Evidence map›Paper›PMID 21196269›Full record

ReviewFrontiers in bioscience (Landmark edition)2011

Emerging metabolic targets in cancer therapy.

Yuhua Zhao, Hao Liu, Adam I Riker, Oystein Fodstad, Susan P Ledoux, Glenn L Wilson, Ming Tan

Abstract readReview
In one paragraph

Review in Frontiers in bioscience (Landmark edition), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Prognostic role of glycolysis for cancer outcome: evidence from 86 studies.Journal of cancer research and clinical oncology · 2019
    Pooled it
  2. International journal of molecular medicine · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
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  15. Metabolomics of papillary thyroid carcinoma tissues: potential biomarkers for diagnosis and promising targets for therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Review
  17. Article
  18. Article
  19. Dysregulated metabolism contributes to oncogenesis.Seminars in cancer biology · 2015
    Review
  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

7 authors.

Yuhua ZhaoMitchell Cancer Institute, University of South Alabama, Mobile, AL 36604, USA.
Hao Liu
Adam I Riker
Oystein Fodstad
Susan P Ledoux
Glenn L Wilson
Ming Tan

Funding

Glucose metabolism and ErbB2-mediated cancer progressionR01CA149646 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI TAN, MING · 2011 to 2016
$1.4M
NCI NIH HHS R01 CA149646
6 · The paper itself

Abstract

Cancer cells are different from normal cells in their metabolic properties. Normal cells mostly rely on mitochondrial oxidative phosphorylation to produce energy. In contrast, cancer cells depend mostly on glycolysis, the aerobic breakdown of glucose into ATP. This altered energy dependency is known as the "Warburg effect" and is a hallmark of cancer cells. In recent years, investigating the metabolic changes within cancer cells has been a rapidly growing area. Emerging evidence shows that oncogenes that drive the cancer-promoting signals also drive the altered metabolism. Although the exact mechanisms underlying the Warburg effect are unclear, the existing evidence suggests that increased glycolysis plays an important role in support malignant behavior of cancer cells. A thorough understanding of the unique metabolism of cancer cells will help to design of more effective drugs targeting metabolic pathways, which will greatly impact the capacity to effectively treat cancer patients. Here we provide an overview of the current understanding of the Warburg effect upon tumor cell growth and survival, and discussion on the potential metabolic targets for cancer therapy.

Indexed as

Adenylate KinaseAntineoplastic AgentsCell ProliferationDrug Resistance, NeoplasmEnergy MetabolismEnzyme InhibitorsGenes, mycGlycolysisHexokinaseHumansHypoxia-Inducible Factor 1NeoplasmsPhosphoinositide-3 Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPyruvate Dehydrogenase Acetyl-Transferring KinaseAdenylate KinaseAntineoplastic AgentsEnzyme InhibitorsHexokinaseHypoxia-Inducible Factor 1Phosphoinositide-3 Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPyruvate Dehydrogenase Acetyl-Transferring KinasePyruvate KinaseTOR Serine-Threonine Kinases

Identifiers

PMID21196269
PMCPMC3117434

What OpenQuestion holds

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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.