My interest in scientific research began with my admission to the Research Initiative for Scientific Enhancement (MBRS-RISE) program my sophomore year of college. This was my first introduction to neuroscience research; I analyzed the function of palmitoyl-protein thioesterase 2 (PPT-2) in zebrafish. The RISE program opened up many opportunities for me and provided my initial research framework, including a nine-week, paid summer undergraduate research internship at the University of Missouri-Columbia. After my undergraduate years, my interest in an academic research career grew, leading me to seek more opportunities to enrich my lab skills and my understanding of hypothesis testing and the scientific process. In 2012, I entered the NIH Post-Baccalaureate Research Program (NIH-PREP) at the University of South Carolina-Columbia, an experience that inspired me to pursue a master's degree in biological sciences.
My master's thesis, "Tp53 and Hras Influence on HPV16 E7 Expression in HPV16-Transformed Human Keratinocytes," was intellectually stimulating and significantly deepened my knowledge of cellular, molecular, and developmental biology. The study focused on the molecular characteristics of HPV-inactive tumors and the mechanisms by which such tumors may lose E6 and E7 oncogene expression, aiming to uncover how HPV-transformed cells can escape the need for continuous E6/E7 expression to proliferate. We tested whether mutated H-Ras (H-RasV12) expression results in changes in E7 mRNA and Rb protein levels in human keratinocytes. Our results indicated that H-RasV12 partially replaces E7 function, and we also demonstrated that shRNA-mediated p53 knockdown could be achieved in human keratinocyte lines transformed with HPV16. Beyond a motivating project, this intense, full-time research experience gave me a much better grasp of scientific workflow and objectives — and initiated my long-term goal of becoming a principal investigator.
After completing my master's in biological sciences (with a focus in cellular, molecular, and developmental biology) in June 2015, I joined Moffitt Cancer Center as a research associate, working as part of Dr. David Morse's team on a project that led to two papers I co-authored. Prior to my joining the group, an Ac-DOTA-MC1RL conjugate had been synthesized in high radiochemical yield and purity and tested in vitro for biostability and MC1R-specific cytotoxicity in uveal melanoma cells, with the lanthanum-DOTA-MC1RL analog tested for binding affinity. I joined this multidisciplinary group to test non–tumor-bearing BALB/c mice for maximum tolerated dose and biodistribution, and to study tumor biodistribution and efficacy in severe combined immunodeficient mice bearing uveal melanoma tumors or engineered MC1R-positive and -negative tumors. We also calculated radiation dosimetry using biodistribution and kinetic data, and demonstrated significantly prolonged survival and decreased metastasis burden after a single administration of 225Ac-DOTA-MC1RL — findings that supported the clinical translation of 225Ac-DOTA-MC1RL as a novel therapy for metastatic uveal melanoma and helped enable approval for a Phase 1 clinical trial. Seeing pre-clinical research have a direct, positive effect on an affected clinical population solidified my decision to pursue a PhD.
I joined Biomedical Sciences at Florida State University College of Medicine in 2018, drawn to a program that would let me develop my interests in neuroscience while grounding me solidly in a human-disease-focused curriculum. Initial laboratory rotations let me sample multiple aspects of cell biology, biochemistry, and neuropharmacology, and I ultimately joined the laboratory of Dr. Gregg Stanwood, whose group studies the neurodevelopmental basis of brain disorders with an emphasis on gene–environment interactions and susceptibility to mental health diseases. My dissertation project focuses on the effect of neuron-subtype-specific loss of dopamine D1 receptors during a critical period of brain development in mice. Our data suggest that D1 receptor expression in a specific subpopulation of cerebral cortical interneurons has previously undiscovered roles in regulating mood and cognition, may contribute to adaptive mechanisms underlying behavioral and cognitive resilience, and may ultimately serve as a previously unexplored target for treating mood and psychotic disorders. Specifically, we identified significant antidepressant-like effects in adult conditional knockout mice, accompanied by reduced basal circulating levels of the stress hormone corticosterone and altered expression of specific neurotrophins and synaptic plasticity genes in the prefrontal cortex — a potentially new mechanism to treat mood disorders, particularly in patients who don't respond effectively to other antidepressants. In ongoing experiments, I continue exploring the roles of cortical interneurons and cortical dopamine signaling in mood regulation, stress responses, and synaptic stabilization, using a combination of behavioral, neurochemical, and molecular approaches.