Claudia Manriquez Roman is a graduate student at Mayo Clinic Graduate School of Biomedical Sciences in Rochester, Minnesota. She received her Bachelor of Science in General Microbiology (Summa Cum Laude) and Master of Science in Biological Sciences from the University of Texas at El Paso (UTEP). She is currently a pre-doctoral candidate at Mayo Clinic Graduate School of Biomedical Sciences in the Virology and Gene Therapy Track and Regenerative Sciences.
As an undergraduate student at UTEP, Claudia led two research projects which involved the evaluation of Chagas' disease (ChD) in animal reservoirs in El Paso, Texas and the expression and purification of Leishmania major methionine aminopeptidase-1 (LmMetAP1), a target for chemotherapeutic agents against cutaneous Leishmaniasis. The animal reservoirs project was an epidemiological study that attempted to identify T. cruzi in stray dogs and cats in the El Paso area. Both these projects were funded by two undergradaute research fellowship that were awarded from the UTEP Campus of Undergraduate Research Initiatives (COURI) program and MERITUS program. As a Master's student, her thesis project focused on the genetic disruption and characterization of UDP-Galactopyranose Mutase (UGM) in T.cruzi mediated by CRISPR/Cas9 via CRISPR/Cas9. Both her undergraduate and master's project at UTEP guided her in understanding the structural, biological and immunological roles of T. cruzi.
Currently, Claudia is pursuing her PhD in Virology and Gene Therapy, as well as Regenerative Sciences, at Mayo Clinic under the mentorship of Dr. Saad Kenderian. Her thesis project aims to modulate CART cell activation and prevent apoptosis as a strategy to enhance its anti-tumor efficacy with the sole goal of translating this therapeutic application into clinical trials. Overall, the aims of her thesis projects are 1) to determine if GM-CSF (Granulocyte Macrophage Colony Stimulating Factor) disruption modulates apoptosis, activation and expansion on CART cells, 2) to enhance CAR-T cell activation via modulation of tumor antigen and 3) to define the role of TNFR2 (Tumor Necrosis Factor Receptor 2) in CAR-T cells as a strategy to prevent apoptosis and enhance CAR-T cell effector functions.
