Evidence map›Paper›PMID 40071465›Full record

ReviewCurrent opinion in oncology2025

Polyamine metabolism in prostate cancer.

Laura A Sena

Abstract readReview
In one paragraph

Review in Current opinion in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. 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

1 author.

Laura A SenaThe Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University; Baltimore, Maryland, USA.

Funding

Synthetic lethal metabolic drug combinations for castration-resistant prostate cancerK08CA273167 · NCI · JOHNS HOPKINS UNIVERSITY · PI Laura A. Sena · 2023 to 2026
$877k
NCI NIH HHS K08 CA273167
6 · The paper itself

Abstract

purpose of reviewNormal and malignant prostate engage in high rates of de novo polyamine synthesis. This review considers how polyamine metabolism regulates prostate cancer initiation and progression. RECENT

findingsThe androgen receptor (AR) establishes a metabolic program to drive robust polyamine synthesis in the normal prostate. Upon malignant transformation, this AR-driven metabolic program persists and is optimized for oncogenesis by the proto-oncogene MYC and/or alterations to PI3K signaling. A deeper understanding of the function of polyamines in prostate cancer may be obtained by considering their function in the normal prostate. SUMMARY: Recent findings support ongoing research into the role of polyamines in driving prostate cancer initiation and progression and suggest targeting polyamine metabolism remains a promising therapeutic strategy for prevention and treatment of prostate cancer.

Indexed as

PolyaminesProstatic NeoplasmsAnimalsHumansMaleProto-Oncogene MasReceptors, AndrogenMAS1 protein, humanPolyaminesProto-Oncogene MasReceptors, Androgenandrogen receptorpolyaminesprostateprostate cancertumor metabolism

Identifiers

PMID40071465
PMCPMC11971019

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.