Evidence map›Paper›PMID 21748469›Full record

ReviewCellular and molecular life sciences : CMLS2011

Androgen receptor and its splice variants in prostate cancer.

Simon Haile, Marianne D Sadar

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
9.5field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 112 citations in OpenAlex.

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5 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 1 institution in 1 country.

Simon HaileGenome Sciences Center, BC Cancer Agency, 675 West 10th Avenue, Vancouver, BC V5Z 1L3, Canada.
Marianne D Sadar
BC Cancer Agency · CA

Funding

Novel compounds that inhibit transactivation of N-terminal domain of the androgenR01CA105304 · NCI · PROVINCIAL HEALTH SERVICES AUTHORITY · PI SADAR, MARIANNE D · 2004 to 2021
$3.7M
CIHR MOP-84325NCI NIH HHS 2R01 CA105304NCI NIH HHS R01 CA105304
6 · The paper itself

Abstract

Androgen receptor (AR) is a transcription factor that becomes active upon binding to androgens via its ligand-binding domain (LBD) or in response to signaling cascades initiated by growth factors and cytokines. The activity of AR requires regions within the N-terminal domain (NTD) in a manner that is distinct from the activation of related steroid hormone receptors. Unequivocal evidence has been amassed to consider that the AR axis is the most critical pathway for the progression of prostate cancer. Qualitatively distinct insights into AR pathobiology have been garnered including that AR-regulated gene expression is stage-specifically modulated during disease progression and that the ligand requirement for AR activity could be rendered dispensable because of the expression of constitutively active AR splice variants that are devoid of LBD. The recent appreciation of the clinical challenge that stems from non-gonadal androgens that are not inhibited by traditional hormonal therapies has been tangibly translated into the development of more potent drugs that can potentially lead towards achieving an androgen-free environment. The pre-clinical evidence that proves that AR NTD is a druggable target also forecasts a further paradigm shift in the management of advanced prostate cancer. These advancements together with the identification of more robust AR antagonists and their promising clinical outcome have renewed the hope that targeting the AR pathway remains a sound strategy in the clinical management of prostate cancer. Here, we address these developments with a greater emphasis on the rapidly growing literature on AR splice variants.

Indexed as

Alternative SplicingAntineoplastic AgentsGene Expression Regulation, NeoplasticHumansMaleModels, BiologicalProstatic NeoplasmsProtein IsoformsReceptors, AndrogenAntineoplastic AgentsProtein IsoformsReceptors, Androgen

Identifiers

PMID21748469
PMCPMC3729216
OpenAlexW2016771357

What OpenQuestion holds

Textmetadata
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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.