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Histone H3.3 K27M Accelerates Spontaneous Brainstem Glioma and Drives Restricted Changes in Bivalent Gene Expression
Highlights • H3.3 K27M mutation enhances neural stem cell self-renewal • Neonatal PDGFRα activation and Trp53 loss induces supratentorial and brainstem glioma • H3.3 K27M preferentially accelerates hindbrain tumorigenesis • H3.3 K27M drives bivalent gene activation associated with neurodevelopment in DIPG Summary Diffuse intrinsic pontine gliomas (DIPGs) are incurable childhood brainstem tumors with frequent histone H3 K27M mutations and recurrent alterations in PDGFRA and TP53.
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