Evidence map›Paper›PMID 31771226›Full record

ArticleCells2019

Diversity of the Senescence Phenotype of Cancer Cells Treated with Chemotherapeutic Agents.

Agnieszka Bojko, Joanna Czarnecka-Herok, Agata Charzynska, Michal Dabrowski, Ewa Sikora

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Therapy-Induced Senescence: Novel Approaches for Markers Identification.International journal of molecular sciences · 2024
    Review
  19. Article
  20. Article

10 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

5 authors at 1 institution in 1 country.

Agnieszka BojkoLaboratory of Molecular Bases of Ageing, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw 02-093, Poland.ORCID 0000-0002-8680-3300
Joanna Czarnecka-HerokLaboratory of Molecular Bases of Ageing, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw 02-093, Poland.ORCID 0000-0002-7287-3615
Agata CharzynskaLaboratory of Bioinformatics, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw 02-093, Poland.ORCID 0000-0003-4761-9831
Michal DabrowskiLaboratory of Bioinformatics, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw 02-093, Poland.
Ewa SikoraLaboratory of Molecular Bases of Ageing, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw 02-093, Poland.ORCID 0000-0002-1111-1748
Instytut Biologii Doświadczalnej im. Marcelego Nenckiego · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is acknowledged that cancer cells are able to undergo senescence in response to clinically used chemotherapeutics. Moreover, recent years have provided evidence that some drugs can selectively remove senescent cells. Therefore, it is essential to properly identify and characterize senescent cells, especially when it comes to cancer. Senescence was induced in various cancer cell lines (A549, SH-SY-5Y, HCT116, MDA-MB-231, and MCF-7) following treatment with doxorubicin, irinotecan, methotrexate, 5-fluorouracil, oxaliplatin, or paclitaxel. Treatment with tested chemotherapeutics resulted in upregulation of p21 and proliferation arrest without cytotoxicity. A comparative analysis with the use of common senescence markers (i.e., morphology, SA-β-galactosidase, granularity, secretory phenotype, and the level of double-stranded DNA damage) revealed a large diversity in response to the chemotherapeutics used. The strongest senescence inducers were doxorubicin, irinotecan, and methotrexate; paclitaxel had an intermediate effect and oxaliplatin and 5-fluorouracil did not induce senescence. In addition, different susceptibility of cancer cells to senescence was observed. A statistical analysis aimed at finding any relationship between the senescence markers applied did not show clear correlations. Moreover, increased SA-β-gal activity coupled with p21 expression proved not to be an unequivocal senescence marker. This points to a need to simultaneously analyze multiple markers, given their individual limitations.

Indexed as

Antineoplastic AgentsCell ProliferationCellular SenescenceCyclin-Dependent Kinase Inhibitor p21DoxorubicinFluorouracilHumansIrinotecanMethotrexateNeoplasmsOxaliplatinPaclitaxelPhenotypeTumor Cells, CulturedAntineoplastic AgentsCyclin-Dependent Kinase Inhibitor p21DoxorubicinFluorouracilIrinotecanMethotrexateOxaliplatinPaclitaxelcancerchemotherapyDNA damageSASPsenescencesenescence markers

Identifiers

PMID31771226
PMCPMC6952928
OpenAlexW2991467764

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.