ArticleJCI insight2021
Resistance to androgen receptor signaling inhibition does not necessitate development of neuroendocrine prostate cancer.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1-mediated cell-intrinsic resistance.Nature communications · 2026Article
- Evaluation of Tissue from Patients with Prostate Cancer Identifies B7-H3 as an Androgen-Regulated, Broadly Expressed, Combinatorial Therapeutic Target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Targeting arginine metabolism overcomes chemotherapy resistance in aggressive-variant prostate cancers.iScience · 2026Article
- Deciphering double-negative prostate cancer: from aggressive subtype to novel therapeutic paradigms.Cell communication and signaling : CCS · 2026Review
- Genetic and epigenetic mechanisms underlying treatment-induced neuroendocrine prostate cancer.Journal of the National Cancer Center · 2026Review
- Characteristics and therapeutic resistance mechanisms of the prostate cancer immune microenvironment: a comprehensive analysis from bench to clinic.Frontiers in pharmacology · 2026Review
- Intratumoral Androgens and Genetic Variants Driving Therapy Resistance in Prostate Cancer.Research (Washington, D.C.) · 2026Review
- Lineage plasticity and histological transformation: tumor histology as a spectrum.Cell research · 2025Review
- Cancer cell plasticity and therapeutic resistance: mechanisms, crosstalk, and translational perspectives.Hereditas · 2025Review
- Patterns of intra- and intertumor phenotypic heterogeneity in lethal prostate cancer.The Journal of clinical investigation · 2025Article
- Intraindividual epigenetic heterogeneity underlying phenotypic subtypes of advanced prostate cancer.Nature communications · 2025Article
- PROX1 is an early driver of lineage plasticity in prostate cancer.The Journal of clinical investigation · 2025Article
- ETV5 reduces androgen receptor expression and induces neural stem-like properties during neuroendocrine prostate cancer development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Framework for the Pathology Workup of Metastatic Castration-Resistant Prostate Cancer Biopsies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- Targeting mRNA-coding genes in prostate cancer using CRISPR/Cas9 technology with a special focus on androgen receptor signaling.Cell communication and signaling : CCS · 2024Review
- AKT Inhibition Sensitizes to Polo-Like Kinase 1 Inhibitor Onvansertib in Prostate Cancer.Molecular cancer therapeutics · 2024Article
- Understanding the function of Pax5 in development of docetaxel-resistant neuroendocrine-like prostate cancers.Cell death & disease · 2024Article
- Proteostasis perturbation of N-Myc leveraging HSP70 mediated protein turnover improves treatment of neuroendocrine prostate cancer.Nature communications · 2024Article
- Systematic Multi-Omics Investigation of Androgen Receptor Driven Gene Expression and Epigenetics changes in Prostate Cancer.bioRxiv : the preprint server for biology · 2024Article
- Plexin D1 emerges as a novel target in the development of neural lineage plasticity in treatment-resistant prostate cancer.Oncogene · 2024Article
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
Resistance to AR signaling inhibitors (ARSis) in a subset of metastatic castration-resistant prostate cancers (mCRPCs) occurs with the emergence of AR- neuroendocrine prostate cancer (NEPC) coupled with mutations/deletions in PTEN, TP53, and RB1 and the overexpression of DNMTs, EZH2, and/or SOX2. To resolve whether the lack of AR is the driving factor for the emergence of the NE phenotype, molecular, cell, and tumor biology analyses were performed on 23 xenografts derived from patients with PC, recapitulating the full spectrum of genetic alterations proposed to drive NE differentiation. Additionally, phenotypic response to CRISPR/Cas9-mediated AR KO in AR+ CRPC cells was evaluated. These analyses document that (a) ARSi-resistant NEPC developed without androgen deprivation treatment; (b) ARS in ARSi-resistant AR+/NE+ double-positive "amphicrine" mCRPCs did not suppress NE differentiation; (c) the lack of AR expression did not necessitate acquiring a NE phenotype, despite concomitant mutations/deletions in PTEN and TP53, and the loss of RB1 but occurred via emergence of an AR-/NE- double-negative PC (DNPC); (d) despite DNPC cells having homogeneous genetic driver mutations, they were phenotypically heterogeneous, expressing basal lineage markers alone or in combination with luminal lineage markers; and (e) AR loss was associated with AR promoter hypermethylation in NEPCs but not in DNPCs.
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