Evidence map›Paper›PMID 32790723›Full record

ArticlePloS one2020

Assessment of STAT5 as a potential therapy target in enzalutamide-resistant prostate cancer.

Holger H H Erb, Julia Bodenbender, Florian Handle, Tamara Diehl, Lukas Donix, Igor Tsaur, Martin Gleave, Axel Haferkamp, Johannes Huber, Susanne Fuessel and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  5. Metabolic changes during prostate cancer development and progression.Journal of cancer research and clinical oncology · 2023
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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

13 authors at 6 institutions in 4 countries.

Holger H H ErbDepartment of Urology, Technische Universität Dresden, Dresden, Germany.ORCID 0000-0001-5209-7914
Julia BodenbenderDepartment of Urology and Pediatric Urology, University Medical Center Mainz, Mainz, Germany.
Florian HandleMolecular Endocrinology Laboratory, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
Tamara DiehlDepartment of Urology and Pediatric Urology, University Medical Center Mainz, Mainz, Germany.
Lukas DonixDepartment of Urology, Technische Universität Dresden, Dresden, Germany.
Igor TsaurDepartment of Urology and Pediatric Urology, University Medical Center Mainz, Mainz, Germany.
Martin GleaveThe Vancouver Prostate Centre, University of British Columbia, Vancouver, Canada.
Axel HaferkampDepartment of Urology and Pediatric Urology, University Medical Center Mainz, Mainz, Germany.
Johannes HuberDepartment of Urology, Technische Universität Dresden, Dresden, Germany.
Susanne FuesselDepartment of Urology, Technische Universität Dresden, Dresden, Germany.
Eva JuengelDepartment of Urology and Pediatric Urology, University Medical Center Mainz, Mainz, Germany.
Zoran CuligExperimental Urology, Department of Urology, University of Innsbruck, Innsbruck, Austria.
Christian ThomasDepartment of Urology, Technische Universität Dresden, Dresden, Germany.
Johannes Gutenberg University Mainz · DETechnische Universität Dresden · DEKU Leuven · BENational Center for Tumor Diseases · DEUniversität Innsbruck · ATUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite enzalutamide's efficacy in delaying the progression of metastatic castration-resistant prostate cancer (CRPC), resistance to this anti-androgen inevitably occurs. Several studies have revealed that the signal transducer and activator of transcription (STAT) 5 plays a role in tumour progression and development of drug resistance such as enzalutamide. Data mining revealed heterogeneous expression of STAT5 in enzalutamide-treated mCRPC patients and enzalutamide-resistant prostate cancer (PCa). Isobologram analysis revealed that the STAT5 inhibitor pimozide combined with enzalutamide has? additive and synergistic inhibitory effects on cell viability in the used models. Functional analysis with siRNA-mediated STAT5 knockdown yielded divergent results. The LNCaP-derived cell line MR49F could be resensitised to enzalutamide by siRNA-mediated STAT5b-knock-down. In contrast, neither STAT5a nor STAT5b knockdown resensitised enzalutamide-resistant LAPC4-EnzaR cells to enzalutamide. In conclusion, our results indicate that STAT5 may be a possible target in a subgroup of enzalutamide-resistant PCa. However, based on the data presented here, a general role of STAT5 in enzalutamide-resistance and its potential as a therapeutic target could not be shown.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsBenzamidesCell Line, TumorGene Expression Regulation, NeoplasticHumansMaleNitrilesPhenylthiohydantoinProstatic NeoplasmsSTAT5 Transcription FactorTumor Suppressor ProteinsAntineoplastic AgentsBenzamidesenzalutamideNitrilesPhenylthiohydantoinSTAT5A protein, humanSTAT5B protein, humanSTAT5 Transcription FactorTumor Suppressor Proteins

Identifiers

PMID32790723
PMCPMC7425943
OpenAlexW3048974830

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.