Evidence map›Paper›PMID 31965409›Full record

ReviewStem cell reviews and reports2020

Plasticity of Cancer Stem Cell: Origin and Role in Disease Progression and Therapy Resistance.

Plabon Kumar Das, Suja Pillai, Md Abdur Rakib, Jahan Ara Khanam, Vinod Gopalan, Alfred K Y Lam, Farhadul Islam

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Stem cell reviews and reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.2field-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

51 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Cancer stem cells in meningiomas: novel insights and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  9. Review
  10. Article
  11. Cell-cell communication: new insights and clinical implications.Signal transduction and targeted therapy · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  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

7 authors at 3 institutions in 2 countries.

Plabon Kumar DasDepartment of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, 6205, Bangladesh.
Suja PillaiSchool of Biomedical Sciences, Faculty of Medicine, University of Queensland, Brisbane, QLD, 4029, Australia. s.pillai@uq.edu.au.
Md Abdur RakibDepartment of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, 6205, Bangladesh.
Jahan Ara KhanamDepartment of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, 6205, Bangladesh.
Vinod GopalanSchool of Medicine, Griffith University Gold Coast Campus, Gold Coast, QLD, 4222, Australia.
Alfred K Y LamSchool of Medicine, Griffith University Gold Coast Campus, Gold Coast, QLD, 4222, Australia.
Farhadul IslamDepartment of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, 6205, Bangladesh. farhad_bio83@ru.ac.bd.ORCID 0000-0001-5262-4702
University of Rajshahi · BDGriffith University · AUThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In embryonic development and throughout life, there are some cells can exhibit phenotypic plasticity. Phenotypic plasticity is the ability of cells to differentiate into multiple lineages. In normal development, plasticity is highly regulated whereas cancer cells re-activate this dynamic ability for their own progression. The re-activation of these mechanisms enables cancer cells to acquire a cancer stem cell (CSC) phenotype- a subpopulation of cells with increased ability to survive in a hostile environment and resist therapeutic insults. There are several contributors fuel CSC plasticity in different stages of disease progression such as a complex network of tumour stroma, epidermal microenvironment and different sub-compartments within tumour. These factors play a key role in the transformation of tumour cells from a stable condition to a progressive state. In addition, flexibility in the metabolic state of CSCs helps in disease progression. Moreover, epigenetic changes such as chromatin, DNA methylation could stimulate the phenotypic change of CSCs. Development of resistance to therapy due to highly plastic behaviour of CSCs is a major cause of treatment failure in cancers. However, recent studies explored that plasticity can also expose the weaknesses in CSCs, thereby could be utilized for future therapeutic development. Therefore, in this review, we discuss how cancer cells acquire the plasticity, especially the role of the normal developmental process, tumour microenvironment, and epigenetic changes in the development of plasticity. We further highlight the therapeutic resistance property of CSCs attributed by plasticity. Also, outline some potential therapeutic options against plasticity of CSCs. Graphical Abstract .

Indexed as

Cell PlasticityDisease ProgressionDrug Resistance, NeoplasmEpigenesis, GeneticHumansNeoplastic Stem CellsTumor MicroenvironmentCancer heterogeneityCancer metabolismCSC plasticityTherapeutic optionsTherapeutic resistanceTumour microenvironment

Identifiers

PMID31965409
OpenAlexW3002568854

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.