Evidence map›Paper›PMID 33879782›Full record

ArticleNature communications2021

Genomic architecture and prediction of censored time-to-event phenotypes with a Bayesian genome-wide analysis.

Sven E Ojavee, Athanasios Kousathanas, Daniel Trejo Banos, Etienne J Orliac, Marion Patxot, Kristi Läll, Reedik Mägi, Krista Fischer, Zoltan Kutalik, Matthew R Robinson

Abstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Genetic association studies using disease liabilities from deep neural networks.medRxiv : the preprint server for health sciences · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
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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

10 authors.

Sven E OjaveeDepartment of Computational Biology, University of Lausanne, Lausanne, Switzerland. svenerik.ojavee@unil.ch.ORCID 0000-0002-7433-7787
Athanasios KousathanasDepartment of Computational Biology, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0001-6265-6521
Daniel Trejo BanosDepartment of Computational Biology, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0001-5268-5759
Etienne J OrliacScientific Computing and Research Support Unit, University of Lausanne, Lausanne, Switzerland.
Marion PatxotDepartment of Computational Biology, University of Lausanne, Lausanne, Switzerland.
Kristi LällEstonian Genome Center, Institute of Genomics, University of Tartu, Tartu, Estonia.
Reedik MägiEstonian Genome Center, Institute of Genomics, University of Tartu, Tartu, Estonia.
Krista FischerEstonian Genome Center, Institute of Genomics, University of Tartu, Tartu, Estonia.
Zoltan KutalikUniversity Center for Primary Care and Public Health, Lausanne, Switzerland.
Matthew R RobinsonInstitute of Science and Technology Austria, Klosterneuburg, Austria. matthew.robinson@ist.ac.at.ORCID 0000-0001-8982-8813

Funding

Medical Research Council MC_PC_17228Medical Research Council MC_QA137853
6 · The paper itself

Abstract

While recent advancements in computation and modelling have improved the analysis of complex traits, our understanding of the genetic basis of the time at symptom onset remains limited. Here, we develop a Bayesian approach (BayesW) that provides probabilistic inference of the genetic architecture of age-at-onset phenotypes in a sampling scheme that facilitates biobank-scale time-to-event analyses. We show in extensive simulation work the benefits BayesW provides in terms of number of discoveries, model performance and genomic prediction. In the UK Biobank, we find many thousands of common genomic regions underlying the age-at-onset of high blood pressure (HBP), cardiac disease (CAD), and type-2 diabetes (T2D), and for the genetic basis of onset reflecting the underlying genetic liability to disease. Age-at-menopause and age-at-menarche are also highly polygenic, but with higher variance contributed by low frequency variants. Genomic prediction into the Estonian Biobank data shows that BayesW gives higher prediction accuracy than other approaches.

Indexed as

Age of OnsetGenome, HumanModels, GeneticMultifactorial InheritanceAge FactorsAlgorithmsBayes TheoremCardiovascular DiseasesComputer SimulationDatabases, GeneticDiabetes Mellitus, Type 2EstoniaFemaleGenetic Association StudiesGenome-Wide Association StudyGenomics

Identifiers

PMID33879782
PMCPMC8058085

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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.