Evidence map›Paper›PMID 31397193›Full record

ReviewCell cycle (Georgetown, Tex.)2019

Chemotherapy-induced senescence, an adaptive mechanism driving resistance and tumor heterogeneity.

Jordan Guillon, Coralie Petit, Bertrand Toutain, Catherine Guette, Eric Lelièvre, Olivier Coqueret

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The Role of Cellular Senescence in Oral Health and Disease.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. State-of-the-Art Liver Cancer Organoids: Modeling Cancer Stem Cell Heterogeneity for Personalized Treatment.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

9 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Jordan GuillonPaul Papin ICO Cancer Center, CRCINA, INSERM, Université de Nantes, Université d'Angers , Angers , France.
Coralie PetitPaul Papin ICO Cancer Center, CRCINA, INSERM, Université de Nantes, Université d'Angers , Angers , France.
Bertrand ToutainPaul Papin ICO Cancer Center, CRCINA, INSERM, Université de Nantes, Université d'Angers , Angers , France.
Catherine GuettePaul Papin ICO Cancer Center, CRCINA, INSERM, Université de Nantes, Université d'Angers , Angers , France.
Eric LelièvrePaul Papin ICO Cancer Center, CRCINA, INSERM, Université de Nantes, Université d'Angers , Angers , France.
Olivier CoqueretPaul Papin ICO Cancer Center, CRCINA, INSERM, Université de Nantes, Université d'Angers , Angers , France.ORCID https://orcid.org/0000-0002-2843-7867
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescence is activated in response to chemotherapy to prevent the propagation of cancer cells. In transformed cells, recent studies have shown that this response is not always definitive and that persistent populations can use senescence as an adaptive pathway to restart proliferation and become more aggressive. Here we discuss the results showing that an incomplete and heterogeneous senescence response plays a key role in chemotherapy resistance. Surviving to successive chemotherapy regimens, chronically existing senescent cells can create a survival niche through paracrine cooperations with neighboring cells. This favors chemotherapy escape of premalignant clones but might also allow the survival of adjacent clones presenting a lower fitness. A better characterization of senescence heterogeneity in transformed cells is therefore necessary. This will help us to understand this incomplete response to therapy and how it could generate clones with increased tumor capacity leading to disease relapse.

Indexed as

Neoplasm Recurrence, LocalAntineoplastic AgentsApoptosisCell ProliferationCellular SenescenceClone CellsDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansNeoplasmsOncogene ProteinsSignal TransductionTumor Suppressor ProteinsAntineoplastic AgentsOncogene ProteinsTumor Suppressor Proteinscancer relapseChemotherapydrug resistancesenescencetumor escape

Identifiers

PMID31397193
PMCPMC6738909
OpenAlexW2966996218

What OpenQuestion holds

Textmetadata
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.