Evidence map›Paper›PMID 39901189›Full record

ArticleCancer cell international2025

EMT-driven plasticity prospectively increases cell-cell variability to promote therapeutic adaptation in breast cancer.

Lauriane Muller, Frédérique Fauvet, Christelle Chassot, Francesca Angileri, Angèle Coutant, Cyril Dégletagne, Laurie Tonon, Pierre Saintigny, Alain Puisieux, Anne-Pierre Morel and 2 more

Abstract read
In one paragraph

Article in Cancer cell international, 2025. 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
–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

5 citing papers in PubMed.

  1. Article
  2. Review
  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

12 authors.

Lauriane MullerIntegrated Analyses of Cancer Dynamics Team, Centre de Recherche en Cancérologie de Lyon (CRCL), Institut Convergence PlasCan, INSERM U1052, CNRSUMR 5286, Centre Léon Bérard, Université Claude Bernard Lyon 1, Lyon, France.
Frédérique FauvetEMT and Cancer Cell Plasticity Team, Centre Léon Bérard, Lyon, France.
Christelle ChassotEMT and Cancer Cell Plasticity Team, Centre Léon Bérard, Lyon, France.
Francesca AngileriIntegrated Analyses of Cancer Dynamics Team, Centre de Recherche en Cancérologie de Lyon (CRCL), Institut Convergence PlasCan, INSERM U1052, CNRSUMR 5286, Centre Léon Bérard, Université Claude Bernard Lyon 1, Lyon, France.
Angèle CoutantIntegrated Analyses of Cancer Dynamics Team, Centre de Recherche en Cancérologie de Lyon (CRCL), Institut Convergence PlasCan, INSERM U1052, CNRSUMR 5286, Centre Léon Bérard, Université Claude Bernard Lyon 1, Lyon, France.
Cyril DégletagnePlateforme de Génomique des Cancers, Centre de Recherche en Cancérologie de Lyon (CRCL), INSERM U1052, CNRS UMR 5286, Centre Léon Bérard, Université Claude Bernard Lyon 1, Lyon, France.
Laurie TononPlateforme de Bioinformatique Gilles Thomas, Synergie Lyon Cancer, Centre Léon Bérard, Lyon, France.
Pierre SaintignyIntegrated Analyses of Cancer Dynamics Team, Centre de Recherche en Cancérologie de Lyon (CRCL), Institut Convergence PlasCan, INSERM U1052, CNRSUMR 5286, Centre Léon Bérard, Université Claude Bernard Lyon 1, Lyon, France.
Alain PuisieuxEquipe Labellisée Ligue Contre le Cancer, CNRS UMR 3666, INSERM U1143, Paris, France.
Anne-Pierre MorelEMT and Cancer Cell Plasticity Team, Centre Léon Bérard, Lyon, France.
Maria OuzounovaEMT and Cancer Cell Plasticity Team, Centre Léon Bérard, Lyon, France.
Pierre MartinezIntegrated Analyses of Cancer Dynamics Team, Centre de Recherche en Cancérologie de Lyon (CRCL), Institut Convergence PlasCan, INSERM U1052, CNRSUMR 5286, Centre Léon Bérard, Université Claude Bernard Lyon 1, Lyon, France. pierre.martinez@lyon.unicancer.fr.

Funding

Alliance Nationale pour les Sciences de la Vie et de la Santé C19045CSLigue Contre le Cancer IP/SC-16639
6 · The paper itself

Abstract

Cellular plasticity enables cancer cells to adapt non-genetically, thereby preventing therapeutic success. The epithelial-mesenchymal transition (EMT) is a type of plasticity linked to resistance and metastasis. However, its exact impact on population diversity and its dynamics under chemotherapy is unknown. We used single-cell transcriptomics to investigate phenotypic diversity dynamics upon treatment in two in vitro models of triple negative breast cancer (TNBC), where EMT-driven plasticity is either induced or spontaneously occurring. We report that EMT-driven plasticity confers higher phenotypic cell-cell variability (p < 0.001) while enriching for stem-like cells. Genetic and phenotypic cell-cell variability were not consistently correlated. High-plasticity populations displayed more pre-adapted cells before treatment (p = 0.03). In a population displaying spontaneous EMT and phenotypic variation, pre-adapted cells were a rare minority of high-scoring outliers whose expression patterns correlated with survival in TNBC patients subjected to chemotherapy (p = 0.03). Higher plasticity was not associated with a partial EMT status. Our results provide novel insights on how EMT-driven plasticity promotes a prospective diversification process increasing population phenotypic diversity, which can yield rare pre-adapted states before treatment. This highlights the need to tackle phenotypic diversity prior to treatment in high-plasticity tumours.

Identifiers

PMID39901189
PMCPMC11789407

What OpenQuestion holds

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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 OpenQuestion graph.