My Research Journey

My interests 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 me with my initial research framework, including a 9-weeks summer undergraduate research paid internship at the University of Missouri-Columbia. After my undergraduate years, my interest in an academic research career blossomed, leading me to seek more opportunities in order to enrich my skill set in the lab, and my understanding of hypothesis testing and the scientific process. Therefore, in 2012 I entered the NIH Post-Baccalaureate Research Program (NIH-PREP) at the University of South Carolina-Columbia. This experience inspired me to pursue a Master’s degree in Biological Sciences.

My master's thesis was very intellectually stimulating and focused on “Tp53 and Hras Influence on HPV16 E7 Expression in HPV16-Transformed Human Keratinocytes”. I significantly increased my knowledge and appreciation for cellular, molecular and developmental biology. This study focused on the molecular characteristics of HPV-inactive tumors and the molecular mechanisms by which these tumors may lose E6 and E7 oncogene expression. This project was aimed towards uncovering specific molecular mechanisms by which HPV-transformed cells can escape the need for continuous E6/E7 expression for proliferation. We tested whether mutated H-Ras (H-RasV12) expression results in changes in E7 mRNA and Rb protein levels in HKc. Our results indicated that H-RasV12 partially replaces E7 function. Additionally, we demonstrated that shRNA-mediated p53 knock-down could be achieved in human keratinocyte lines transformed with HPV16 (HKc/HPV16). In addition to a motivating project, this intense full-time research experience allowed me to gain a better grasp of scientific workflows and objectives, and most importantly, initiated my long-term goal of becoming a principal investigator.

After acquiring my masters in Biological science (with a focus in Cellular, Molecular and Developmental Biology) in June 2015, I was offered an opportunity to work at Moffitt Cancer Center as a research associate. I was fortunate to have been part of Dr. David Morse’s team and participated in a very exciting project which led to two papers that I co-authored. Prior to joining the group, Ac-DOTA-MC1RL conjugate was synthesized in high radiochemical yield and purity and was tested in vitro for biostability and for MC1R-specific cytotoxicity in uveal melanoma cells, and the lanthanum-DOTA-MC1RL analog was tested for binding affinity. I was invited to join this multidisciplinary group of scientists to test non–tumor-bearing BALB/c mice for maximum tolerated dose and biodistribution; and studied tumors for biodistribution and efficacy on severe combined immunodeficient mice bearing uveal melanoma tumors or engineered MC1R-positive and -negative tumors. In addition, radiation dosimetry was calculated using biodistribution and kinetic data. We demonstrated significantly prolonged survival and decreased metastasis burden after a single administration of 225Ac-DOTA-MC1RL; this demonstrated potential for the clinical translation of 225Ac-DOTA-MC1RL as a novel therapy for metastatic uveal melanoma. I was able to personally experience how pre-clinical research can have a direct positive effect on an affected clinical population of study, since those previous findings were needed to allow for approval for a phase 1 clinical trial. This experience, most importantly, solidified my decision to pursue a PhD.

I joined Biomedical Sciences at Florida State University College of Medicine in 2018, I knew this PhD program would allowed me to further develop my interests and skills in neuroscience, while also grounding me solidly in a human disease-focused curriculum. Initial laboratory rotations gave me an opportunity to sample multiple aspects of cell biology, biochemistry and neuropharmacology. I am engaged in thesis work in the laboratory of Dr. Gregg Stanwood; his laboratory 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 expression of D1 receptors in a specific subpopulation of cerebral cortical interneurons has previously undiscovered roles in regulating mood and cognition, may contribute to adaptive mechanisms sub-serving behavioral and cognitive resilience, and may ultimately serve as a previously unexplored target for the treatment of mood and psychotic disorders. More specifically, we have 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. We may therefore have discovered a new and exciting mechanism to treat mood disorders, particularly in a subpopulation of patients that do not respond effectively to other antidepressants. In ongoing experiments, I am exploring roles for cortical interneurons and cortical dopamine signaling in mood regulation, stress responses, and synaptic stabilization using a combination of behavioral, neurochemical and molecular approaches.