ArticleThe Journal of clinical investigation2017
A mouse model of MYCN-driven retinoblastoma reveals MYCN-independent tumor reemergence.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Targeting MYCN Degradation by HLB-0532259 Induces Senescence in Retinoblastoma.Investigative ophthalmology & visual science · 2026Article
- Retinoblastoma: unveiling molecular pathogenesis and pioneering organoid-driven therapeutic innovations.Stem cell research & therapy · 2026Review
- Human Retinal Organoid Modeling Defines Developmental Window and Therapeutic Vulnerabilities in MYCN-Amplified Retinoblastoma.International journal of molecular sciences · 2025Article
- Targeting the MYCN-MDM2 pathways for cancer therapy: Are they druggable?Genes & diseases · 2025Review
- In vitro model of retinoblastoma derived tumor and stromal cells for tumor microenvironment (TME) studies.Cell death & disease · 2024Article
- Histone Deacetylases in Retinoblastoma.International journal of molecular sciences · 2024Review
- Piperlongumine inhibits proliferation and oncogenic MYCN expression in chemoresistant metastatic retinoblastoma cells directly and through extracellular vesicles.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
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- Characterizing DNA methylation signatures of retinoblastoma using aqueous humor liquid biopsy.Nature communications · 2022Article
- MYCN induces cell-specific tumorigenic growth in RB1-proficient human retinal organoid and chicken retina models of retinoblastoma.Oncogenesis · 2022Article
- Basal cell carcinomas acquire secondary mutations to overcome dormancy and progress from microscopic to macroscopic disease.Cell reports · 2022Article
- pRB-Depleted Pluripotent Stem Cell Retinal Organoids Recapitulate Cell State Transitions of Retinoblastoma Development and Suggest an Important Role for pRB in Retinal Cell Differentiation.Stem cells translational medicine · 2022Article
- Mesenchymal Mycn participates in odontoblastic lineage commitment by regulating Krüppel-like Factor 4 (Klf4) in mice.Stem cell research & therapy · 2022Article
- The OncogeneCancers · 2021Article
- Retinoblastoma from human stem cell-derived retinal organoids.Nature communications · 2021Article
- Advances in immunotherapeutic targets for childhood cancers: A focus on glypican-2 and B7-H3.Pharmacology & therapeutics · 2021Review
- Temporal evolution of cellular heterogeneity during the progression to advanced AR-negative prostate cancer.Nature communications · 2021Article
- The Role of Glypicans in Cancer Progression and Therapy.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Silencing of the Long Noncoding RNA MYCNOS1 Suppresses Activity of MYCN-Amplified Retinoblastoma Without RB1 Mutation.Investigative ophthalmology & visual science · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The most frequent focal alterations in human retinoblastoma are mutations in the tumor-suppressor gene retinoblastoma (RB) and amplification of the oncogene MYCN. Whether MYCN overexpression drives retinoblastoma has not been assessed in model systems. Here, we have shown that Rb inactivation collaborates strongly with MYCN overexpression and leads to retinoblastoma in mice. Overexpression of human MYCN in the context of Rb inactivation increased the expression of MYC-, E2F-, and ribosome-related gene sets, promoted excessive proliferation, and led to retinoblastoma with anaplastic changes. We then modeled responses to MYCN-directed therapy by suppressing MYCN expression in MYCN-driven retinoblastomas. Initially, MYCN suppression led to proliferation arrest and partial tumor regression with loss of anaplasia. However, over time, retinoblastomas reemerged, typically without reactivation of human MYCN or amplification of murine Mycn. A subset of returning retinoblastomas showed genomic amplification of a Mycn target gene encoding the miR cluster miR-17~92, while most retinoblastomas reemerged without clear genetic alterations in either Mycn or known Mycn targets. This Rb/MYCN model recapitulates key genetic driver alterations seen in human retinoblastoma and reveals the emergence of MYCN independence in an initially MYCN-driven tumor.
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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.