Evidence map›Paper›PMID 26572708›Full record

Trial reportEuropean urology2016

The Early Effects of Rapid Androgen Deprivation on Human Prostate Cancer.

Greg L Shaw, Hayley Whitaker, Marie Corcoran, Mark J Dunning, Hayley Luxton, Jonathan Kay, Charlie E Massie, Jodi L Miller, Alastair D Lamb, Helen Ross-Adams and 11 more

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in European urology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 66 citations in OpenAlex.

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  15. HyperpolarisedNature communications · 2022
    Article
  16. Frontiers in cell and developmental biology · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 5 institutions in 2 countries.

Greg L ShawCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK; Department of Urology, Cambridge University Hospitals NHS Trust, Cambridge, UK; University College Hospitals NHS Trust, UK. Electronic address: gregshaw@doctors.org.uk.
Hayley WhitakerCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK; University College London, London, UK.
Marie CorcoranDepartment of Urology, Cambridge University Hospitals NHS Trust, Cambridge, UK.
Mark J DunningCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK.
Hayley LuxtonCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK; University College London, London, UK.
Jonathan KayCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK; University College London, London, UK.
Charlie E MassieCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK.
Jodi L MillerCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK.
Alastair D LambCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK; Department of Urology, Cambridge University Hospitals NHS Trust, Cambridge, UK.
Helen Ross-AdamsCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK.
Roslin RussellCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK.
Adam W NelsonCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK; Department of Urology, Cambridge University Hospitals NHS Trust, Cambridge, UK.
Matthew D EldridgeCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK.
Andrew G LynchCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK.
Antonio Ramos-MontoyaCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK.
Ian G MillsProstate Cancer Research Group, Nordic EMBL Partnership, Centre for Molecular Medicine Norway (NCMM), University of Oslo, Oslo, Norway; Departments of Cancer Prevention and Urology, Institute of Cancer Research and Oslo University Hospitals, Oslo, Norway; Prostate Cancer UK/Movember Centre of Excellence for Prostate Cancer Research, Centre for Cancer Research and Cell Biology, Queens University Belfast, Belfast, UK.
Angela E TaylorCentre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Egbaston, Birmingham, UK.
Wiebke ArltCentre for Endocrinology, Diabetes and Metabolism, University of Birmingham, Egbaston, Birmingham, UK.
Nimish ShahDepartment of Urology, Cambridge University Hospitals NHS Trust, Cambridge, UK.
Anne Y WarrenDepartment of Pathology, Cambridge University Hospitals NHS Trust, Cambridge, UK.
David E NealCancer Research UK Cambridge Institute, Li Ka Shing Centre, Cambridge, UK; Department of Urology, Cambridge University Hospitals NHS Trust, Cambridge, UK; Nuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Headington, Oxford, UK.
Cancer Research UK Cambridge Center · GBCambridge University Hospitals NHS Foundation Trust · GBUniversity College London · GBUniversity of Birmingham · GBProstate Cancer UK · GB

Funding

Cancer Research UK 20406Medical Research Council G0801473Medical Research Council G0900567Medical Research Council G116/172Medical Research Council MR/L00156X/1Prostate Cancer UK G2012/50Prostate Cancer UK PA14-022
6 · The paper itself

Abstract

unlabelledThe androgen receptor (AR) is the dominant growth factor in prostate cancer (PCa). Therefore, understanding how ARs regulate the human transcriptome is of paramount importance. The early effects of castration on human PCa have not previously been studied 27 patients medically castrated with degarelix 7 d before radical prostatectomy. We used mass spectrometry, immunohistochemistry, and gene expression array (validated by reverse transcription-polymerase chain reaction) to compare resected tumour with matched, controlled, untreated PCa tissue. All patients had levels of serum androgen, with reduced levels of intraprostatic androgen at prostatectomy. We observed differential expression of known androgen-regulated genes (TMPRSS2, KLK3, CAMKK2, FKBP5). We identified 749 genes downregulated and 908 genes upregulated following castration. AR regulation of α-methylacyl-CoA racemase expression and three other genes (FAM129A, RAB27A, and KIAA0101) was confirmed. Upregulation of oestrogen receptor 1 (ESR1) expression was observed in malignant epithelia and was associated with differential expression of ESR1-regulated genes and correlated with proliferation (Ki-67 expression). PATIENT SUMMARY: This first-in-man study defines the rapid gene expression changes taking place in prostate cancer (PCa) following castration. Expression levels of the genes that the androgen receptor regulates are predictive of treatment outcome. Upregulation of oestrogen receptor 1 is a mechanism by which PCa cells may survive despite castration.

Indexed as

Prostatic NeoplasmsEstrogen Receptor alphaGene Expression ProfilingGene Expression Regulation, NeoplasticHormone AntagonistsHumansImmunohistochemistryMaleOligopeptidesPreoperative CareProstateProstatectomyReceptors, AndrogenSpectrum Analysisacetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ILys-prolyl-alaninamideESR1 protein, humanEstrogen Receptor alphaHormone AntagonistsOligopeptidesReceptors, AndrogenAndrogen receptorCastrationClinical trialGene transcriptionImmunohistochemistryProstate cancer

Identifiers

PMID26572708
PMCPMC4926724
OpenAlexW2164746240

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.