Evidence map›Paper›PMID 21778211›Full record

ReviewEndocrine-related cancer2011

Alternatively spliced androgen receptor variants.

Scott M Dehm, Donald J Tindall

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine-related cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 223 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
223citing papers in PubMed, 1 pooled it
25.4field-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

223 citing papers in PubMed, 1 synthesis or guideline pooled it, 377 citations in OpenAlex.

  1. Pooled it
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163 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

2 authors at 2 institutions in 1 country.

Scott M DehmDepartment of Laboratory Medicine and Pathology, Masonic Cancer Center, University of Minnesota, Mayo Mail Code 806, 420 Delaware Street SE, Minneapolis, Minnesota 55455, USA. dehm@umn.edu
Donald J Tindall
University of Minnesota · USWinnMed · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Douglas Yee · 1998 to 2026
$100.4M
Utility of serum and Tissue Biomarkers for Predicting Response to Androgen DeprivP50CA091956 · NCI · MAYO CLINIC ROCHESTER · PI TINDALL, DONALD J. · 2001 to 2010
$23.4M
Coregulators in Androgen-Refractory Prostate CancerR01CA121277 · NCI · MAYO CLINIC ROCHESTER · PI TINDALL, DONALD J. · 2006 to 2010
$1.3M
Androgenic Inactivation of FOXO1 in Prostate CancerR01CA125747 · NCI · MAYO CLINIC ROCHESTER · PI TINDALL, DONALD J. · 2007 to 2011
$1.3M
AR Transcriptional Activation Domains in Prostate Cancer ProgressionR21CA141011 · NCI · UNIVERSITY OF MINNESOTA · PI DEHM, SCOTT M. · 2009 to 2010
$365k
NCI NIH HHS CA121277NCI NIH HHS CA125747NCI NIH HHS CA141011NCI NIH HHS CA91956NCI NIH HHS P30 CA077598NCI NIH HHS P50 CA091956NCI NIH HHS R01 CA121277NCI NIH HHS R01 CA125747NCI NIH HHS R21 CA141011PHS HHS P30 077598
6 · The paper itself

Abstract

Alternative splicing is an important mechanism for increasing functional diversity from a limited set of genes. Deregulation of this process is common in diverse pathologic conditions. The androgen receptor (AR) is a steroid receptor transcription factor with functions critical for normal male development as well as the growth and survival of normal and cancerous prostate tissue. Studies of AR function in androgen insensitivity syndrome (AIS) and prostate cancer (PCa) have demonstrated loss-of-function AR alterations in AIS and gain-of-function AR alterations in PCa. Over the past two decades, AR gene alterations have been identified in various individuals with AIS, which disrupt normal AR splicing patterns and yield dysfunctional AR protein variants. Recently, altered AR splicing patterns have been identified as a mechanism of PCa progression and resistance to androgen depletion therapy. Several studies have described the synthesis of alternatively spliced transcripts encoding truncated AR isoforms that lack the ligand-binding domain, which is the ultimate target of androgen depletion. Many of these truncated AR isoforms function as constitutively active, ligand-independent transcription factors that can support androgen-independent expression of AR target genes, as well as the androgen-independent growth of PCa cells. In this review, we will summarize the various alternatively spliced AR variants that have been discovered, with a focus on their role and origin in the pathologic conditions of AIS and PCa.

Indexed as

Alternative SplicingAndrogen-Insensitivity SyndromeAnimalsExonsGene Expression Regulation, NeoplasticHumansMaleProstatic NeoplasmsProtein IsoformsReceptors, AndrogenAR protein, humanProtein IsoformsReceptors, Androgen

Identifiers

PMID21778211
PMCPMC3235645
OpenAlexW2136344158

What OpenQuestion holds

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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.