Evidence map›Paper›PMID 41735769›Full record

ReviewEndocrinology2026

Androgen metabolism in prostate cancer: recent advances.

Nima Sharifi

Abstract readReview
In one paragraph

Review in Endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Nima SharifiDesai Sethi Urology Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.ORCID 0000-0003-1281-3474

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Androgen biosynthesis is physiologically necessary for generating the principal stimulus for androgen receptor (AR) signaling and thus plays an essential role for development of the normal prostate, prostate cancer growth, and the development of resistance to hormonal therapies. Testosterone and dihydrotestosterone are both potent endogenous androgens that stimulate AR signaling. While the role of gonadal androgens in stimulating prostate cancer progression has been recognized for over 80 years, the appreciation for nongonadal precursor steroids in prostate cancer has been more limited in duration of time, attention, and focus in the field. Nevertheless, the very clearly established role of nongonadal androgens in enabling prostate cancer progression, especially in the absence of gonadal testosterone, frames the essentiality of androgen metabolic processes for dictating prostate cancer clinical behavior. Here, the role of androgen metabolism in prostate cancer is reviewed, particularly within the context of hormonal therapy and hormone therapy resistance, and with emphasis on recent advances.

Indexed as

AndrogensProstatic NeoplasmsAnimalsHumansMaleReceptors, AndrogenSignal TransductionAndrogensReceptors, Androgenandrogensenzymesmetabolismprostate cancersteroids

Identifiers

PMID41735769
PMCPMC13016875

What Socratic 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 Socratic graph.