My goal as a cellular & molecular biologist is to uncover actionable therapeutic strategies through discovery of molecular targets for the treatment of Gastrointestinal (GI) and central nervous system (CNS) diseases to improve disease outcomes. During my doctoral work, I described a mechanism through which CNS glial cells, known oligodendrocyte progenitor cells, respond to the extracellular matrix protein laminin to promote proliferation through inducing metalloprotease mediated cleavage of its receptor, dystroglycan. I was the first to develop and established protocols to study metalloproteases in the lab.

To continue training in molecular mechanisms of disease in addition to pedagogical training, I was awarded a postdoctoral fellowship through the Alliance for Graduate Education in the Professoriate-Transformation (AGEP-T) program at Stony Brook University, funded by the National Science Foundation. In the lab of Dr. Thomas Floyd, I described how a group of glial cells known as astrocytes respond to mild-moderate hypoxic stress in vitro and in vivo through molecular mechanisms that involve hypoxic response systems and metabolic adaptation to maintain homeostatic functions that impact cognitive processes such as memory (Leiton et al., in review). I was among a selected group of investigators accepted into an NIH-sponsored Metabolomics training workshop at the University of Alabama, and through this training, I developed protocols to study metabolomic flux in our model systems. I also had the opportunity to train and teach students ranging from high school to medical school, through experimental design, execution, analysis, and interpretation in our laboratory, leading them to present their work at local and national competitions and conferences.

With a strong interest in translational research, I am currently continuing my postdoctoral training in the lab of Dr. Kenneth Shroyer in the department of Pathology at Stony Brook University, where my goal is to uncover molecular mechanisms of how a prognostic biomarker that our laboratory discovered, Keratin 17, drives pancreatic cancer aggression. Building on our lab’s previous discovery that this intermediate filament protein can solubilize and translocate to the nucleus, we have discovered that it can also target tumor suppressor proteins and regulate transcription, two major mechanisms that may change cellular behaviors and drive tumor aggression. We are exploring strategies for therapeutic targeting that may additionally synergistically result in sensitivity to existing chemotherapeutics. In addition to establishing pancreatic cancer models, continuing to teach and train students, I have most recently initiated grantsmanship training under the mentorship of my research advisor and study collaborators.