Fred Bunz
Stress-activated pathways and anti-cancer therapies
Associate Professor
Department of Radiation Oncology and Molecular Radiation Sciences
School of Medicine
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.
Selected Publications
- Bunz, Fred. Principles of cancer genetics, 3rd Edition (textbook). Springer, 2022.
- Jang Y, Bunz F. AdenoBuilder: A platform for the modular assembly of recombinant adenoviruses. STAR Protocols, 2022.
- Miciak J, Bunz F. Long story short: p53 mediates innate immunity. Biochimica et Biophysica acta, 2016.
- Chung JH, Larsen AR, Chen E, Bunz F. A PTCH1 homolog transcriptionally activated by p53 suppresses Hedgehog signaling. Journal of Biological Chemistry, 2014.
- Wilsker D, Chung JH, Pradilla I, Petermann E, Helleday T, Bunz F. Targeted mutations in the ATR pathway define agent-specific requirements for cancer cell growth and survival. Molecular cancer therapeutics, 2012.