Evidence map›Paper›PMID 27184811›Full record

ReviewProstate cancer and prostatic diseases2016

Androgen receptor variant-driven prostate cancer: clinical implications and therapeutic targeting.

E S Antonarakis, A J Armstrong, S M Dehm, J Luo

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Prostate cancer and prostatic diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 3 pooled it
–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

111 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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  16. Discovery of BMS-986365, a First-in-Class Dual Androgen Receptor Ligand-Directed Degrader and Antagonist, for the Treatment of Advanced Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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51 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

4 authors.

E S AntonarakisDepartments of Oncology and Urology, Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD, USA.
A J ArmstrongDepartments of Medicine, Surgery, and Pharmacology and Cancer Biology, Divisions of Medical Oncology and Urology, Duke Cancer Institute, Durham, NC, USA.
S M DehmMasonic Cancer Center and Departments of Laboratory Medicine and Pathology and Urology, University of Minnesota, Minneapolis, MN, USA.
J LuoDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University, Baltimore, MD, USA.

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
AR Gene Rearrangements and AR Signaling in Prostate CancerR01CA174777 · NCI · UNIVERSITY OF MINNESOTA · PI Scott M. Dehm · 2013 to 2026
$4.9M
The aberrant androgen receptor underlies abiraterone/enzalutamide resistanceR01CA185297 · NCI · JOHNS HOPKINS UNIVERSITY · PI ANTONARAKIS, EMMANUEL S., LUO, JUN · 2015 to 2018
$1.5M
NCI NIH HHS P30 CA006973NCI NIH HHS R01 CA174777NCI NIH HHS R01 CA185297
6 · The paper itself

Abstract

While there are myriad mechanisms of primary and acquired resistance to conventional and next-generation hormonal therapies in prostate cancer, the potential role of androgen receptor splice variants (AR-Vs) has recently gained momentum. AR-Vs are abnormally truncated isoforms of the androgen receptor (AR) protein that lack the COOH-terminal domain but retain the NH2-terminal domain and DNA-binding domain and are thus constitutively active even in the absence of ligands. Although multiple preclinical studies have previously implicated AR-Vs in the development of castration resistance as well as resistance to abiraterone and enzalutamide, recent technological advances have made it possible to reliably detect and quantify AR-Vs from human clinical tumor specimens including blood samples. Initial clinical studies have now shown that certain AR-Vs, in particular AR-V7, may be associated with resistance to abiraterone and enzalutamide but not taxane chemotherapies when detected in circulating tumor cells. Efforts are now underway to clinically validate AR-V7 as a relevant treatment-selection biomarker in the context of other key genomic aberrations in men with metastatic castration-resistant prostate cancer. Additional efforts are underway to therapeutically target both AR and AR-Vs either directly or indirectly. Whether AR-Vs represent drivers of castration-resistant prostate cancer, or whether they are simply passenger events associated with aggressive disease or clonal heterogeneity, will ultimately be answered only through these types of clinical trials.

Indexed as

Genetic VariationAlternative SplicingAndrogen Receptor AntagonistsAndrogensAnimalsAntineoplastic Agents, HormonalBiomarkers, TumorCell Transformation, NeoplasticClinical Trials as TopicDrug Evaluation, PreclinicalDrug Resistance, NeoplasmEpitheliumGene Expression Regulation, NeoplasticHumansMaleMolecular Targeted TherapyAndrogen Receptor AntagonistsAndrogensAntineoplastic Agents, HormonalBiomarkers, TumorReceptors, Androgen

Identifiers

PMID27184811
PMCPMC5493501

What OpenQuestion holds

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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.