D. Hambardzumyan

H3.3-G34R Mutation-Mediated Epigenetic Reprogramming Leads to Enhanced Efficacy of Immune Stimulatory Gene Therapy in Diffuse Hemispheric Gliomas

This study shows that H3.3-G34R mutations reprogram the tumor immune microenvironment in diffuse hemispheric gliomas, enhancing the efficacy of immune stimulatory gene therapy and leading to long-term survival in treated mice.

BRAF/MEK Inhibition Induces Cell State Transitions Boosting Immune CheckpointSensitivity in BRAFV600E-mutant Glioma

This study shows that BRAF/MEK inhibition induces cell state transitions in BRAFV600E-mutant gliomas, leading to PD-L1 upregulation and immune evasion, which can be overcome by combining with immune checkpoint inhibition.

The novel compensatory reciprocal interplay between neutrophils and monocytes drives cancer progression

This paper shows that eliminating monocyte chemoattraction increases neutrophil infiltration in glioblastoma, promoting tumor aggression, and that targeting both monocytes and neutrophils improves survival in mouse models.

A paracrine circuit of IL-1b/IL-1R1 between myeloid and tumor cells drives glioblastoma progression

The paper identifies a paracrine IL-1β/IL-1R1 circuit between myeloid and tumor cells that drives glioblastoma progression and shows that antagonizing this circuit reduces tumor growth and extends survival.

Spatial patterning and immunosuppression of glioblastoma immune contexture in hypoxic niches

This study identifies hypoxia-driven immunosuppression in glioblastoma by tracking TAM dynamics and reveals niche factors that promote immunotolerant states and poor prognosis.

Cell Surface Multimeric Assemblies Regulate Canonical and Noncanonical EphA2 Receptor Tyrosine Kinase Signaling

This study identifies molecular interfaces that mediate EphA2 receptor assembly and distinguishes between canonical and noncanonical signaling pathways.

Brain aging-dependent glioma traits reversible by NAD+/BDNF-mediated neuronal reactivation

This study shows that aging reduces neuronal signaling in gliomas, but NAD+ and BDNF can reverse these effects, improving outcomes in older mice.

G-CSF SECRETED BY EPIGENETICALLY REPROGRAMMED MUTANT IDH1 GLIOMA STEM CELLS REVERSES THE MYELOID CELLS'-MEDIATED IMMUNOSUPPRESSIVE TUMOR MICROENVIRONMENT

The paper shows that mIDH1 glioma stem cells secrete G-CSF, which reprograms myeloid cells to become non-immunosuppressive, altering the tumor microenvironment.