Evidence map›Paper›PMID 27548914›Full record

ArticleNature cell biology2016

A single dividing cell population with imbalanced fate drives oesophageal tumour growth.

Julia Frede, Philip Greulich, Tibor Nagy, Benjamin D Simons, Philip H Jones

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

43 citing papers in PubMed, 96 citations in OpenAlex.

  1. A modeller's guide for biomedical discovery.Disease models & mechanisms · 2026
    Article
  2. Article
  3. Review
  4. Epithelial architecture and signaling activity in the adult human esophagus.Frontiers in cell and developmental biology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. NNature communications · 2022
    Article
  20. Making sense of fragmentation and merging in lineage tracing experiments.Frontiers in cell and developmental biology · 2022
    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 2 institutions in 1 country.

Julia FredeWellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.
Philip GreulichCavendish Laboratory, Department of Physics, University of Cambridge, J.J. Thomson Avenue, Cambridge CB3 0HE, UK.
Tibor NagyWellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.
Benjamin D SimonsCavendish Laboratory, Department of Physics, University of Cambridge, J.J. Thomson Avenue, Cambridge CB3 0HE, UK.
Philip H JonesWellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.
Wellcome Sanger Institute · GBUniversity of Cambridge · GB

Funding

Cancer Research UK 17257Cancer Research UK C609/A17257Medical Research Council MC_PC_12009Medical Research Council MC_UU_12022/5Wellcome TrustWellcome Trust 098357/Z/12/Z
6 · The paper itself

Abstract

Understanding the cellular mechanisms of tumour growth is key for designing rational anticancer treatment. Here we used genetic lineage tracing to quantify cell behaviour during neoplastic transformation in a model of oesophageal carcinogenesis. We found that cell behaviour was convergent across premalignant tumours, which contained a single proliferating cell population. The rate of cell division was not significantly different in the lesions and the surrounding epithelium. However, dividing tumour cells had a uniform, small bias in cell fate so that, on average, slightly more dividing than non-dividing daughter cells were generated at each round of cell division. In invasive cancers induced by Kras(G12D) expression, dividing cell fate became more strongly biased towards producing dividing over non-dividing cells in a subset of clones. These observations argue that agents that restore the balance of cell fate may prove effective in checking tumour growth, whereas those targeting cycling cells may show little selectivity.

Indexed as

AnimalsCell DifferentiationCell DivisionCell LineageCell ProliferationCell Transformation, NeoplasticEsophageal MucosaEsophageal NeoplasmsHumansMice, TransgenicMutation

Identifiers

PMID27548914
PMCPMC5870829
OpenAlexW2513121575

What OpenQuestion holds

Textmetadata
LicenceTDM
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.