Evidence map›Paper›PMID 33869685›Full record

ReviewRegenerative therapy2021

Molecular pathology underlying the robustness of cancer stem cells.

Go J Yoshida, Hideyuki Saya

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Regenerative therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.8field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. An overview of current research on cancer stem cells: a bibliometric analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Epithelial-Mesenchymal Transition in Acute Leukemias.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Go J YoshidaDivision of Gene Regulation, Institute for Advanced Medical Research (IAMR), Keio University School of Medicine, Tokyo, Japan.
Hideyuki SayaDivision of Gene Regulation, Institute for Advanced Medical Research (IAMR), Keio University School of Medicine, Tokyo, Japan.
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intratumoral heterogeneity is tightly associated with the failure of anticancer treatment modalities including conventional chemotherapy, radiation therapy, and molecularly targeted therapy. Such heterogeneity is generated in an evolutionary manner not only as a result of genetic alterations but also by the presence of cancer stem cells (CSCs). CSCs are proposed to exist at the top of a tumor cell hierarchy and are undifferentiated tumor cells that manifest enhanced tumorigenic and metastatic potential, self-renewal capacity, and therapeutic resistance. Properties that contribute to the robustness of CSCs include the abilities to withstand redox stress, to rapidly repair damaged DNA, to adapt to a hyperinflammatory or hyponutritious tumor microenvironment, and to expel anticancer drugs by the action of ATP-binding cassette transporters as well as plasticity with regard to the transition between dormant CSC and transit-amplifying progenitor cell phenotypes. In addition, CSCs manifest the phenomenon of metabolic reprogramming, which is essential for maintenance of their self-renewal potential and their ability to adapt to changes in the tumor microenvironment. Elucidation of the molecular underpinnings of these biological features of CSCs is key to the development of novel anticancer therapies. In this review, we highlight the pathological relevance of CSCs in terms of their hallmarks and identification, the properties of their niche-both in primary tumors and at potential sites of metastasis-and their resistance to oxidative stress dependent on system xc (-).

Indexed as

ABC, ATP-binding cassetteALDH, Aldehyde dehydrogenaseBMP, Bone morphogenetic proteinCAF, Cancer-associated fibroblastCagA, Cytotoxin-associated gene ACancer stem cellCD44 variantCD44v, CD44 variantCSC, Cancer stem cellCTC, Circulating tumor cellDTC, Disseminated tumor cellECM, Extracellular matrixEGF, Epidermal growth factorE/M, Epithelial/mesenchymalEMT, Epithelial-to-mesenchymal transitionEpCAM, Epithelial cell adhesion moleculeEEpithelial-to-mesenchymal transition (EMT)GSC, Glioma stem cellGSH, reduced glutathioneHGF, Hepatocyte growth factorHNSCC, Head and neck squamous cell cancerIL, InterleukinIntratumoral heterogeneityMAPK, mitogen-activated protein kinaseMET, mesenchymal-to-epithelial transitionNicheNrf2, nuclear factor erythroid 2–related factor 2NSCLC, non–small cell lung cancerOXPHOS, Oxidative phosphorylationPlasticityPrrx1, Paired-related homeodomain transcription factor 1ROS, Reactive oxygen speciesSRP1, Epithelial splicing regulatory protein 1TGF-β, Transforming growth factor–β

Identifiers

PMID33869685
PMCPMC8024885
OpenAlexW3144644259

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.