Evidence map›Paper›PMID 37444583›Full record

ReviewCancers2023

Lactate as Key Metabolite in Prostate Cancer Progression: What Are the Clinical Implications?

Paolo Chetta, Renuka Sriram, Giorgia Zadra

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Targeting Lactate and Lactylation in Cancer Metabolism and Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. FDG/PSMA discordance in [Frontiers in oncology · 2026
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Cellular Signaling of Amino Acid Metabolism in Prostate Cancer.International journal of molecular sciences · 2025
    Review
  19. Review
  20. 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 at 3 institutions in 2 countries.

Paolo ChettaDepartment of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA.
Renuka SriramDepartment of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA 94143, USA.ORCID 0000-0003-3505-2479
Giorgia ZadraInstitute of Molecular Genetics, National Research Council (IGM-CNR), 27100 Pavia, Italy.
Massachusetts General Hospital · USNational Research Council · ITUniversity of California, San Francisco · US

Funding

TR&D3: Open-Source Tools for Processing Hyperpolarized MR DataP41EB013598 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Daniel B Vigneron · 2011 to 2026
$19.9M
Preclinical imaging characterization and resource development of PDX SCNC prostate cancer murine modelsU24CA253377 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KURHANEWICZ, JOHN, PEEHL, DONNA M. · 2020 to 2024
$3.4M
NCI NIH HHS U24 CA253377NIBIB NIH HHS P41 EB013598
6 · The paper itself

Abstract

Advanced prostate cancer represents the fifth leading cause of cancer death in men worldwide. Although androgen-receptor signaling is the major driver of the disease, evidence is accumulating that disease progression is supported by substantial metabolic changes. Alterations in de novo lipogenesis and fatty acid catabolism are consistently reported during prostate cancer development and progression in association with androgen-receptor signaling. Therefore, the term "lipogenic phenotype" is frequently used to describe the complex metabolic rewiring that occurs in prostate cancer. However, a new scenario has emerged in which lactate may play a major role. Alterations in oncogenes/tumor suppressors, androgen signaling, hypoxic conditions, and cells in the tumor microenvironment can promote aerobic glycolysis in prostate cancer cells and the release of lactate in the tumor microenvironment, favoring immune evasion and metastasis. As prostate cancer is composed of metabolically heterogenous cells, glycolytic prostate cancer cells or cancer-associated fibroblasts can also secrete lactate and create "symbiotic" interactions with oxidative prostate cancer cells via lactate shuttling to sustain disease progression. Here, we discuss the multifaceted role of lactate in prostate cancer progression, taking into account the influence of the systemic metabolic and gut microbiota. We call special attention to the clinical opportunities of imaging lactate accumulation for patient stratification and targeting lactate metabolism.

Indexed as

biomarkerslactatemetabolic imagingmonocarboxylate transportersprostate cancertumor microenvironment

Identifiers

PMID37444583
PMCPMC10340474
OpenAlexW4383105300

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.