Evidence map›Paper›PMID 42324329›Full record

ArticleScientific reports2026

UCA1 copy number gain in serum cfDNA predicts next-generation antiandrogen resistance in metastatic castration-resistant prostate cancer.

Anita Csizmarik, Áron Soós, Melinda Váradi, Balázs Magyar, Martin Puhr, Ákos Nagy, Balázs Győrffy, Gergő Holló, Gero Kramer, Mulham Al-Nader and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

14 authors.

Anita CsizmarikDepartment of Urology, Semmelweis University, Üllői street 78/b, Budapest, H-1082, Hungary.
Áron SoósDepartment of Urology, Semmelweis University, Üllői street 78/b, Budapest, H-1082, Hungary.
Melinda VáradiDepartment of Urology, Semmelweis University, Üllői street 78/b, Budapest, H-1082, Hungary.
Balázs MagyarDepartment of Urology, Semmelweis University, Üllői street 78/b, Budapest, H-1082, Hungary.
Martin PuhrDepartment of Urology, Medical University of Innsbruck, Innsbruck, Austria.
Ákos NagyHCEMM-SE Molecular Oncohematology Research Group, Department of Pathology, Experimental Cancer Research, Semmelweis University, Budapest, Hungary.
Balázs GyőrffyDepartment of Bioinformatics, Semmelweis University, Budapest, Hungary.
Gergő HollóDepartment of Bioinformatics, Semmelweis University, Budapest, Hungary.
Gero KramerDepartment of Urology, Medical University of Vienna, Vienna, Austria.
Mulham Al-NaderDepartment of Urology, University Hospital Essen, University of Duisburg-Essen, Hufelandstr. 55, Essen, D-45147, Germany.
Osama MahmoudDepartment of Urology, University Hospital Essen, University of Duisburg-Essen, Hufelandstr. 55, Essen, D-45147, Germany.
Boris HadaschikDepartment of Urology, University Hospital Essen, University of Duisburg-Essen, Hufelandstr. 55, Essen, D-45147, Germany.
Péter NyirádyDepartment of Urology, Semmelweis University, Üllői street 78/b, Budapest, H-1082, Hungary.
Tibor SzarvasDepartment of Urology, Semmelweis University, Üllői street 78/b, Budapest, H-1082, Hungary. szarvas.tibor@semmelweis.hu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enzalutamide (ENZA) is a second-generation antiandrogen therapy that provides overall survival (OS) benefit for prostate cancer (PC) patients. However, many patients have baseline or develop resistance to ENZA. Currently, no biomarkers are used in clinical decision making to predict the efficacy of ENZA therapy. We aimed to identify cell-free DNA (cfDNA) biomarkers for metastatic castration-resistant prostate cancer (mCRPC) predictive to ENZA response. Comparative whole-exome and transcriptome sequencing was performed on three ENZA-resistant and parental ENZA-sensitive PC cell line pairs. Bioinformatic analysis identified UCA1, ORM1, and androgen receptor (AR) as candidate markers for serum cfDNA testing. Digital droplet PCR was used to analyze UCA1, ORM1 and AR in cfDNA from serum samples of mCRPC patients who underwent ENZA (n = 20), abiraterone (ABI; n = 20) and 40 docetaxel (DOC; n = 40) treatment. UCA1 copy number gain was significantly associated with reduced OS in ENZA-treated patients (p = 0.030). AR gain correlated with poorer OS in ABI-treated patients (p = 0.039), whereas no association was observed in DOC-treated patients. Normal AR and UCA1 levels were associated with significantly better OS in ENZA and ABI-treated patients. These findings suggest that UCA1 gain may predict reduced efficacy of ENZA treatment, while AR gain indicates decreased effectiveness of ABI but not ENZA and DOC therapies. These results may help support therapeutic decisions in the clinical settings.

Indexed as

Androgen AntagonistsCell-Free Nucleic AcidsDNA Copy Number VariationsDrug Resistance, NeoplasmProstatic Neoplasms, Castration-ResistantAgedAndrostenesBenzamidesBiomarkers, TumorCell Line, TumorDocetaxelHumansMaleMiddle AgedNeoplasm MetastasisNitrilesabirateroneAndrogen AntagonistsAndrostenesBenzamidesBiomarkers, TumorCell-Free Nucleic AcidsDocetaxelenzalutamideNitrilesPhenylthiohydantoinReceptors, AndrogenRNA, Long NoncodingUCA1 RNA, humanAndrogen receptorBiomarkerCell-free DNA (cfDNA)Prostate cancerUCA1

Identifiers

PMID42324329
PMCPMC13562513

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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.