Evidence map›Paper›PMID 26779810›Full record

ReviewOncogenesis2016

Energy disruptors: rising stars in anticancer therapy?

F Bost, A-G Decoux-Poullot, J F Tanti, S Clavel

Open access · goldAbstract readReview
In one paragraph

Review in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
6.5field-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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. The Combined Metabolically Oriented Effect of Fucoidan from the Brown AlgaInternational journal of molecular sciences · 2023
    Article
  13. The role of the SNF1 signaling pathway in the growth of Saccharomyces cerevisiae in different carbon and nitrogen sources.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. RETRACTED: Metformin and Breast Cancer: Where Are We Now?International journal of molecular sciences · 2022
    Review
  20. A Multi-enzyme Cascade for the Biosynthesis of AICA Ribonucleoside Di- and Triphosphate.Chembiochem : a European journal of chemical biology · 2022
    Article

8 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

4 authors at 2 institutions in 1 country.

F BostINSERM, C3M, U1065, Team Cellular and Molecular Physiopathology of Obesity and Diabetes, Nice, France.
A-G Decoux-PoullotINSERM, C3M, U1065, Team Cellular and Molecular Physiopathology of Obesity and Diabetes, Nice, France.
J F TantiINSERM, C3M, U1065, Team Cellular and Molecular Physiopathology of Obesity and Diabetes, Nice, France.
S ClavelINSERM, C3M, U1065, Team Cellular and Molecular Physiopathology of Obesity and Diabetes, Nice, France.
Inserm · FRUniversité Côte d'Azur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The metabolic features of tumor cells diverge from those of normal cells. Otto Warburg was the first to observe that cancer cells dramatically increase their glucose consumption to generate ATP. He also claimed that cancer cells do not have functional mitochondria or oxidative phosphorylation (OXPHOS) but simply rely on glycolysis to provide ATP to the cell, even in the presence of oxygen (aerobic glycolysis). Several studies have revisited this observation and demonstrated that most cancer cells contain metabolically efficient mitochondria. Indeed, to sustain high proliferation rates, cancer cells require functional mitochondria to provide ATP and intermediate metabolites, such as citrate and cofactors, for anabolic reactions. This difference in metabolism between normal and tumors cells causes the latter to be more sensitive to agents that can disrupt energy homeostasis. In this review, we focus on energy disruptors, such as biguanides, 2-deoxyglucose and 5-aminoimidazole-4-carboxamide ribonucleotide, that interfere with the main metabolic pathways of the cells, OXPHOS, glycolysis and glutamine metabolism. We discuss the preclinical data and the mechanisms of action of these disruptors at the cellular and molecular levels. Finally, we consider whether these drugs can reasonably contribute to the antitumoral therapeutic arsenal in the future.

Identifiers

PMID26779810
PMCPMC4728676
OpenAlexW2418589037

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.