Our work focuses on how dendritic cells coordinate immune responses within the tumor microenvironment. Using a high-throughput in vivo tumor array platform that enables longitudinal, lesion-level analysis within individual animals, we study how immune responses emerge, diverge, and ultimately determine tumor fate. This system captures responder and non-responder lesions in the same host, allowing direct interrogation of microenvironmental control of immunity. Our prior work has identified a critical role for spatially organized interactions between conventional type 1 dendritic cells (cDC1s) and CD8⁺ T cells in sustaining cytotoxic function within tumors.

Building on this framework, we are applying this approach to clinically important therapeutic contexts. In PDAC, we use genetically defined KPC-derived models to test how RAS inhibition reshapes tumor-immune states and whether it drives productive immune conversion or partial, non-durable responses. By combining longitudinal imaging with immune profiling, we aim to define the cellular and spatial correlates of response versus resistance and establish a framework for rational combination with immunotherapy.

In neuroblastoma, we focus on anti-GD2 therapy, which engages natural killer (NK) cells but frequently fails to produce durable responses for patients. We hypothesize that sustained tumor control requires coordination across an NK-cDC1-CD8⁺ T cell circuit, and that this circuit is disrupted by tumor-derived suppressive pathways, including prostaglandin E2 and galectin-9. Using integrated in vivo tumor array models and controlled in vitro systems, we are defining how these signals modulate dendritic cell function and exploring strategies to restore coordinated anti-tumor immunity.

Together, this work aims to define actionable, indication-specific principles of tumor immunity to guide the development of immunotherapies for currently intractable cancers.