Evidence map›Paper›PMID 36151426›Full record

ReviewJournal of cancer research and clinical oncology2023

Metabolic changes during prostate cancer development and progression.

Alicia-Marie K Beier, Martin Puhr, Matthias B Stope, Christian Thomas, Holger H H Erb

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2023. 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
5.6field-weighted citation impact, top 3% 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, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Targeting mitochondria and programmed cell death as potential interventions for metastatic castration-resistant prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  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 5 institutions in 2 countries.

Alicia-Marie K BeierDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Martin PuhrDepartment of Urology, Medical University of Innsbruck, Innsbruck, Austria.
Matthias B StopeDepartment of Gynecology and Gynecological Oncology, University Hospital Bonn, Bonn, Germany.
Christian ThomasDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Holger H H ErbDepartment of Urology, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany. holger.erb@uniklinikum-dresden.de.ORCID http://orcid.org/0000-0001-5209-7914
German Cancer Research Center · DEInnsbruck Medical University · ATNational Center for Tumor Diseases · DEUniversity Hospital Bonn · DEUniversity Hospital Carl Gustav Carus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming has been recognised as a hallmark in solid tumours. Malignant modification of the tumour's bioenergetics provides energy for tumour growth and progression. Otto Warburg first reported these metabolic and biochemical changes in 1927. In prostate cancer (PCa) epithelial cells, the tumour metabolism also changes during development and progress. These alterations are partly driven by the androgen receptor, the key regulator in PCa development, progress, and survival. In contrast to other epithelial cells of different entities, glycolytic metabolism in prostate cells sustains physiological citrate secretion in the normal prostatic epithelium. In the early stages of PCa, citrate is utilised to power oxidative phosphorylation and fuel lipogenesis, enabling tumour growth and progression. In advanced and incurable castration-resistant PCa, a metabolic shift towards choline, amino acid, and glycolytic metabolism fueling tumour growth and progression has been described. Therefore, even if the metabolic changes are not fully understood, the altered metabolism during tumour progression may provide opportunities for novel therapeutic strategies, especially in advanced PCa stages. This review focuses on the main differences in PCa's metabolism during tumourigenesis and progression highlighting glutamine's role in PCa.

Indexed as

Prostatic NeoplasmsProstatic Neoplasms, Castration-ResistantCitratesEnergy MetabolismGlycolysisHumansMaleProstateReceptors, AndrogenCitratesReceptors, AndrogenCRPCGlutamineMetabolic reprogramming

Identifiers

PMID36151426
PMCPMC10097763
OpenAlexW4297087537

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.