Evidence map›Paper›PMID 24079832›Full record

ReviewBioscience reports2013

How does the metabolism of tumour cells differ from that of normal cells.

Nívea Dias Amoêdo, Juan Perez Valencia, Mariana Figueiredo Rodrigues, Antonio Galina, Franklin David Rumjanek

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Journal of cardiovascular development and disease · 2023
    Article
  7. Article
  8. Targeting Energy Metabolism in Cancer Treatment.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Entrapment ofPharmaceutics · 2019
    Article
  15. Widespread gene transfer to malignant gliomas with In vitro-to-In vivo correlation.Journal of controlled release : official journal of the Controlled Release Society · 2019
    Article
  16. Article
  17. Article
  18. Dysregulation of Glucose Metabolism by Oncogenes and Tumor Suppressors in Cancer CellsAsian Pacific journal of cancer prevention : APJCP · 2018
    Review
  19. Article
  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

5 authors at 1 institution in 1 country.

Nívea Dias Amoêdo*Instituto de Bioquímica Médica, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Cidade Universitária, Av, Carlos Chagas Filho 373, Ilha do Fundão CEP 21941-590, Rio de Janeiro, Brazil.
Juan Perez Valencia*Instituto de Bioquímica Médica, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Cidade Universitária, Av, Carlos Chagas Filho 373, Ilha do Fundão CEP 21941-590, Rio de Janeiro, Brazil.
Mariana Figueiredo Rodrigues*Instituto de Bioquímica Médica, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Cidade Universitária, Av, Carlos Chagas Filho 373, Ilha do Fundão CEP 21941-590, Rio de Janeiro, Brazil.
Antonio Galina*Instituto de Bioquímica Médica, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Cidade Universitária, Av, Carlos Chagas Filho 373, Ilha do Fundão CEP 21941-590, Rio de Janeiro, Brazil.
Franklin David Rumjanek*Instituto de Bioquímica Médica, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Cidade Universitária, Av, Carlos Chagas Filho 373, Ilha do Fundão CEP 21941-590, Rio de Janeiro, Brazil.
Universidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour cells thrive in environments that would be hostile to their normal cell counterparts. Survival depends on the selection of cell lines that harbour modifications of both, gene regulation that shifts the balance between the cell cycle and apoptosis and those that involve the plasticity of the metabolic machinery. With regards to metabolism, the selected phenotypes usually display enhanced anaerobic glycolysis even in the presence of oxygen, the so-called Warburg effect, and anabolic pathways that provide precursors for the synthesis of lipids, proteins and DNA. The review will discuss the original ideas of Otto Warburg and how they initially led to the notion that mitochondria of tumour cells were dysfunctional. Data will be presented to show that not only the organelles are viable and respiring, but that they are key players in tumorigenesis and metastasis. Likewise, interconnecting pathways that stand out in the tumour phenotype and that require intact mitochondria such as glutaminolysis will be addressed. Furthermore, comments will be made as to how the peculiarities of the biochemistry of tumour cells renders them amenable to new forms of treatment by highlighting possible targets for inhibitors. In this respect, a case study describing the effect of a metabolite analogue, the alkylating agent 3BP (3-bromopyruvate), on glycolytic enzyme targets will be presented.

Indexed as

AnimalsAntineoplastic AgentsEnergy MetabolismGlutamineGlycolysisHumansMitochondriaMolecular Targeted TherapyNeoplasmsAntineoplastic AgentsGlutamine

Identifiers

PMID24079832
PMCPMC3828821
OpenAlexW2035591142

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.