Cambridge, Massachusetts, United States
Cancer cells reside in a complex microenvironment and interact with many stromal and immune cell components. During tumorigenesis, highly reactive oxygen species (ROS) accumulate due to increased basal metabolic activity, mitochondrial dysfunction, uncontrolled cytokine signaling, and deregulation of genes that control redox signaling. The resulting oxidative stress promotes tumor initiation and progression, and increasing evidence suggests a role for oxidative stress in signaling to the immune system. However, little is known about how the generation and modulation of ROS within the tumor can impact the interplay between the tumor cell and the microenvironment.
Our laboratory would like to explore how such tumor intrinsic factors impact immune cell infiltration and influence response to immunotherapy. To this end, we perform functional genomics to interrogate the role of clinically-relevant oncogenes and tumor suppressors on the tumor metabolic environment and subsequent impact on immune function. Understanding such causal factors should enable new therapeutic approaches that may facilitate beneficial immune infiltrates into tumors and expand the fraction of patients capable of responding to novel immunotherapies.