ArticleNeoplasia (New York, N.Y.)2016
A Novel Mouse Model of Diffuse Intrinsic Pontine Glioma Initiated in Pax3-Expressing Cells.
Article in Neoplasia (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Synergistic cell-cycle repression by HDAC/EZH2 co-targeting in H3K27-altered diffuse midline glioma.Molecular therapy. Oncology · 2026Article
- Oncohistone inhibition reshapes tumor-microenvironment communication in Diffuse Midline Glioma (DMG).bioRxiv : the preprint server for biology · 2026Article
- Therapeutic approaches for targeting the pediatric brain tumor microenvironment.Drug delivery and translational research · 2025Review
- Effects of combination therapy of a CDK4/6 and MEK inhibitor in diffuse midline glioma preclinical models.PloS one · 2025Article
- The Landscape of Pediatric High-Grade Gliomas: The Virtues and Pitfalls of Pre-Clinical Models.Biology · 2024Review
- Preclinical pediatric brain tumor models for immunotherapy: Hurdles and a way forward.Neuro-oncology · 2024Review
- Feasibility of probe washing after stereotactic needle biopsy as a novel technique for developing cell lines and xenografts of H3 K27-altered diffuse midline gliomas.Journal of neurosurgery. Pediatrics · 2023Article
- Oncohistones and disrupted development in pediatric-type diffuse high-grade glioma.Cancer metastasis reviews · 2023Review
- Article
- The Intricate Epigenetic and Transcriptional Alterations in Pediatric High-Grade Gliomas: Targeting the Crosstalk as the Oncogenic Achilles' Heel.Biomedicines · 2022Review
- Review
- Current knowledge on the immune microenvironment and emerging immunotherapies in diffuse midline glioma.EBioMedicine · 2021Review
- Development of a prognostic index based on immunogenomic landscape analysis in glioma.Immunity, inflammation and disease · 2021Article
- Advanced Pediatric Diffuse Pontine Glioma Murine Models Pave the Way towards Precision Medicine.Cancers · 2021Review
- Diffuse intrinsic pontine glioma: current insights and future directions.Chinese neurosurgical journal · 2021Review
- Ad-CD40L mobilizes CD4 T cells for the treatment of brainstem tumors.Neuro-oncology · 2020Article
- Immune-stimulatory (TK/Flt3L) gene therapy opens the door to a promising new treatment strategy against brainstem gliomas.Oncotarget · 2020Article
- Magnetic Resonance Imaging-Guided Focused Ultrasound-Based Delivery of Radiolabeled Copper Nanoclusters to Diffuse Intrinsic Pontine Glioma.ACS applied nano materials · 2020Article
- Senescence Induced by BMI1 Inhibition Is a Therapeutic Vulnerability in H3K27M-Mutant DIPG.Cell reports · 2020Article
- Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy.International journal of molecular sciences · 2020Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Diffuse intrinsic pontine glioma (DIPG) is a rare and incurable brain tumor that arises predominately in children and involves the pons, a structure that along with the midbrain and medulla makes up the brainstem. We have previously developed genetically engineered mouse models of brainstem glioma using the RCAS/Tv-a system by targeting PDGF-B overexpression, p53 loss, and H3.3K27M mutation to Nestin-expressing brainstem progenitor cells of the neonatal mouse. Here we describe a novel mouse model targeting these same genetic alterations to Pax3-expressing cells, which in the neonatal mouse pons consist of a Pax3+/Nestin+/Sox2+ population lining the fourth ventricle and a Pax3+/NeuN+ parenchymal population. Injection of RCAS-PDGF-B into the brainstem of Pax3-Tv-a mice at postnatal day 3 results in 40% of mice developing asymptomatic low-grade glioma. A mixture of low- and high-grade glioma results from injection of Pax3-Tv-a;p53(fl/fl) mice with RCAS-PDGF-B and RCAS-Cre, with or without RCAS-H3.3K27M. These tumors are Ki67+, Nestin+, Olig2+, and largely GFAP- and can arise anywhere within the brainstem, including the classic DIPG location of the ventral pons. Expression of the H3.3K27M mutation reduces overall H3K27me3 as compared with tumors without the mutation, similar to what has been previously shown in human and mouse tumors. Thus, we have generated a novel genetically engineered mouse model of DIPG, which faithfully recapitulates the human disease and represents a novel platform with which to study the biology and treatment of this deadly disease.
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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.