
The study demonstrates that acquired castration-resistant prostate cancer (CRPC) LNCaP sublines have a homologous recombination repair (HRR) defect and increased sensitivity to olaparib and cisplatin due to impaired RAD51 expression and recruitment. Ex vivo tumor slice cultures from CRPC patients and patient-derived tumor organoids (PDOs) also showed enhanced sensitivity to olaparib and cisplatin. PDOs can help identify individualized drug screening and translate treatment sensitivities into tailored clinical therapy recommendations.
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