Evidence map›Paper›PMID 40008000›Full record

ReviewFrontiers in oncology2025

Androgen receptor dynamics in prostate cancer: from disease progression to treatment resistance.

Caihong Li, Dongkai Cheng, Peng Li

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

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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.

Caihong LiCenter for Reproductive Medicine, Shenyang Jinghua Hospital, Shenyang, China.
Dongkai ChengCenter for Reproductive Medicine, Shenyang Jinghua Hospital, Shenyang, China.
Peng LiCenter for Reproductive Medicine, Shenyang Jinghua Hospital, Shenyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is the most common cancer among men worldwide, especially in those over 65, and is a leading cause of cancer-related mortality. The disease typically advances from an androgen-dependent state to castration-resistant prostate cancer (CRPC), which poses significant treatment challenges. The androgen receptor (AR) on the X chromosome is a central driver in this process, activating genes that govern proliferation and survival. Mutations and amplifications of the AR are closely associated with disease progression and treatment resistance. While traditional therapies such as androgen deprivation therapy (ADT) and AR antagonists like enzalutamide have been effective, resistance persists due to reactivation of AR signaling through mechanisms like ligand-independent activation. Recent research highlights the role of epigenetic modifications in enhancing AR activity and drug resistance. The tumor microenvironment, particularly interactions with cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs), further complicates treatment by promoting aggressive tumor behavior and immune evasion. Future directions include developing next-generation AR antagonists, identifying AR-related biomarkers for personalized therapy, and exploring combinations with immune checkpoint inhibitors. Additionally, basal cell-lumen-derived organoids provide innovative models that can enhance understanding and treatment strategies in prostate cancer.

Indexed as

androgen receptor (AR)drug resistanceepigeneticspersonalized therapyprostate cancer

Identifiers

PMID40008000
PMCPMC11850250

What OpenQuestion holds

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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.