernando Riveros-MckayGenomics Ltd, Oxford, UK.
Nilesh J SamaniDivision of Cardiovascular Sciences, University of Leicester, BHF Cardiovascular Research Centre, Leicester, UK.ORCID http://orcid.org/0000-0002-3286-8133
Daniel WellsGenomics Ltd, Oxford, UK.
Vincent PlagnolGenomics Ltd, Oxford, UK.
Gil McVeanGenomics Ltd, Oxford, UK.
Euan A AshleyDivision of Cardiology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0001-9418-9577
Peter DonnellyGenomics Ltd, Oxford, UK.
Seamus Harrison *Genomics Ltd, Oxford, UK.
Jack W O'Sullivan *Division of Cardiology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA. jackos@stanford.edu.ORCID http://orcid.org/0000-0003-3629-2546

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polygenic risk scores (PRS) have demonstrated predictive validity across a range of cohorts and diseases, but quantifying their clinical utility remains a challenge. As PRS can be derived from a single biological sample and remains stable throughout life, we explore the potential of PRS to optimize existing screening programs. Via an integrated modelling approach, we quantify the potential clinical benefits arising from a knowledge of PRS across seven diseases with existing screening programs (abdominal aortic aneurysm, breast cancer, colorectal cancer, coronary artery disease, hypertension, prostate cancer, and type 2 diabetes). We identify individuals at high genetic risk (PRS OR>2) and very high genetic risk (PRS OR>3) and estimate the optimal screening ages for these genetically high-risk individuals, based on the equivalent risk to population-level risk at recommended screening ages. We then leverage published data on differential mortality and other outcomes, with and without screening-based interventions, to assess the potential benefits of tailoring screening age based on genetic risk. Very high risk individuals reach the risk level associated with usual starting screening age on average 10.8 years earlier, high risk individuals 8.9 years earlier and reduced risk individuals (OR<0.5) 16.8 years later. During this time, case enrichment (the ratio of the percentage of cases in the high PRS risk group and in the total population) in the high risk group is between 1.7 and 3.0, depending on the disease. Across all seven diseases, appropriate interventions following PRS-guided screening could reduce premature deaths in high-risk individuals by 23.3%. Knowledge of genetic risk, measured using PRS, has the potential to deliver substantial public health benefits when aggregated across conditions, and could reduce premature mortality by tailoring existing screening programs.

Indexed as

Mortality, PrematureMultifactorial InheritanceAortic Aneurysm, AbdominalColorectal NeoplasmsCoronary Artery DiseaseDiabetes Mellitus, Type 2FemaleGenetic Predisposition to DiseaseGenetic Risk ScoreHumansHypertensionMaleMass ScreeningProstatic NeoplasmsRisk Factors

Identifiers

PMID41559068
PMCPMC12876942

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.