Magdalena Zakrzewska

TL;DR: The presence of H3F3A/ATRX-DAXX/TP53 mutations was strongly associated with alternative lengthening of telomeres and specific gene expression profiles, suggesting that defects of the chromatin architecture underlie paediatric and young adult GBM pathogenesis.

TL;DR: It is demonstrated that each H3F3A mutation defines an epigenetic subgroup of GBM with a distinct global methylation pattern, and that they are mutually exclusive with IDH1 mutations, which characterize a third mutation-defined subgroup.

TL;DR: Results suggest that mutations disrupting the histone code at H3K36, including H3.3 G34R/V, IDH1 and/or SETD2 mutations, are central to the genesis of hemispheric HGGs in older children and young adults.

TL;DR: Detailed integrated genetic and epigenetic analyses of ETMR samples suggest a potential oncogenic re-engagement of an early developmental program in ETMR via epigenetic alteration mediated by an embryonic, brain-specific DNMT3B isoform.

TL;DR: Constitutional and somatic FGFR1 alterations and MAP kinase pathway activation are key events in the pathogenesis of DNET and point the way towards existing targeted therapies.