Janet L Funk, MD

Cancer Biology Program
Janet L Funk, MD

Biography

Janet Funk, MD, MS, is a Professor of Medicine with a joint appointment as a Professor of Nutritional Sciences at the University of Arizona. She earned her BS in chemistry from Stanford University, MS in chemistry from Cornell University with Barbara Baird (IgE receptor membrane dynamics) including work at the National Institutes of Health, and MD from the University of California, San Francisco (UCSF). Following internal medicine residency training at George Washington University, she completed a clinical and research fellowship at UCSF in Endocrinology, Diabetes and Metabolism with Carl Grunfeld and Kenneth Feingold, studying hormonal and lipid responses to inflammation. Dr. Funk joined the UCSF faculty as an Assistant Professor of Medicine before moving to the University of Arizona in 1995 to join the Division of Endocrinology, Diabetes and Metabolism in the Department of Medicine.  Her research seeks to identify novel molecular targets to combat bone diseases commonly affecting women, including arthritis, osteoporosis and breast cancer. Understanding bone protective effects of dietary polyphenols, as well as the interplay of obesity, inflammation and hormonal changes across the lifespan on bone disorders are primary research interests.

Cancer Focus

Bone metastases affecting the majority of women with stage IV breast cancer are a major focus of study in the Funk research group. An initial research effort, which identified a protective effect of dietary polyphenols in blocking the progression of breast cancer bone metastases, has led to current work clarifying the importance of bone specific metabolism of these dietary compounds for bioactivity, and our development of unique and more clinical relevant (ER+) models of breast cancer bone metastases.  Clinical studies are underway to examine associations between dietary polyphenols and bone in breast cancer survivors, and pre-clinical studies are testing novel therapeutic approaches for targeting dormant or hormone-resistant ER+ cells in bone.