Evidence map›Paper›PMID 23860689›Full record

ReviewHormones & cancer2013

On the origins of the androgen receptor low molecular weight species.

Maria Mudryj, Clifford G Tepper

Open access · bronzeAbstract readReview
In one paragraph

Review in Hormones & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. The androgen receptor in bladder cancer.Nature reviews. Urology · 2023
    Review
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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

2 authors at 2 institutions in 1 country.

Maria MudryjVeterans Affairs-Northern California Health Care System, Mather, CA 95655, USA. mmudryj@ucdavis.edu
Clifford G Tepper
University of California, Davis · USVA Northern California Health Care System · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura Marcu · 2002 to 2026
$84.9M
Modeling E2F3 isoform specificity in prostate cancerI01BX001079 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI MUDRYJ, MARIA · 2011 to 2014
–
BLRD VA I01 BX001079NCI NIH HHS P30 CA093373
6 · The paper itself

Abstract

Prostate cancer (CaP), a commonly diagnosed malignancy, is readily treated by androgen ablation. This treatment temporarily halts the disease, but castration-resistant neoplasms that are refractory to current therapies emerge. While these neoplasms are no longer dependent on physiological levels of androgens, they remain reliant on the expression of the androgen receptor (AR). There are multiple mechanisms by which CaP cells circumvent androgen ablation therapies. These include AR mutations that broaden ligand specificity, AR overexpression, AR activation by growth factors and cytokines, overexpression of AR co-activators, altered steroid metabolism, and a locus-wide histone transcriptional activation of some AR targets. This review focuses on a more recently described mechanism: the expression of low molecular weight AR species that are missing the ligand-binding domain and function independently of ligand to drive proliferation. The etiology, biological activity, unique features, predictive value, and therapeutic implication of these androgen receptor isoforms are discussed in depth.

Indexed as

AndrogensHumansMaleMolecular WeightProstatic Neoplasms, Castration-ResistantReceptors, AndrogenAndrogensReceptors, Androgen

Identifiers

PMID23860689
PMCPMC4353596
OpenAlexW2091472631

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.