I continued my education at UNC-Chapel Hill by obtaining a PhD in Genetics and Molecular Biology in the lab of Terry Van Dyke, where I designed and created a new transgenic mouse model of prostate cancer that demonstrated the important role the microenvironment plays in tumor progression. As a Damon Runyon postdoctoral fellow with Dr. Hong Wu at UCLA, I chose to focus on pancreatic adenocarcinoma (PDAC), an under-researched disease with a high mortality rate, poor prognosis, and few therapeutic options. I developed mouse models to recapitulate the complexities of human PDAC in order to uncover new therapeutic strategies that could be translated to the human disease.
My lab utilizes genetic models to address fundamental questions about how cell autonomous (e.g. genetic alteration) and cell non-autonomous (e.g. inflammation) mechanisms affect pancreatic cancer development. My focus is to uncover the central mechanisms through which the microenvironment aids tumor initiation, progression, and therapeutic resistance. A better understanding of these processes will not only help the development of more effective treatments for pancreatic cancer, but can be expanded to applications in a wide range of other diseases.