Evidence map›Paper›PMID 39796613›Full record

ReviewNutrients2025

Targeting Asparagine Metabolism in Solid Tumors.

Keita Hanada, Kenji Kawada, Kazutaka Obama

Abstract readReview
In one paragraph

Review in Nutrients, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Biomedicines · 2025
    Article
  5. Review
  6. 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

3 authors.

Keita HanadaDepartment of Gastrointestinal Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan.
Kenji KawadaDepartment of Gastrointestinal Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan.ORCID 0000-0003-4336-6937
Kazutaka ObamaDepartment of Gastrointestinal Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan.ORCID 0000-0003-2924-6701

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reprogramming of energy metabolism to support cellular growth is a "hallmark" of cancer, allowing cancer cells to balance the catabolic demands with the anabolic needs of producing the nucleotides, amino acids, and lipids necessary for tumor growth. Metabolic alterations, or "addiction", are promising therapeutic targets and the focus of many drug discovery programs. Asparagine metabolism has gained much attention in recent years as a novel target for cancer therapy. Asparagine is widely used in the production of other nutrients and plays an important role in cancer development. Nutritional inhibition therapy targeting asparagine has been used as an anticancer strategy and has shown success in the treatment of leukemia. However, in solid tumors, asparagine restriction alone does not provide ideal therapeutic efficacy. Tumor cells initiate reprogramming processes in response to asparagine deprivation. This review provides a comprehensive overview of asparagine metabolism in cancers. We highlight the physiological role of asparagine and current advances in improving survival and overcoming therapeutic resistance.

Indexed as

AsparagineNeoplasmsAnimalsAntineoplastic AgentsEnergy MetabolismHumansAntineoplastic AgentsAsparagineasparagine metabolismcancerglutamine metabolismmetabolic adaptation

Identifiers

PMID39796613
PMCPMC11722615

What OpenQuestion holds

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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.