Nada Jabado

This study shows that USP15 deletion in astrocytes and microglia reduces neuroinflammation and slows synucleinopathy progression in mice, with human data linking USP15 expression to Parkinson's disease risk.

The paper identifies ependymomas as originating from the pre-neural crest/roof plate lineage using single-cell transcriptomics and lineage tracing.

The paper shows that H3K27me3 spreading regulates chromatin architecture and gene repression, with implications for cell fate and tumor development.

This study examines the dynamic changes in the immune microenvironment of paediatric solid tumours over time, revealing a shift toward immunosuppressive and tolerogenic states.

This study investigates how BLBS-causing H3.3 mutations affect H3K36 methylation and effector protein binding, revealing molecular similarities across mutations.

This study identifies CD155 as a key regulator of tumor growth and immune evasion in diffuse midline glioma, showing that targeting CD155 or its downstream target FOXM1 can inhibit tumor progression.

The paper identifies O-mannosylation and protein maturation as therapeutic targets in BRAF fusion oncogenesis by showing their necessity for fusion-induced transformation.

This study identifies FGFR alterations in pediatric gliomas, their association with specific histologies, and their response to targeted therapies.

The paper identifies SUZ12's nucleic acid-binding domain as critical for regulating PRC2 activity in H3 K27M gliomas, showing how it constrains enzymatic function and maintains targeted gene silencing.

This study investigates age-dependent tumor-immune interactions in pediatric cancer using mouse models and patient samples, finding that pediatric tumors have distinct immune profiles and poor response to immunotherapy, which can be improved by modulating the tumor microenvironment.

The paper investigates how multiple FGFR1 mutations affect tumorigenic mechanisms in glioneuronal tumors by analyzing their interactomes and functional impacts.

This study investigates the combination of DNA methyltransferase inhibitor decitabine and PD-1 inhibitor in high-risk pediatric brain tumor models, finding improved survival in some subtypes.

The paper uses single-cell transcriptomics to show childhood cerebellar tumors mirror fetal cerebellar cell lineages, linking tumor subtypes to specific developmental stages.