Evidence map›Paper›PMID 26318637›Full record

ArticleWorld journal of urology2016

Inhibition of IGF-1R diminishes transcriptional activity of the androgen receptor and its constitutively active, C-terminally truncated counterparts Q640X and AR-V7.

Friedemann Zengerling, Anca Azoitei, Alexander Herweg, Florian Jentzmik, Marcus V Cronauer

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Article in World journal of urology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Friedemann ZengerlingDepartment of Urology, Ulm University Medical Center, Prittwitzstrasse 43, 89075, Ulm, Germany.
Anca AzoiteiDepartment of Urology, Ulm University Medical Center, Prittwitzstrasse 43, 89075, Ulm, Germany.
Alexander HerwegDepartment of Urology, Ulm University Medical Center, Prittwitzstrasse 43, 89075, Ulm, Germany.
Florian JentzmikDepartment of Urology, Ulm University Medical Center, Prittwitzstrasse 43, 89075, Ulm, Germany.
Marcus V CronauerDepartment of Urology, Ulm University Medical Center, Prittwitzstrasse 43, 89075, Ulm, Germany. marcus.cronauer@uni-ulm.de.
Universität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeFailure of endocrine treatment in castration-resistant prostate cancer (CRPC) is often associated with the emergence of C-terminally truncated androgen receptor variants that function as constitutively active transcription factors (i.e., AR∆LBD). The mechanisms involved in the regulation of AR∆LBD signaling are largely unknown. Since the IGF-1 pathway was repeatedly shown to affect AR function, we studied whether an inhibition of IGF-1R could also affect AR∆LBD signaling.

methodsRegulation of androgen receptor (AR) and AR∆LBD signaling was analyzed by reporter gene assays, immunoblotting, ELISA and quantitative RT-PCR.

resultsInhibition of IGF-1R with the small-molecule inhibitor NVP-AEW541 reduced the transcriptional activity of the AR and its truncated counterparts Q640X and AR-V7. As shown in Q640X, the inhibition of transcriptional activity was paralleled by a decreased receptor phosphorylation.

conclusionsInhibition of IGF-1R leads to a down-regulation of AR∆LBD signaling and provides a rationale for CRPC therapies targeting growth factor receptors.

Indexed as

Signal TransductionHumansInsulin-Like Growth Factor IMaleProstatic Neoplasms, Castration-ResistantReceptors, AndrogenTumor Cells, CulturedAR protein, humanInsulin-Like Growth Factor IReceptors, AndrogenAR-V7Castration-resistant prostate cancerIGF-1 receptorQ640X

Identifiers

PMID26318637
OpenAlexW1892663535

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.