Evidence map›Paper›PMID 30237440›Full record

ArticleOncogene2019

A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer.

Anne Y Warren, Charlie E Massie, Kate Watt, Katarina Luko, Folake Orafidiya, Luke A Selth, Hisham Mohammed, Brinder S Chohan, Suraj Menon, Ajoeb Baridi and 17 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2019. 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
2.0field-weighted citation impact, top 13% 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, 23 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

27 authors at 7 institutions in 4 countries.

Anne Y WarrenDepartment of Pathology, Addenbrooke's Cambridge University Hospital, Cambridge, UK.
Charlie E MassieEarly Detection Programme, Cancer Research UK Cambridge Centre, Department of Oncology, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-2314-4843
Kate WattInstitute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Katarina LukoInstitute of Human Genetics, Jena University Hospital, Jena, Germany.
Folake OrafidiyaInstitute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Luke A SelthDame Roma Mitchell Cancer Research Laboratories, School of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia.
Hisham MohammedCancer Early Detection Advanced Research Center, Knight Cancer Institute, OHSU, Portland, USA.
Brinder S ChohanDepartment of Pathology, Addenbrooke's Cambridge University Hospital, Cambridge, UK.
Suraj MenonCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Ajoeb BaridiCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Wanfeng ZhaoDepartment of Pathology, Addenbrooke's Cambridge University Hospital, Cambridge, UK.
Carles EscriuCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Thanakorn PungsrinontInstitute of Human Genetics, Jena University Hospital, Jena, Germany.
Clive D'SantosCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Xiaoping YangCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Chris TaylorCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Arham QureshiCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Vincent R ZecchiniCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Greg L ShawCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Scott M DehmMasonic Cancer Center, University of Minnesota, Minneapolis, USA.ORCID http://orcid.org/0000-0002-7827-5579
Ian G MillsProstate Cancer UK/Movember Centre of Excellence, CCRCB, Queens University, Belfast, UK.
Jason S CarrollCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Wayne D TilleyDame Roma Mitchell Cancer Research Laboratories, School of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia.
Iain J McEwanInstitute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Aria BaniahmadInstitute of Human Genetics, Jena University Hospital, Jena, Germany.
David E NealCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Mohammad AsimCancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK. m.asim@surrey.ac.uk.
University of Cambridge · GBJena University Hospital · DEUniversity of Aberdeen · GBFreemasons Foundation Centre for Men's Health · AUOHSU Knight Cancer InstituteQueen's University Belfast · GBUniversity of Minnesota Medical Center · US

Funding

AR Gene Rearrangements and AR Signaling in Prostate CancerR01CA174777 · NCI · UNIVERSITY OF MINNESOTA · PI Scott M. Dehm · 2013 to 2026
$4.9M
Cancer Research UK 20411NCI NIH HHS R01 CA174777
6 · The paper itself

Abstract

Elucidation of mechanisms underlying the increased androgen receptor (AR) activity and subsequent development of aggressive prostate cancer (PrCa) is pivotal in developing new therapies. Using a systems biology approach, we interrogated the AR-regulated proteome and identified PDZ binding kinase (PBK) as a novel AR-regulated protein that regulates full-length AR and AR variants (ARVs) activity in PrCa. PBK overexpression in aggressive PrCa is associated with early biochemical relapse and poor clinical outcome. In addition to its carboxy terminus ligand-binding domain, PBK directly interacts with the amino terminus transactivation domain of the AR to stabilise it thereby leading to increased AR protein expression observed in PrCa. Transcriptome sequencing revealed that PBK is a mediator of global AR signalling with key roles in regulating tumour invasion and metastasis. PBK inhibition decreased growth of PrCa cell lines and clinical specimen cultured ex vivo. We uncovered a novel interplay between AR and PBK that results in increased AR and ARVs expression that executes AR-mediated growth and progression of PrCa, with implications for the development of PBK inhibitors for the treatment of aggressive PrCa.

Indexed as

Signal TransductionCell Line, TumorGene Expression RegulationHumansMaleMitogen-Activated Protein Kinase KinasesNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsProstatic NeoplasmsProtein Kinase InhibitorsReceptors, AndrogenMitogen-Activated Protein Kinase KinasesNeoplasm ProteinsPDZ-binding kinaseProtein Kinase InhibitorsReceptors, Androgen

Identifiers

PMID30237440
PMCPMC6514849
OpenAlexW2890079584

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.