Evidence map›Paper›PMID 39313617›Full record

ArticleNature genetics2024

Self-sustaining long-term 3D epithelioid cultures reveal drivers of clonal expansion in esophageal epithelium.

Albert Herms, David Fernandez-Antoran, Maria P Alcolea, Argyro Kalogeropoulou, Ujjwal Banerjee, Gabriel Piedrafita, Emilie Abby, Jose Antonio Valverde-Lopez, Inês S Ferreira, Irene Caseda and 12 more

Abstract read
In one paragraph

Article in Nature genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Precancerous microenvironment: A signalling perspective.Current opinion in cell biology · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Epithelial architecture and signaling activity in the adult human esophagus.Frontiers in cell and developmental biology · 2025
    Review
  11. 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

22 authors.

Albert Herms *Wellcome Sanger Institute, Hinxton, UK.ORCID http://orcid.org/0000-0003-2999-8196
David Fernandez-Antoran *Wellcome Sanger Institute, Hinxton, UK.ORCID http://orcid.org/0000-0003-1608-570X
Maria P Alcolea *Cambridge Stem Cell Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-8396-6454
Argyro KalogeropoulouWellcome Sanger Institute, Hinxton, UK.
Ujjwal BanerjeeWellcome Sanger Institute, Hinxton, UK.
Gabriel PiedrafitaWellcome Sanger Institute, Hinxton, UK.ORCID http://orcid.org/0000-0001-8701-1084
Emilie AbbyWellcome Sanger Institute, Hinxton, UK.ORCID http://orcid.org/0000-0003-0284-4760
Jose Antonio Valverde-LopezWellcome/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, UK.
Inês S FerreiraWellcome/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-2937-7728
Irene CasedaDepartment of Biomedical Sciences, Universitat de Barcelona, Barcelona, Spain.
Maria T BejarCambridge Stem Cell Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-8850-0178
Stefan C DentroWellcome Sanger Institute, Hinxton, UK.
Sara Vidal-NotariDepartment of Biochemistry and Molecular Biology, Complutense University of Madrid, Madrid, Spain.ORCID http://orcid.org/0009-0002-7741-4976
Swee Hoe OngWellcome Sanger Institute, Hinxton, UK.ORCID http://orcid.org/0000-0002-3629-5387
Bartomeu ColomWellcome Sanger Institute, Hinxton, UK.ORCID http://orcid.org/0000-0001-6256-6462
Kasumi MuraiWellcome Sanger Institute, Hinxton, UK.
Charlotte KingWellcome Sanger Institute, Hinxton, UK.ORCID http://orcid.org/0000-0003-2543-1993
Krishnaa MahbubaniDepartment of Surgery, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-1327-2334
Kourosh Saeb-ParsyDepartment of Surgery, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-0633-3696
Alan R LoweInstitute for Structural and Molecular Biology, University College London, London, UK.
Moritz GerstungEuropean Molecular Biology Laboratory, European Bioinformatics Institute, Cambridge, UK.
Philip H JonesWellcome Sanger Institute, Hinxton, UK. pj3@sanger.ac.uk.ORCID http://orcid.org/0000-0002-5904-795X

Funding

Agencia Canaria de Investigación, Innovación y Sociedad de la Información (ACIISI) PID2020-116163GA-I00Cancer Research UK (CRUK) C17918/A28870Cancer Research UK (CRUK) C609/A17257Cancer Research UK (CRUK) C609/A27326EC | EC Seventh Framework Programm | FP7 Nuclear Fission, Safety and Radiation Protection (FP7-EURATOM-FISSION - EURATOM: Nuclear Fission and Radiation Protection) 323267European Molecular Biology Organization (EMBO) EMBO ALTF885-2015Leverhulme Trust RPG-2023-136Medical Research Council MC_PC_17230National Centre for the Replacement Refinement and Reduction of Animals in Research (NC3Rs) NC/X000885/1RCUK | Medical Research Council (MRC) MR/P019013/1Royal Society 105942/Z/14/ARoyal Society 105942/Z/14/ZWellcome TrustWellcome Trust (Wellcome) 108413/A/15/DWellcome Trust (Wellcome) 296194Worldwide Cancer Research 23-0063
6 · The paper itself

Abstract

Aging epithelia are colonized by somatic mutations, which are subjected to selection influenced by intrinsic and extrinsic factors. The lack of suitable culture systems has slowed the study of this and other long-term biological processes. Here, we describe epithelioids, a facile, cost-effective method of culturing multiple mouse and human epithelia. Esophageal epithelioids self-maintain without passaging for at least 1 year, maintaining a three-dimensional structure with proliferative basal cells that differentiate into suprabasal cells, which eventually shed and retain genomic stability. Live imaging over 5 months showed that epithelioids replicate in vivo cell dynamics. Epithelioids support genetic manipulation and enable the study of mutant cell competition and selection in three-dimensional epithelia, and show how anti-cancer treatments modulate competition between transformed and wild-type cells. Finally, a targeted CRISPR-Cas9 screen shows that epithelioids recapitulate mutant gene selection in aging human esophagus and identifies additional drivers of clonal expansion, resolving the genetic networks underpinning competitive fitness.

Indexed as

EsophagusAnimalsCell Culture TechniquesCell Culture Techniques, Three DimensionalCell DifferentiationCell ProliferationCRISPR-Cas SystemsEpithelial CellsEpitheliumEsophageal MucosaHumansMiceMutation

Identifiers

PMID39313617
PMCPMC11525200

What Socratic 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 Socratic graph.