Fujifilm Fellowship

I grew up in New York City and attended Stanford University, where I earned my BS in Bioengineering and MS in Computer Science. Previously, I conducted research in bioengineering, immuno-oncology, computational biology, genetics, and AI at Stanford University, Karolinska Institutet, ETH Zürich, Memorial Sloan Kettering Cancer Center, and Rockefeller University. My undergraduate and master’s research focused on characterizing and therapeutically targeting an immune checkpoint protein implicated in cancer and autoimmune diseases. I also completed software engineering internships at Verily Life Sciences and Microsoft. For my PhD, I was excited to return to the East Coast and immerse myself in the unique biotech scene encompassing Harvard Medical School and Boston. The network of hospitals and academic institutions here offers me an incredible opportunity to pursue research in cellular therapy.

CAR T cell therapy has revolutionized the treatment of hematological malignancies and can lead to cancer remission. Although progress has been made in CAR T cell therapy for liquid tumors, solid tumors pose challenges. The effects of CAR T cell therapy are limited in solid tumors due to a combination of factors, including an immunosuppressive tumor microenvironment, inadequate tumor trafficking and infiltration, tumor heterogeneity, and antigen escape. I aim to engineer CAR T cells to improve the treatment of solid cancers.

I grew up near Los Angeles, CA, studied molecular biology at Brigham Young University, and was a research fellow at the National Institute of Allergy and Infectious Diseases during the SARS-CoV-2 pandemic. Before graduate school, I had accrued research experience in epigenetics, structural biology, and immunology. Harvard’s immunology PhD program offered a unique opportunity to conduct research at the intersection of these fields and allowed me to pursue basic research in a therapeutically relevant discipline.

The genes in the Major Histocompatibility Complex locus play critical roles in an immune response. They are also major risk factors for various autoimmune diseases, and their regulatory elements that contribute to disease susceptibility are poorly understood. My work aims to paint a better picture of how these genes are regulated differently across individuals, and how variable regulation contributes to autoimmunity. The results of this work can advance autoimmune diagnostics and provide insight for early-intervention therapeutics.

I was born and raised in Wilmington, Delaware. I completed my B.S. and M.S. in biochemistry at Brandeis University, where I investigated the biosynthetic mechanisms of sesquiterpene synthases in the lab of Dr. Daniel Oprian. This experience, combined with recent advances in protein structure prediction, sparked my interest in using powerful new computational methods to investigate novel protein-ligand interactions. I chose to pursue this interest at HMS because it offers a uniquely collaborative and multidisciplinary environment for translating insights from computational modeling into therapeutic development.

Deubiquitinases comprise a family of proteases that catalyze the cleavage of ubiquitin from other proteins, thereby altering the fate of their substrates. Deubiquitinases are important modulators of cell cycle control, apoptosis, and DNA damage repair, and are implicated in cardiomyopathies, neurodegenerative disorders, cancer, and more. My research combines bioinformatic techniques with protein structure prediction to identify the roles deubiquitinases have in human disease. I also employ protein-ligand co-folding and molecular dynamics simulations to accelerate the development of small-molecule therapeutics that specifically modulate deubiquitinase activity.