Athanassios Dovas

Paired Tumor Biopsies Reveal Spatiotemporal Myeloid Remodeling After Local Chemotherapy in Glioblastoma

This study examines the spatiotemporal myeloid response to chemotherapy in glioblastoma using multiple models, showing chemotherapy-induced genotoxic stress and inflammatory remodeling in myeloid cells.

Microtubule Acetylation Regulates the Malignant Phenotype of Glioblastoma and is a Promising Therapeutic Target

This study identifies ATAT1 as a therapeutic target in glioblastoma by showing its role in promoting tumor invasion, proliferation, and resistance, with potential for combination therapies.

IDH-mutant inhibitors enhance the sensitivity of IDH1-mutant gliomas to cysteine-methionine deprivation and ferroptosis

This study shows that IDH1-mutant glioma cells are more sensitive to cysteine-methionine deprivation and ferroptosis inducers, and that IDH inhibitors enhance this sensitivity.

MT-125 Inhibits Non-Muscle Myosin IIA and IIB, Synergizes with Oncogenic Kinase Inhibitors, and Prolongs Survival in Glioblastoma

Glioma-Induced Alterations in Excitatory Neurons are Reversed by mTOR Inhibition

This study investigates how mTOR inhibition reverses glioma-induced changes in excitatory neurons, showing effects on mRNA, dendritic spines, and neuronal activity.

Resistance to Spindle Inhibitors in Glioblastoma Depends on STAT3 and Therapy Induced Senescence

This study identifies STAT3 as a key driver of resistance to spindle inhibitors in glioblastoma, showing that therapy-induced senescence contributes to drug resistance by promoting quiescence and secreting factors that induce quiescence in proliferating cells.

Glioma-induced alterations in neuronal activity and neurovascular coupling during disease progression

This study tracks glioma progression in mice, showing decreased neuronal synchrony, disrupted neurovascular coupling, and seizure-related hypoxia in infiltrated cortex.

Single-cell based elucidation of molecularly-distinct glioblastoma states and drug sensitivity

The paper identifies four molecularly distinct glioblastoma subtypes using single-cell protein-activity analysis and shows drug sensitivity is state-dependent.