ArticleJournal of experimental & clinical cancer research : CR2025
Multi-layer stratified oncology platform utilizing transcriptomics, prostate cancer organoids, and modeling of drug response.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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.
Who cites it
3 citing papers in PubMed.
- Cancer Heterogeneity and Cancer Cell Plasticity: Molecular Mechanisms and Precision Therapy.MedComm · 2026Review
- PU.1 is a mediator of the reactive stromal response associated with castration-resistant prostate cancer.Communications biology · 2026Article
- Organoids glimpse: the nexus for diverse tumor heterogeneity.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
The high intra-patient heterogeneity in multifocal primary prostate cancer (PCa) has curtailed the efficacy of current treatment options. By employing twin biopsies from multiple lesions with matched patient-derived organoids (PDO) models, the PCa molecular heterogeneity was investigated. We utilized genomics, transcriptomics and machine learning (ML) approaches to elucidate and predict the underlying mechanisms of pharmacological heterogeneity. Our data indicate a vulnerability of primary PCa organoids for small molecule inhibitors targeting receptor tyrosine kinases (MET, ALK, SRC). By exploring gene expression data from matched parental tissue in an unsupervised manner, we identified two distinct clusters of samples. Interestingly, the PDO drug responses were significantly different between the two clusters for 4/11 compounds tested. We developed a transcriptomics-based, cluster prediction model, which can accurately stratify samples into the two clusters. Notably, our prediction model is based on tissue profiles, therefore, it can be utilized to rapidly evaluate new cases and suggest promising drug candidates, even when PDO derivation is not feasible. Taken together, we propose a novel flexible stratified oncology approach that can swiftly and accurately highlight promising drug vulnerabilities of PCa patients.
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Registered trials
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.