Dr. Zhang is developing a new form of cancer immunotherapy with improved safety and controllability. Redirecting the immune system to launch attacks on tumor cells has emerged as an extremely promising approach to fight cancer. One such strategy, named bispecific T cell engager antibody (BiTE) has shown remarkable efficacy against blood cancers, but it is also associated with severe toxicity. Using tools of synthetic organic chemistry, he aims to build a “chemical switch” that can be used to rapidly tune the activity of BiTE, thus allowing the circumvention of toxic side effects without diminishing therapeutic potential. The ultimate goal of this project is to develop a cancer immunotherapy that can be safely employed at doses effective for the treatment of solid tumors.

CAR T cell therapy, in which a patient’s own immune cells are reprogrammed to recognize and kill cancer, has revolutionized the treatment of blood cancers. Unfortunately, however, a significant portion of treated patients relapse, and CAR T cell therapy for aggressive solid tumors has been largely ineffective. A major roadblock preventing this therapy from curing more patients is the gradual loss of CAR T cells’ ability to kill tumor cells, which results in tumor progression or relapse. Dr. Weber aims to develop optimized killer CAR T cells that stay in the fight against cancer. His lab has developed a novel, high-throughput method of analysis that can be used to identify T cell characteristics, genes, and other biological features that enable CAR T cells to serially kill cancer cells. These insights will provide a roadmap for reprogramming T cells with enhanced tumor killing function, paving the way for more efficacious CAR T cell therapies and potentially other cancer immunotherapies for patients in need.

Many different kinds of mutations affect cancer genomes, but the most recurrent are copy number alterations, resulting in a cancer cell with more or fewer copies of a gene than a normal genome. Dr. Baslan is focused on developing novel therapies that target this class of mutations with an emphasis on deletion events. More specifically, using a combination of advanced algorithms and chemical biology tools, Dr. Baslan is investigating specific vulnerabilities that are associated with deletion events and developing strategies to target these sensitivities in pancreatic cancers. Ultimately, Dr. Baslan aims to explore the generalizability of these therapeutic strategies across cancers, as the majority of cancer genomes contain recurrent deletions.

Kinase pathways control how cells grow, divide, and survive. When they malfunction, they drive many forms of cancer. Abnormal kinase signaling also contributes to resistance against current therapies. Rather than blocking these pathways as traditional treatments do, Dr. Zhou’s research explores ways to change the outcome of aberrant kinase signaling. By redirecting these pathways toward anti-tumor responses, this approach has the potential to provide more durable treatments for cancers that evade existing therapies.

Many cancers evade immune attack by creating a local environment that suppresses immune cells, thereby preventing sustained anti-tumor responses. Dr. Carnevale’s research focuses on dendritic cells, which play a central role in activating cancer-fighting T cells. She seeks to understand how these cells can be reprogrammed to function within tumors despite suppressive signals. In addition, she plans to develop new approaches to engineer dendritic cells so they can physically and functionally coordinate multiple types of T cells within tumors, strengthening local immune responses. Ultimately, this research aims to uncover new strategies to harness dendritic cells to overcome immune resistance in cancer.

While much progress has been made in understanding cancer immune responses, natural killer T (NKT) cells remain understudied. These immune cells act as a bridge between innate and adaptive immunity, rapidly responding to targets through their distinctive receptor. This receptor recognizes lipid molecules, but we currently do not know what tumor lipids can activate NKTs or how NKTs help the immune system attack tumors. Dr. Ferris will investigate how NKTs are involved in the cancer immune response, with the goal of defining how NKT cells are activated by tumor lipids and what those lipids are. This research not only seeks to expand our understanding of fundamental immunological processes but also holds potential to develop immunotherapies to target multiple cancer types using NKT cells.

Subyeta is a graduate of the Macaulay Honors College at Hunter College, New York, where she earned a BA in Biological Sciences with a minor in Public Health. Born and raised in New York City, Subyeta’s personal medical experiences exposed her to the profound impact of medicine and scientific discovery. These experiences, coupled with clinical volunteer work in hospitals and nursing homes, solidified her aspiration to pursue a career that intersects both cancer research and medicine. She explored this passion through research experiences in Dr. Ross Levine’s lab at Memorial Sloan Kettering Cancer Center, where she contributed to projects focused on acute myeloid leukemia. In the summer of 2024, she deepened her research experience as a Harvard-Amgen Scholar at Boston Children’s Hospital, studying clonal hematopoiesis in the lab of Dr. Vijay G. Sankaran, current Sponsor to a Damon Runyon Fellow and Damon Runyon-St. Jude Fellow. Subyeta’s research efforts were recognized with the Horace W. Goldsmith Scholar Award from Macaulay Honors College. In her free time, she enjoys exploring New York City, building Legos, and unwinding with a good movie. 

Isabella [National Mah Jongg League Scholar] was born and raised in Puyallup, Washington. She graduated from Pacific Lutheran University, Tacoma, with a BS in Biological Sciences with minors in Chemistry and Business Administration. Her motivation to pursue cancer research stems from her own health struggles, which sparked a strong interest in human health and biology from an early age. Over time, that interest has evolved into a deep intellectual curiosity about the molecular mechanisms of cancer. During her undergraduate studies, she had the opportunity to work as a summer intern in the laboratory of Christina M. Termini, PhD, where she investigated how inhibiting isoprenoid production impacts hematopoietic stem cell (HSC) maintenance, expansion, and survival. Her ultimate goal is to contribute meaningfully to improving patient outcomes by developing safe, accessible, and effective cancer treatments. Outside the lab, she enjoys being outdoors, cooking, dancing, and spending quality time with her family. 

Many cancers develop when crucial “cellular machinery” malfunctions. One component of this machinery is the ring ATPase, which harnesses the energy from ATP to perform essential tasks such as maintaining protein homeostasis and ensuring genome stability—processes vital for preventing uncontrolled cell growth. Understanding precisely how these complex human ring ATPases operate and coordinate their actions remains a significant challenge. Dr. Xu’s [HHMI Fellow] research focuses on a mechanically similar, yet structurally simpler, ring ATPase found in the φ29 bacteriophage. By filming high-resolution “movies” of this viral ring ATPase in action using advanced single-molecule techniques, Dr. Xu aims to uncover the fundamental principles of its mechanochemical cycle. This will reveal, step-by-step, how it converts chemical energy into the precise mechanical forces and coordinated movements required to stabilize DNA. This work is relevant to a range of cancers where cellular ring ATPases are dysregulated, and the insights gained could pave the way for novel therapeutic strategies targeting these essential molecular machines. Dr. Xu received his PhD from Vrije Universiteit, Amsterdam, his MS from the University of Chinese Academy of Sciences, Beijing, and his BS from Northeast Agriculture University, Harbin.

Genetic disturbances can disrupt normal cellular programs, promote unrestricted proliferation (i.e., tumor growth), and expose vulnerabilities that can be targeted therapeutically. However, how cells dynamically respond to such changes over time remains incompletely understood. Dr. Torre will use cutting-edge genetic tools, such as CRISPR and single-cell RNA sequencing, to study the precise sequence of molecular events triggered upon silencing of key regulators of cell identity and proliferation in human cells. By combining single-cell data with advanced statistical modeling, this work will reveal how gene perturbations dynamically alter cellular networks and drive survival or cell death, thus helping inform the development of novel cancer treatments. Dr. Torre received his PhD from the Icahn School of Medicine at Mount Sinai, New York, and his BS from the University of Trieste, Trieste.