Evidence map›Paper›PMID 23752196›Full record

ReviewOncogene2014

Androgen receptor functions in castration-resistant prostate cancer and mechanisms of resistance to new agents targeting the androgen axis.

X Yuan, C Cai, S Chen, S Chen, Z Yu, S P Balk

Abstract readReview
In one paragraph

Review in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 2 pooled it
25.6field-weighted citation impact, top 1% 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

213 citing papers in PubMed, 2 syntheses or guidelines pooled it, 381 citations in OpenAlex.

  1. Pooled it
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  7. Lipid Droplets in Cancer: New Insights and Therapeutic Potential.International journal of molecular sciences · 2026
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153 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

X YuanHematology Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
C CaiHematology Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
S ChenHematology Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
S ChenHematology Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Z YuHematology Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
S P BalkHematology Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

Molecular basis of androgen receptor mediated gene transcriptional repressionK99CA166507 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CAI, CHANGMENG · 2012 to 2013
$270k
NCI NIH HHS K99 CA166507
6 · The paper itself

Abstract

The metabolic functions of androgen receptor (AR) in normal prostate are circumvented in prostate cancer (PCa) to drive tumor growth, and the AR also can acquire new growth-promoting functions during PCa development and progression through genetic and epigenetic mechanisms. Androgen deprivation therapy (ADT, surgical or medical castration) is the standard treatment for metastatic PCa, but patients invariably relapse despite castrate androgen levels (castration-resistant PCa, CRPC). Early studies from many groups had shown that AR was highly expressed and transcriptionally active in CRPC, and indicated that steroids from the adrenal glands were contributing to this AR activity. More recent studies showed that CRPC cells had increased expression of enzymes mediating androgen synthesis from adrenal steroids, and could synthesize androgens de novo from cholesterol. Phase III clinical trials showing a survival advantage in CRPC for treatment with abiraterone (inhibitor of the enzyme CYP17A1 required for androgen synthesis that markedly reduces androgens and precursor steroids) and for enzalutamide (new AR antagonist) have now confirmed that AR activity driven by residual androgens makes a major contribution to CRPC, and led to the recent Food and Drug Administration approval of both agents. Unfortunately, patients treated with these agents for advanced CRPC generally relapse within a year and AR appears to be active in the relapsed tumors, but the molecular mechanisms mediating intrinsic or acquired resistance to these AR-targeted therapies remain to be defined. This review outlines AR functions that contribute to PCa development and progression, the roles of intratumoral androgen synthesis and AR structural alterations in driving AR activity in CRPC, mechanisms of action for abiraterone and enzalutamide, and possible mechanisms of resistance to these agents.

Indexed as

Drug Resistance, NeoplasmAndrogen Receptor AntagonistsAndrogensAnimalsCell Transformation, NeoplasticDisease ProgressionGene Expression Regulation, NeoplasticHumansMaleProstatic Neoplasms, Castration-ResistantReceptors, AndrogenRepressor ProteinsSteroid 17-alpha-HydroxylaseTrans-ActivatorsTranscription, GeneticAndrogen Receptor AntagonistsAndrogensCYP17A1 protein, humanReceptors, AndrogenRepressor ProteinsSteroid 17-alpha-HydroxylaseTrans-Activators

Identifiers

PMID23752196
PMCPMC4890635
OpenAlexW2077438659

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.