Fred Bunz

Research Overview

Dr. Bunz’s research objective is to understand how stress-activated signaling pathways affect the cellular responses to anti-cancer therapy. A longstanding interest is p53, a central node within a complex network of DNA damage-response pathways involved in tumor suppression. It is well-known that cancer associated p53 mutations impact the efficacy of DNA damage-based anticancer therapies, such as radiotherapy. It is now apparent that p53 also controls immune recognition, and thereby influences the efficacy of immune-based therapies. 

Recent work in the lab is focused on understanding the mechanistic basis for these effects, and on the development of therapeutic viral agents that can stimulate neoantigen-specific anti-cancer immune responses. The long-term goal is to better understand how current therapies work, and to develop new and improved cancer treatments.