Brain-wide circuit remodeling in cancer

Brain cancer cells not only infiltrate throughout the brain but also depend on the function of neurons and circuits in distant regions, a phenomenon which has been increasingly recognized as a vicious cycle underpinning brain cancer progression. We investigate the brain regions responsible for the behavioral and cognitive symptoms that frequently occur in cancer patients and worsen disease prognosis. Our goal is to uncover the fundamental principles of long-range communication between cancer and brain-wide circuits, leveraging this understanding to develop novel therapeutic strategies that preserve brain function and improve prognosis in cancer patients.

Clinical translation: from bench to bedside

We are committed to translating our understanding of neuron-cancer networks into tangible benefits for patients with brain tumors. We test pharmacological strategies that modulate neuronal activity and disrupt tumor-promoting circuit interactions, with the dual aim of slowing tumor progression and improving patients' quality of life by alleviating behavioral and cognitive symptoms. In parallel, we study how targeting these networks intersects with current treatment modalities to identify rational combinations and avoid unintended interference. By bridging mechanistic discovery with clinical application, we aim to translate our understanding of neuron-cancer circuitry into therapies that meaningfully extend and improve the lives of patients.

Color-enhanced MRI scans of two human brains viewed from above, showing various brain structures in colors like purple, blue, and green.

Microenvironmental contributions to circuit remodeling in brain cancer

Non-neuronal cell types - including microglia, astrocytes, and oligodendroglia - are known to contribute to circuit remodeling in both the healthy and cancer-infiltrated brain. These cells can sense changes in electrical activity and also modulate it to affect brain-wide circuits. Our laboratory investigates how these brain-resident cells actively participate in neuron-cancer networks and what mechanisms recruit them into this electrically active circuitry. Our goal is to leverage this understanding to reprogram cell types and states in order to dampen electrical activity within tumor networks.