Student Presenter(s): James Virga
Faculty Mentor: Haotian Zhao
School/College: Osteopathic Medicine, Old Westbury

Tumors of the choroid plexus (CP) arise from neuroepithelium and predominantly occur in children. During development, specific developmental programs assure the fate of CP epithelial cells via SHH signaling, resulting in a pseudostratified sheet of multiciliated epithelial cells. Phenotypically, CP tumors exhibit a monociliated phenotype driven by repression of the Gemc1 transcriptional network. As previously shown, mouse models with persistent SHH and NOTCH signals, or loss of Trp53 and Rb, result in CP tumors recapitulating CP carcinoma (CPC) in humans, featuring monociliated epithelial cells. Pediatric cancers are notorious for displaying dysregulated transcriptional mechanisms resulting in tumorigenesis. Master transcription factor Sox2 plays a role in development in the ventricular zone, CP, and roof plate, while also contributing to cancer stemness, tumorigenesis, and drug resistance. Sox2 is highly expressed in roof plate progenitors yet significantly reduced in epithelial cells. Gene expression studies demonstrate aberrant Sox2 expression in human CP tumors, implicating a role in tumor development. Considering the potential for Sox2 to coordinate various transcriptional programs in development and cancer, we hypothesize that Sox2 plays a vital role in CP tumor formation.