ArticleMolecular oncology2023
Preclinical patient-derived modeling of castration-resistant prostate cancer facilitates individualized assessment of homologous recombination repair deficient disease.
Article in Molecular oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Functional and omics-based rationale for the induction of BRCAness by androgen receptor pathway inhibitors to sensitize prostate cancer to PARP inhibition, regardless of HRR status.British journal of cancer · 2026Article
- Overexpression of the ERG oncogene in prostate cancer identifies candidates for PARP inhibitor-based radiosensitization.The Journal of clinical investigation · 2026Article
- Article
- Patient-derived prostate cancer organoids: model development, therapeutic applications, and challenges for precision oncology.Frontiers in oncology · 2026Review
- Precision-cut tumor slices: a biomimetic tool for accelerating oncological development from basic research to clinical translation.Frontiers in physiology · 2026Review
- Endocrine cancer organoids in basic and translational medical research.Science China. Life sciences · 2025Review
- [Olaparib for high-risk biochemically recurrent prostate cancer following prostatectomy].Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2025Article
- Facilitation of Tumor Stroma-Targeted Therapy: Model Difficulty and Co-Culture Organoid Method.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Patient-derived tumor organoids: A preclinical platform for personalized cancer therapy.Translational oncology · 2025Review
- Organoids: An Emerging Precision Medicine Model for Prostate Cancer Research.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 4 countries.
Funding
Abstract
The use of mutation analysis of homologous recombination repair (HRR) genes to estimate PARP-inhibition response may miss a larger proportion of responding patients. Here, we provide preclinical models for castration-resistant prostate cancer (CRPC) that can be used to functionally predict HRR defects. In vitro, CRPC LNCaP sublines revealed an HRR defect and enhanced sensitivity to olaparib and cisplatin due to impaired RAD51 expression and recruitment. Ex vivo-induced castration-resistant tumor slice cultures or tumor slice cultures derived directly from CRPC patients showed increased olaparib- or cisplatin-associated enhancement of residual radiation-induced γH2AX/53BP1 foci. We established patient-derived tumor organoids (PDOs) from CRPC patients. These PDOs are morphologically similar to their primary tumors and genetically clustered with prostate cancer but not with normal prostate or other tumor entities. Using these PDOs, we functionally confirmed the enhanced sensitivity of CRPC patients to olaparib and cisplatin. Moreover, olaparib but not cisplatin significantly decreased the migration rate in CRPC cells. Collectively, we present robust patient-derived preclinical models for CRPC that recapitulate the features of their primary tumors and enable individualized drug screening, allowing translation of treatment sensitivities into tailored clinical therapy recommendations.
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