Our lab is focused on the functions of oncogenic drivers found in several types of both pediatric and adult brain tumors, including Glioma, Meningioma, and Supratentorial (ST) Ependymoma. Pediatric and adult tumors can differ dramatically in their genetic markup and their underlying mutations. While adult cancers frequently harbor a highly aberrant genome with gains and losses of entire chromosomal regions, the genomes of pediatric cancers are oftentimes relatively more stable and are enriched for more defined mutations, such as gene fusions. Pediatric cancers that harbor targetable gene fusions are ideal candidates for targeted therapies. However, even though clinical trials targeting gene fusions have achieved promising initial responses (such as Larotrectinib in NTRK fusion positive tumors), these effects are usually only partial, and the tumors ultimately recur due to the occurrence of resistance mutations. Our lab utilizes genetically-engineered mouse models in order to study how specific oncogenes (such as gene fusions) drive tumor development, how these tumors respond to targeted therapies in vivo, and what mechanisms of resistance lead to treatment failure and tumor recurrence in order to develop novel adjuvant therapies that can increase treatment success and survival.