Evidence map›Paper›PMID 29743249›Full record

ReviewThe Biochemical journal2018

Cancer stem cells (CSCs): metabolic strategies for their identification and eradication.

Ernestina M De Francesco, Federica Sotgia, Michael P Lisanti

Abstract readReview
In one paragraph

Review in The Biochemical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed
–field-weighted citation impact
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

158 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Circular RNAs: key regulators in cancer stem cell dynamics.Molecular genetics and genomics : MGG · 2026
    Review
  5. Metabolic reprogramming and plasticity of cancer stem cells.Frontiers in cell and developmental biology · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
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  15. Review
  16. Understanding and overcoming multidrug resistance in cancer.Nature reviews. Clinical oncology · 2025
    Review
  17. Review
  18. Review
  19. Diethyldithiocarbamate-CuNanomedicine (London, England) · 2025
    Article
  20. Article

98 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

3 authors.

Ernestina M De FrancescoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Federica SotgiaTranslational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, U.K.
Michael P LisantiTranslational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC), University of Salford, Greater Manchester, U.K. michaelp.lisanti@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenotypic and functional heterogeneity is one of the most relevant features of cancer cells within different tumor types and is responsible for treatment failure. Cancer stem cells (CSCs) are a population of cells with stem cell-like properties that are considered to be the root cause of tumor heterogeneity, because of their ability to generate the full repertoire of cancer cell types. Moreover, CSCs have been invoked as the main drivers of metastatic dissemination and therapeutic resistance. As such, targeting CSCs may be a useful strategy to improve the effectiveness of classical anticancer therapies. Recently, metabolism has been considered as a relevant player in CSC biology, and indeed, oncogenic alterations trigger the metabolite-driven dissemination of CSCs. More interestingly, the action of metabolic pathways in CSC maintenance might not be merely a consequence of genomic alterations. Indeed, certain metabotypic phenotypes may play a causative role in maintaining the stem traits, acting as an orchestrator of stemness. Here, we review the current studies on the metabolic features of CSCs, focusing on the biochemical energy pathways involved in CSC maintenance and propagation. We provide a detailed overview of the plastic metabolic behavior of CSCs in response to microenvironment changes, genetic aberrations, and pharmacological stressors. In addition, we describe the potential of comprehensive metabolic approaches to identify and selectively eradicate CSCs, together with the possibility to 'force' CSCs within certain metabolic dependences, in order to effectively target such metabolic biochemical inflexibilities. Finally, we focus on targeting mitochondria to halt CSC dissemination and effectively eradicate cancer.

Indexed as

Metabolic Networks and PathwaysHumansNeoplasmsNeoplastic Stem CellsOxidative PhosphorylationTumor Microenvironmentcancer stem cellsmetabolismmitochondria

Identifiers

PMID29743249
PMCPMC5941316

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.