Cancer is fundamentally a disease of lost tissue integrity, in which cells fail to properly coordinate and regulate one another, leading to abnormal cell growth and invasion within tissues. Dr. Hung aims to uncover basic principles of how cells combine chemical and mechanical signals to maintain tissue integrity. Using flatworms that are capable of tissue regeneration as a model, he will employ live whole-worm imaging of tissue regeneration to study mechanical and chemical signaling at the cellular level. This project will provide key insights about the logic of multicellular signaling circuits for maintaining normal tissue integrity and clues about how these signaling circuits can be dysregulated in cancer. Dr. Hung received his PhD from Stanford University, Stanford, and his BS from the University of Washington, Seattle.

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.

Cells have a built-in defense system that detects double-stranded RNA (dsRNA), a molecule often associated with viruses. Although this system evolved to fight microbial infections, activating it can also help the body recognize and attack cancer, especially when combined with treatments that make tumors easier for immune cells to detect. However, tumors can escape this immune pathway by producing high levels of a protein called ADAR, which edits dsRNA by changing one of its building blocks, adenosine, into inosine. These edits prevent the dsRNA from being recognized, allowing cancer cells to stay hidden even during treatment. Dr. Nichols’ [Merck Fellow] research aims to understand how these RNA changes block immune detection and to identify which RNA molecules are most likely to trigger an immune response. By uncovering how cancer cells use this editing process to escape detection, he hopes to support the development of better immunotherapy treatments. Dr. Nichols received his PhD from the University of Colorado, Anschutz Medical Campus, Aurora, and his BA from Lewis and Clark College, Portland.