Evidence map›Paper›PMID 37468606›Full record

ArticleCommunications biology2023

Mutations observed in somatic evolution reveal underlying gene mechanisms.

Michael W J Hall, David Shorthouse, Rachel Alcraft, Philip H Jones, Benjamin A Hall

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. EarlybioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Review
  5. 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

5 authors at 3 institutions in 1 country.

Michael W J HallWellcome Sanger Institute, Hinxton, CB10 1SA, UK.ORCID 0000-0003-2904-6902
David ShorthouseDepartment of Medical Physics and Biomedical Engineering, Malet Place Engineering Building, University College London, Gower Street, London, WC1E 6BT, UK.ORCID 0000-0002-3207-3584
Rachel AlcraftAdvanced Research Computing, University College London, London, UK.ORCID 0000-0003-2674-6321
Philip H JonesWellcome Sanger Institute, Hinxton, CB10 1SA, UK.ORCID 0000-0002-5904-795X
Benjamin A HallDepartment of Medical Physics and Biomedical Engineering, Malet Place Engineering Building, University College London, Gower Street, London, WC1E 6BT, UK. b.hall@ucl.ac.uk.ORCID 0000-0003-0355-2946
University College London · GBUniversity of Cambridge · GBWellcome Sanger Institute · GB

Funding

Cancer Research UK C609/A17257Cancer Research UK C609/A27326Medical Research Council MC_UU_12022/9Medical Research Council MR/S000216/1Medical Research Council MR/S000216/2Wellcome TrustWellcome Trust 098051Wellcome Trust 296194
6 · The paper itself

Abstract

Highly sensitive DNA sequencing techniques have allowed the discovery of large numbers of somatic mutations in normal tissues. Some mutations confer a competitive advantage over wild-type cells, generating expanding clones that spread through the tissue. Competition between mutant clones leads to selection. This process can be considered a large scale, in vivo screen for mutations increasing cell fitness. It follows that somatic missense mutations may offer new insights into the relationship between protein structure, function and cell fitness. We present a flexible statistical method for exploring the selection of structural features in data sets of somatic mutants. We show how this approach can evidence selection of specific structural features in key drivers in aged tissues. Finally, we show how drivers may be classified as fitness-enhancing and fitness-suppressing through different patterns of mutation enrichment. This method offers a route to understanding the mechanism of protein function through in vivo mutant selection.

Indexed as

Clonal EvolutionProteinsMutationSequence Analysis, DNAProteins

Identifiers

PMID37468606
PMCPMC10356810
OpenAlexW4384652529

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.