Evidence map›Paper›PMID 24298908›Full record

ReviewMolecular cancer2013

Tumor glycolysis as a target for cancer therapy: progress and prospects.

Shanmugasundaram Ganapathy-Kanniappan, Jean-Francois H Geschwind

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 785 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
785citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 1% 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

785 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,443 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Significance of GSH and HRedox report : communications in free radical research · 2026
    Review
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  14. Metabolic-epigenetic reprogrammingActa pharmaceutica Sinica. B · 2026
    Article
  15. Article
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  19. Lactate-induced miR-7-5p/TRIM33 reprograms metabolic flux to suppress tumor growth and viral reactivation.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  20. On why cancer cells require a great amount of glucose.Quantitative biology (Beijing, China) · 2026
    Article

725 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

2 authors at 2 institutions in 1 country.

Shanmugasundaram Ganapathy-KanniappanRussell H Morgan Department of Radiology & Radiological Sciences, Division of Interventional Radiology, Johns Hopkins University School of Medicine, 600 N, Wolfe Street, Blalock Building 340, 21287 Baltimore, MD, USA. gshanmu1@jhmi.edu.
Jean-Francois H Geschwind
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered energy metabolism is a biochemical fingerprint of cancer cells that represents one of the "hallmarks of cancer". This metabolic phenotype is characterized by preferential dependence on glycolysis (the process of conversion of glucose into pyruvate followed by lactate production) for energy production in an oxygen-independent manner. Although glycolysis is less efficient than oxidative phosphorylation in the net yield of adenosine triphosphate (ATP), cancer cells adapt to this mathematical disadvantage by increased glucose up-take, which in turn facilitates a higher rate of glycolysis. Apart from providing cellular energy, the metabolic intermediates of glycolysis also play a pivotal role in macromolecular biosynthesis, thus conferring selective advantage to cancer cells under diminished nutrient supply. Accumulating data also indicate that intracellular ATP is a critical determinant of chemoresistance. Under hypoxic conditions where glycolysis remains the predominant energy producing pathway sensitizing cancer cells would require intracellular depletion of ATP by inhibition of glycolysis. Together, the oncogenic regulation of glycolysis and multifaceted roles of glycolytic components underscore the biological significance of tumor glycolysis. Thus targeting glycolysis remains attractive for therapeutic intervention. Several preclinical investigations have indeed demonstrated the effectiveness of this therapeutic approach thereby supporting its scientific rationale. Recent reviews have provided a wealth of information on the biochemical targets of glycolysis and their inhibitors. The objective of this review is to present the most recent research on the cancer-specific role of glycolytic enzymes including their non-glycolytic functions in order to explore the potential for therapeutic opportunities. Further, we discuss the translational potential of emerging drug candidates in light of technical advances in treatment modalities such as image-guided targeted delivery of cancer therapeutics.

Indexed as

GlycolysisAdenosine TriphosphateAnimalsAntineoplastic AgentsEnzymesHumansMolecular Targeted TherapyNeoplasmsAdenosine TriphosphateAntineoplastic AgentsEnzymes

Identifiers

PMID24298908
PMCPMC4223729
OpenAlexW2129824771

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.