What genetic alterations are commonly associated with Diffuse Midline Gliomas, aside from IDH1 mutation and EGFR amplification, and often linked to p53 overexpression, ATRX loss, and monosomy 10?
[' transgenes are sufficient to reduce the amounts of H3K27me3 in vitro and in vivo.", "In contrast, thalamic gliomas with wild-type H3F3A had DNA methylation profiles similar to those of hemispheric glioblastomas.CONCLUSION: We found that high-grade thalamic gliomas from young adults, like those from children and adolescents, frequently had H3F3A K27M.", "Gliomas with H3F3A K27M from pediatric or young adult patients had similar, characteristic DNA methylation profiles.", "Although the K27M mutation was frequently observed in adult brainstem and thalamic gliomas, this mutation tended to be associated with a poorer prognosis in brainstem gliomas but not in thalamic gliomas.", "Diffuse Midline Gliomas with Histone H3-K27M Mutation: A Series of 47 Cases Assessing the Spectrum of Morphologic Variation and Associated Genetic Alterations.", "In this series, histone H3-K27M mutation was mutually exclusive with IDH1 mutation and EGFR amplification, rarely co-occurred with BRAF-V600E mutation, and was commonly associated with p53 overexpression, ATRX loss (except in pontine gliomas), and monosomy 10.", "The H3.3 K27M mutation results in a poorer prognosis in brainstem gliomas than thalamic gliomas in adults.", "K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas.", "Recently, sequencing of tumor cells revealed that histone H3 is frequently mutated in pediatric HGG, with up to 78\\u00a0% of diffuse intrinsic pontine gliomas (DIPGs) carrying K27M and 36\\u00a0% of non-brainstem gliomas carrying either K27M or G34R/V mutations.", "Interestingly, the G34 mutations, the K36M mutations, and the majority of K27M mutations occur in genes encoding the replacement histone H3.3."]']
The H3.3 K27M mutation is commonly associated with Diffuse Midline Gliomas, aside from IDH1 mutation and EGFR amplification, and often linked to p53 overexpression, ATRX loss, and monosomy 10.
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