Associate Professor
Radiation Oncology and Molecular Radiation Sciences Department, 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.
Cancer Biology | Cellular Stress and Cell Signaling | Translational Research
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.