Evidence map›Paper›PMID 37627015›Full record

ReviewBiology2023

Metabolic Heterogeneity, Plasticity, and Adaptation to "Glutamine Addiction" in Cancer Cells: The Role of Glutaminase and the GTωA [Glutamine Transaminase-ω-Amidase (Glutaminase II)] Pathway.

Arthur J L Cooper, Thambi Dorai, John T Pinto, Travis T Denton

Open access · goldAbstract readReview
In one paragraph

Review in Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Targeting the Glutaminolysis Pathway in Glaucoma-Associated Fibrosis.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Inhibitory Effect of L-Methionine onJournal of fungi (Basel, Switzerland) · 2024
    Article
  12. Article
  13. Review
  14. Review
  15. 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

4 authors at 2 institutions in 1 country.

Arthur J L CooperDepartment of Biochemistry and Molecular Biology, New York Medical College, 15 Dana Road, Valhalla, NY 10595, USA.ORCID 0000-0002-9143-8504
Thambi DoraiDepartment of Biochemistry and Molecular Biology, New York Medical College, 15 Dana Road, Valhalla, NY 10595, USA.
John T PintoDepartment of Biochemistry and Molecular Biology, New York Medical College, 15 Dana Road, Valhalla, NY 10595, USA.ORCID 0000-0003-4249-0856
Travis T DentonDepartment Pharmaceutical Sciences, College of Pharmacy & Pharmaceutical Sciences, Washington State University Health Sciences Spokane, Spokane, WA 99202, USA.ORCID 0000-0002-1222-2538
New York Medical College · USGleason (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many cancers utilize l-glutamine as a major energy source. Often cited in the literature as "l-glutamine addiction", this well-characterized pathway involves hydrolysis of l-glutamine by a glutaminase to l-glutamate, followed by oxidative deamination, or transamination, to α-ketoglutarate, which enters the tricarboxylic acid cycle. However, mammalian tissues/cancers possess a rarely mentioned, alternative pathway (the glutaminase II pathway): l-glutamine is transaminated to α-ketoglutaramate (KGM), followed by ω-amidase (ωA)-catalyzed hydrolysis of KGM to α-ketoglutarate. The name glutaminase II may be confused with the glutaminase 2 (GLS2) isozyme. Thus, we recently renamed the glutaminase II pathway the "glutamine transaminase-ω-amidase (GTωA)" pathway. Herein, we summarize the metabolic importance of the GTωA pathway, including its role in closing the methionine salvage pathway, and as a source of anaplerotic α-ketoglutarate. An advantage of the GTωA pathway is that there is no net change in redox status, permitting α-ketoglutarate production during hypoxia, diminishing cellular energy demands. We suggest that the ability to coordinate control of both pathways bestows a metabolic advantage to cancer cells. Finally, we discuss possible benefits of GTωA pathway inhibitors, not only as aids to studying the normal biological roles of the pathway but also as possible useful anticancer agents.

Indexed as

asparaginaseasparaginase II pathwayGLS1GLS2glutaminase IIglutamine transaminaseGTωA pathwayl-glutamatel-glutaminel-glutamine addictionα-ketoglutaramateα-ketoglutarateα-ketosuccinamateω-amidase

Identifiers

PMID37627015
PMCPMC10452834
OpenAlexW4385805372

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.