David A. Nathanson

High-throughput spheroid profiling reveals BMP-driven rewiring of glioma cell death responses

This study uses high-throughput spheroid profiling to show BMP2 and BMP4 rewire glioma cell death responses by suppressing standard therapies and priming for lipid-dependent necrosis.

Glutamatergic neuron-tumor synapses shape human glioblastoma cell states through radial glia plasticity

This study shows that glutamatergic neuron-tumor synapses influence glioblastoma cell states by modulating radial glia plasticity and transcriptional programs.

Predictable clonal hierarchies from restricted progenitors provide a framework for cell type-specific therapies in glioblastoma

The paper maps clonal hierarchies in glioblastoma using lineage-resolved single-cell data, revealing multiple non-redundant progenitors and identifying cell type-specific therapeutic targets.

Human Organoid Tumor Transplantation Identifies Functional Glioblastoma - Microenvironmental Communication Mediated by PTPRZ1

The paper uses a human organoid tumor transplantation system to study glioblastoma-microenvironment interactions, identifying PTPRZ1 as a key mediator of intercellular communication.

A Human Tumor-Immune Organoid Model of Glioblastoma

Autologous co-culture of patient glioblastoma cells and matched peripheral blood mononuclear cells in human cortical organoids (iHOTT) preserves tumor-immune crosstalk and recapitulates patient T cell responses to pembrolizumab.

Beyond Cell Cycle Control: CDKN2A Loss Orchestrates NAD⁺ Metabolic Plasticity and NAMPT Inhibitor Sensitivity in Glioblastoma

The paper shows CDKN2A loss in glioblastoma affects NAD+ metabolism and increases sensitivity to NAMPT inhibitors, beyond its role in cell cycle control.

A neurovascular progenitor sits at the nexus of glioblastoma lineage trajectories

This study identifies a neurovascular progenitor cell type in glioblastoma that links distinct malignant lineages and influences tumor composition and survival.

Combined Treatment with Dopamine Receptor Antagonists and Radiation Creates a Metabolic Vulnerability in Mouse Models of Glioblastoma

This study shows that combining quetiapine, atorvastatin, and radiation extends survival in glioblastoma mouse models by exploiting a metabolic vulnerability.