Evidence map›Paper›PMID 34572787›Full record

ReviewCancers2021

Cellular Plasticity: A Route to Senescence Exit and Tumorigenesis.

Hadrien De Blander, Anne-Pierre Morel, Aruni P Senaratne, Maria Ouzounova, Alain Puisieux

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Current Methodologies to Assess Cellular Senescence in Cancer.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  13. uPAR Immuno-PET in Pancreatic Cancer, Aging, and Chemotherapy-Induced Senescence.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 2 institutions in 1 country.

Hadrien De BlanderEquipe Labellisée Ligue Contre le Cancer "EMT and Cancer Cell Plasticity", CNRS 5286, INSERM 1052, Centre Léon Bérard, Cancer Research Center of Lyon, Université Claude Bernard Lyon 1, 69008 Lyon, France.
Anne-Pierre MorelEquipe Labellisée Ligue Contre le Cancer "EMT and Cancer Cell Plasticity", CNRS 5286, INSERM 1052, Centre Léon Bérard, Cancer Research Center of Lyon, Université Claude Bernard Lyon 1, 69008 Lyon, France.ORCID 0000-0001-9794-9615
Aruni P SenaratneUMR3664-Nuclear Dynamics, Development, Biology, Cancer, Genetics and Epigenetics, Institut Curie, PSL Research University, 75005 Paris, France.
Maria OuzounovaEquipe Labellisée Ligue Contre le Cancer "EMT and Cancer Cell Plasticity", CNRS 5286, INSERM 1052, Centre Léon Bérard, Cancer Research Center of Lyon, Université Claude Bernard Lyon 1, 69008 Lyon, France.ORCID 0000-0001-8934-3461
Alain PuisieuxEquipe Labellisée Ligue Contre le Cancer "EMT and Cancer Cell Plasticity", CNRS 5286, INSERM 1052, Centre Léon Bérard, Cancer Research Center of Lyon, Université Claude Bernard Lyon 1, 69008 Lyon, France.
Université Claude Bernard Lyon 1 · FRUniversité Paris Sciences et Lettres · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescence is a dynamic, multistep program that results in permanent cell cycle arrest and is triggered by developmental or environmental, oncogenic or therapy-induced stress signals. Senescence is considered as a tumor suppressor mechanism that prevents the risk of neoplastic transformation by restricting the proliferation of damaged cells. Cells undergoing senescence sustain important morphological changes, chromatin remodeling and metabolic reprogramming, and secrete pro-inflammatory factors termed senescence-associated secretory phenotype (SASP). SASP activation is required for the clearance of senescent cells by innate immunity. Therefore, escape from senescence and the associated immune editing would be a prerequisite for tumor initiation and progression as well as therapeutic resistance. One of the possible mechanisms for overcoming senescence could be the acquisition of cellular plasticity resulting from the accumulation of genomic alterations and genetic and epigenetic reprogramming. The modified composition of the SASP produced by these reprogrammed cancer cells would create a permissive environment, allowing their immune evasion. Additionally, the SASP produced by cancer cells could enhance the cellular plasticity of neighboring cells, thus hindering their recognition by the immune system. Here, we propose a comprehensive review of the literature, highlighting the role of cellular plasticity in the pro-tumoral activity of senescence in normal cells and in the cancer context.

Indexed as

cellular plasticityepithelial-mesenchymal transitionimmune evasionreprogrammingsenescence

Identifiers

PMID34572787
PMCPMC8468602
OpenAlexW3201458839

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.