Ewing sarcoma is a rare and aggressive bone cancer that affects children and young adults. A key genetic fusion in these tumors disrupts normal cell behavior, driving rapid growth and weakening the body’s immune defenses. Studying this cancer in the lab is difficult because traditional cell cultures cannot fully capture the diversity of cells and immune interactions present in real tumors. Clevenger aims to bridge this gap by using advanced single-cell techniques to study how Ewing sarcoma cells build and reorganize their internal structures. By combining these novel approaches with analyses of patient tumor samples, her research will uncover how changes inside cancer cells help them evade the immune system and will point to new strategies for developing combination therapies for pediatric solid tumors. Clevenger received her PhD from Texas A&M University and her BS from Trinity University. 

Ewing sarcoma remains one of the most difficult pediatric cancers to treat, especially in relapsed or metastatic cases. Current therapies have changed little for decades and often cause serious long-term side effects, highlighting the need for more precise and less toxic treatments. Abbott’s research focuses on a protein that cells rely on to copy and repair their DNA, and his work shows that Ewing sarcoma cells are unusually dependent on it — suggesting it may represent an Achilles’ heel. Abbott aims to understand why this protein is so important for Ewing sarcoma cells and to evaluate whether blocking it could form the basis of a new therapy. His work may uncover a previously unrecognized vulnerability in Ewing sarcoma and help pave the way for safer, more effective treatments for children with this challenging cancer. Abbott received his PhD from the Massachusetts Institute of Technology and his BS from the University of California, Santa Cruz. 

Osteosarcoma is the most common bone tumor and primarily affects children and adolescents. Unfortunately, treatment approaches and outcomes for osteosarcoma patients have not significantly improved for 40 years. Dr. Morrow’s work is focused on understanding normal bone development and how this development goes awry, giving rise to osteosarcoma. He hopes this improved understanding will lead to new treatment approaches for pediatric osteosarcoma patients. Dr. Morrow received his MD and PhD from Case Western Reserve University School of Medicine, Cleveland and his BS from The Pennsylvania State University, State College.

In the past decade, new therapies that train the immune system to recognize and kill tumor cells have revolutionized cancer care. Unfortunately, immunotherapies have been largely ineffective in pediatric solid tumors, including osteosarcoma, the most common bone cancer. Dr. Smith aims to understand why immunotherapies have failed by studying a mouse model closely resembling human osteosarcoma. Importantly, these mice have an intact immune system, unlike models that transplant human tumors into mice. By combining complex modeling with single cell and spatial techniques, Dr. Smith hopes to uncover barriers to immune control of osteosarcoma and identify potential therapeutic approaches. Based on these findings, he plans to test novel immunotherapies in the mouse model to prepare for the next generation of osteosarcoma human clinical trials. Dr. Smith received his MD and PhD from the University of California, San Francisco and his BA from Harvard College, Cambridge.

Chromatin remodelers are complex protein machines responsible for packaging DNA and regulating gene expression. Their dysfunction is strongly implicated in cancer. For example, certain types of sarcoma and ovarian cancer are driven by mutations in a chromatin remodeler called BAF. Combining experiments with theoretical work, Dr. Owen’s research aims to understand how remodelers recognize their target sites in the cell’s nucleus. By expanding our understanding of chromatin remodeling, the findings of this research will provide the groundwork for more effective cancer treatments—suggesting how drugs might target chromatin remodelers—as well as enhance our understanding of how existing drugs that target remodeler-adjacent mechanisms might work.

A central aim of this project is the development of new, quantitative models to explain the behavior of chromatin remodelers seen in experiments. Dr. Owen will achieve this by successive rounds of passing between theory and experiments repeatedly—measuring, modeling, then measuring again. For comparison to experiments, model predictions will be extracted computationally (e.g., numerically solving ODEs, or by exact stochastic simulation using Gillespie’s algorithm) or analytically (e.g., by the King-Altman procedure, and variants), as appropriate.