ArticleCancer cell2016
N-Myc Induces an EZH2-Mediated Transcriptional Program Driving Neuroendocrine Prostate Cancer.
Article in Cancer cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 399 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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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.
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Who cites it
399 citing papers in PubMed, 1 synthesis or guideline pooled it, 555 citations in OpenAlex.
- A systematic review on the culture methods and applications of 3D tumoroids for cancer research and personalized medicine.Cellular oncology (Dordrecht, Netherlands) · 2025Pooled it
- Epigenetic reprogramming of lineage switching in cancer.FEBS letters · 2026Review
- Beyond androgen deprivation therapy: Next-generation hormonal therapies and emerging combination approaches in advanced prostate cancer.Urologic oncology · 2026Review
- Neuromedin U 'innervation' reprograms myeloid immunosuppression in neuroendocrine prostate cancer.Oncogene · 2026Article
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- TMEM59L promotes neuroendocrine differentiation and enzalutamide resistance in prostate cancer by regulating MUC1/β-catenin/MYC axis.Clinical and translational medicine · 2026Article
- Pathological Pathways of Olfactory Neuroblastoma: From Molecular Mechanisms to Targeted Therapy: A Narrative Review.Cancers · 2026Review
- WSB1-Mediated PSMA Ubiquitination Promotes Enzalutamide-Induced Neuroendocrine-like Transition in Patient-Derived Prostate Cancer Spheroids.International journal of molecular sciences · 2026Article
- MAP2K6 reprograms NADCell death & disease · 2026Article
- A forward genetic screen identifies Sirtuin1 as a driver of neuroendocrine prostate cancer.The Journal of experimental medicine · 2026Article
- Low-PSMA hormone-sensitive prostate cancer: a distinct clinical and molecular state.Molecular medicine (Cambridge, Mass.) · 2026Article
- A MYC family switch: L-MYC drives and maintains neuroendocrine lineage programs in prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- Article
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- Epigenetic plasticity in cancer drug resistance: mechanistic insights and strategies for therapeutic intervention.Acta pharmacologica Sinica · 2026Review
- Cancer stem cell plasticity in shaping drug resistance landscapes in prostate cancer.Journal of advanced research · 2026Review
- 3D genome architecture and epigenetic regulation of lineage identity in advanced prostate cancer.Endocrinology · 2026Review
- IGFBP3-SphK1/S1P Signaling Axis Drives Enzalutamide Resistance in Advanced Prostate Cancer.Molecular cancer therapeutics · 2026Article
- Loss of luminal lineage drives resistance to next-generation ERα antagonists in pretreated ERNature communications · 2026Article
- Serotonin Modulates Lineage Plasticity in Neuroendocrine Prostate Cancer via Epigenetic Reprogramming.Cancer discovery · 2026Article
339 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 9 institutions in 3 countries.
Funding
Abstract
The transition from castration-resistant prostate adenocarcinoma (CRPC) to neuroendocrine prostate cancer (NEPC) has emerged as an important mechanism of treatment resistance. NEPC is associated with overexpression and gene amplification of MYCN (encoding N-Myc). N-Myc is an established oncogene in several rare pediatric tumors, but its role in prostate cancer progression is not well established. Integrating a genetically engineered mouse model and human prostate cancer transcriptome data, we show that N-Myc overexpression leads to the development of poorly differentiated, invasive prostate cancer that is molecularly similar to human NEPC. This includes an abrogation of androgen receptor signaling and induction of Polycomb Repressive Complex 2 signaling. Altogether, our data establishes N-Myc as an oncogenic driver of NEPC.
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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.