ArticleCell reports. Medicine2024
Castrate-resistant prostate cancer response to taxane is determined by an HNF1-dependent apoptosis resistance circuit.
Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Integrative molecular analyses of lineage identity and morphology in aggressive variant prostate cancer.NPJ precision oncology · 2026Article
- Molecular decoupling of lineage identity and morphology in aggressive variant prostate cancer.medRxiv : the preprint server for health sciences · 2026Article
- Nanotechnology in Prostate Cancer: PSMA-Targeted Nanoplatforms, TME-Responsive Therapy, Immunomodulation, and Clinical Translation Challenges.International journal of nanomedicine · 2026Review
- Missense and Intronic Variants inInternational journal of medical sciences · 2026Article
- CRP and HNF1A collaborate to regulate the progression of laryngeal cancer through the Wnt signaling pathway.Functional & integrative genomics · 2025Article
- Transcriptional profiling clarifies a program of enzalutamide extreme non-response in lethal prostate cancer.NPJ precision oncology · 2025Article
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastatic castrate-resistant prostate cancer (mCRPC) is a genetically and phenotypically heterogeneous cancer where advancements are needed in biomarker discovery and targeted therapy. A critical and often effective component of treatment includes taxanes. We perform a high-throughput screen across a cohort of 30 diverse patient-derived castrate-resistant prostate cancer (CRPC) organoids to a library of 78 drugs. Combining quantitative response measures with transcriptomic analyses demonstrates that HNF1 homeobox A (HNF1A) drives a transcriptional program of taxane resistance, commonly dependent upon cellular inhibitor of apoptosis protein 2 (cIAP2). Monotherapy with cIAP2 inhibitor LCL161 is sufficient to treat HNF1A+ models of mCRPC previously resistant to docetaxel. These data may be useful in future clinical trial designs.
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