ArticleJournal of neuro-oncology2016
Tumor location, but not H3.3K27M, significantly influences the blood-brain-barrier permeability in a genetic mouse model of pediatric high-grade glioma.
Article in Journal of neuro-oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Pediatric low-grade brainstem glioma: a review of current diagnosis and treatment paradigms in the molecular era.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2025Pooled it
- Trial
- Current State-of-the-Art Animal Models of Pediatric Brain Tumors.Brain sciences · 2025Review
- H3K27-Altered Diffuse Midline Glioma of the Brainstem: From Molecular Mechanisms to Targeted Interventions.Cells · 2024Review
- Focused ultrasound-mediated blood-brain barrier opening is safe and feasible with moderately hypofractionated radiotherapy for brainstem diffuse midline glioma.Journal of translational medicine · 2024Article
- PNOC015: Repeated convection-enhanced delivery of MTX110 (aqueous panobinostat) in children with newly diagnosed diffuse intrinsic pontine glioma.Neuro-oncology · 2023Article
- Fifty years of DIPG: looking at the future with hope.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2023Review
- Standardized brain tumor imaging protocols for clinical trials: current recommendations and tips for integration.Frontiers in radiology · 2023Review
- H3K27-altered diffuse midline glioma: a paradigm shifting opportunity in direct delivery of targeted therapeutics.Expert opinion on therapeutic targets · 2023Review
- The intrinsic and microenvironmental features of diffuse midline glioma: Implications for the development of effective immunotherapeutic treatment strategies.Neuro-oncology · 2022Article
- Immunogenic Cell Death Enhances Immunotherapy of Diffuse Intrinsic Pontine Glioma: From Preclinical to Clinical Studies.Pharmaceutics · 2022Review
- Oncohistones: Hijacking the histone code.Annual review of cancer biology · 2022Article
- Tumour immune landscape of paediatric high-grade gliomas.Brain : a journal of neurology · 2021Review
- Computational immune infiltration analysis of pediatric high-grade gliomas (pHGGs) reveals differences in immunosuppression and prognosis by tumor location.Computational and systems oncology · 2021Article
- Defining tumor-associated vascular heterogeneity in pediatric high-grade and diffuse midline gliomas.Acta neuropathologica communications · 2021Article
- Leveraging Open Science Drug Development for PET: Preliminary Neuroimaging ofACS medicinal chemistry letters · 2021Article
- Focused ultrasound mediated blood-brain barrier opening is safe and feasible in a murine pontine glioma model.Scientific reports · 2021Article
- Advancements in Neuroimaging to Unravel Biological and Molecular Features of Brain Tumors.Cancers · 2021Review
- A combined approach of convection-enhanced delivery of peptide nanofiber reservoir to prolong local DM1 retention for diffuse intrinsic pontine glioma treatment.Neuro-oncology · 2020Article
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Pediatric high-grade gliomas (pHGGs) occur with strikingly different frequencies in infratentorial and supratentorial regions. Although histologically these malignancies appear similar, they represent distinct diseases. Recent genomic studies have identified histone K27M H3.3/H3.1 mutations in the majority of brainstem pHGGs; these mutations are rarely encountered in pHGGs that arise in the cerebral cortex. Previous research in brainstem pHGGs suggests a restricted permeability of the blood-brain-barrier (BBB). In this work, we use dynamic contrast-enhanced (DCE) MRI to evaluate BBB permeability in a genetic mouse model of pHGG as a function of location (cortex vs. brainstem, n = 8 mice/group) and histone mutation (mutant H3.3K27M vs. wild-type H3.3, n = 8 mice/group). The pHGG models are induced either in the brainstem or the cerebral cortex and are driven by PDGF signaling and p53 loss with either H3.3K27M or wild-type H3.3. T2-weighted MRI was used to determine tumor location/extent followed by 4D DCE-MRI for estimating the rate constant (K (trans) ) for tracer exchange across the barrier. BBB permeability was 67 % higher in cortical pHGGs relative to brainstem pHGGs (t test, p = 0.012) but was not significantly affected by the expression of mutant H3.3K27M versus wild-type H3.3 (t-test, p = 0.78). Although mice became symptomatic at approximately the same time, the mean volume of cortical tumors was 3.6 times higher than the mean volume of brainstem tumors. The difference between the mean volume of gliomas with wild-type and mutant H3.3 was insignificant. Mean K (trans) was significantly correlated to glioma volume. These results present a possible explanation for the poor response of brainstem pHGGs to systemic therapy. Our findings illustrate a potential role played by the microenvironment in shaping tumor growth and BBB permeability.
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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.