Chris C. Benz, M.D., Professor and Program Director
Understanding breast cancer biology to develop better treatment and prevention approaches
Christopher Benz, M.D., is internationally recognized for his research in breast cancer. He is a practicing oncologist at UCSF’s Carol Franc Buck Breast Care Center, and a senior member of the UCSF Cancer Center’s Breast Oncology Program.
The Benz lab examines the link between aging and the onset of breast cancer — in particular, why the incidence of breast cancer increases with age, and how breast cancer biology is altered by the aging process. Benz was among the first to publish studies proving that breast cancer is age-dependent; he believes this finding will lead to age-tailored breast cancer therapies. Among specific areas of interest, the Benz lab focuses on a family of breast cancers that overexpress the estrogen receptor (ER), a biomarker that identifies the most rapidly increasing form of breast cancer worldwide and a critical target for prevention and treatment by endocrine agents like anti-estrogens and aromatase inhibitors.
The lab was the first to demonstrate that among Caucasian women living in Marin County, California there is a selective risk for developing hormone-dependent breast cancer (“ER-positive” and “PR-positive” breast cancers), indicating that women from similar geographic populations are exposed to specific risk factors that promote the development of these cancers. Dr. Benz played a key role in the 2006 launch of the region’s first community-wide scientific survey and biospecimen collection known as the Marin Women’s Study (MWS).
The Benz lab, with international collaborators, has completed a study showing how aging actually alters the biology of breast cancer at the level of DNA and RNA. The Benz lab has also galvanized a Buck interdisciplinary team effort to address the seemingly intractable problem of measuring the extent to which various exogenous (i.e., environmental agents) and endogenous (e.g., physiologic/metabolic changes) chemical exposures can modify intracellular ER structure, thereby altering its function and potential for encouraging breast tumors. Addressing a different area of breast cancer research, the Benz lab has long been developing targeted molecular therapeutics to manage one of the most aggressive forms of human breast cancer, those driven by amplification of the ERBB2 oncogene. The Benz lab uncovered a previously unknown mechanism by which a unique class of investigational agents, histone deacetylase (HDAC) inhibitors, can selectively silence the ERBB2 oncogene.
