Evidence map›Paper›PMID 26907571›Full record

ReviewCurrent opinion in oncology2016

Metabolic targets for potential prostate cancer therapeutics.

Jeffrey Twum-Ampofo, De-Xue Fu, Antonino Passaniti, Arif Hussain, M Minhaj Siddiqui

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Metabolic adaptations in prostate cancer.British journal of cancer · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Carbon sources and pathways for citrate secreted by human prostate cancer cells determined by NMR tracing and metabolic modeling.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Targeting Mitochondrial Metabolism in Prostate Cancer with Triterpenoids.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Review
  18. Review
  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 2 institutions in 1 country.

Jeffrey Twum-AmpofoaDivision of Urology, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland bThe George Washington University School of Medicine and Health Sciences, Washington, DC cDepartment of Pathology dDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine eThe Veteran's Health Administration Research and Development Service fGreenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, USA.
De-Xue Fu
Antonino Passaniti
Arif Hussain
M Minhaj Siddiqui
George Washington University · USUniversity of Maryland, Baltimore · US

Funding

Transcriptional regulation of tumor growthI01BX002205 · VA · BALTIMORE VA MEDICAL CENTER · PI PASSANITI, ANTONINO · 2014 to 2017
–
BLRD VA I01 BX000545BLRD VA I01 BX002205
6 · The paper itself

Abstract

purpose of reviewProstate cancer (PCa) demonstrates characteristic changes in metabolism and bioenergetics in the transition from benign to malignant tissue. It is feasible that some of these changes may be targetable for therapeutic purposes. This review will highlight some of the current metabolically targeted therapies being investigated for the treatment of prostate cancer. RECENT

findingsThe transition from benign to malignant prostate cells is characterized by decreased intracellular zinc concentration and subsequent release of inhibition of the tricarboxylic acid cycle enzyme m-aconitase, which leads to the decrease in citrate concentration within the cancer tissue. Instead of the largely glycolytic phenotype exhibited by most cancers, PCa relies on glutamine and lipids for survival and proliferation. Early studies are beginning to demonstrate that targeting some of the upregulated pathways with inhibitors of key enzymes, such as glutaminase, fatty acid synthase, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, hexokinase, zinc transport, or complex I in the mitochondria may have significant metabolic effects and therapeutic potential. SUMMARY: The unique metabolic profile of PCa allows for many potential avenues of treatment. Future studies will continue to test if the metabolic characterization and treatment of PCa could be an important approach to provide personalized treatment for the disease.

Indexed as

AnimalsHumansMaleMolecular Targeted TherapyPrecision MedicineProstatic Neoplasms

Identifiers

PMID26907571
PMCPMC7306925
OpenAlexW2324502461

What OpenQuestion holds

Textmetadata
LicenceTDM
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.