Kerry L. Burnstein, PhD

Kerry Burnstein, Ph. D.,  joined University of Miami in 1991 and is currently a Professor in the Department of Molecular and Cellular Pharmacology.

Dr. Burnstein has a strong commitment to graduate and post-graduate training and has been the Graduate Program Director for the Department of Molecular and Cellular Pharmacology since 2001, recruiting and advising trainees and developing/updating the graduate curriculum and contributing to programs offered for post-docs.

Dr. Burnstein's research interests include: steroid hormone receptors, hormonal regulation of cell cycle in prostate cancer. Dr. Burnstein's research focuses on mechanisms of signaling cross talk that control cellular responses to steroid hormones. Their relevance to hormone sensitive cancers is investigated using breast, prostate and head and neck cancer models. A major interest is the antiproliferative action of the hormonal form of vitamin D (1,25 dihydroxyvitamin D3), which is mediated by the vitamin D receptor (VDR), a member of the steroid receptor family. VDRs have a wide tissue distribution and affect a broad array of cell types. She and others showed that vitamin D inhibits the growth of cancer cells by promoting cell cycle arrest in the G1 phase. More recently, Dr. Burnstein made the novel discovery that vitamin D stabilizes cell cycle inhibitor, p27, and promotes the nuclear exclusion of cyclin dependent kinase 2 (cdk2) thereby decreasing its activity and leading to cell cycle arrest. Current efforts are to understand vitamin D/VDR regulation of cyclin dependent kinase 2 nucleocytoplasmic trafficking in cancer cells. Drs. Slingerland and Fontoura collaborate in this project. 

The Burnstein lab has also investigated possible intracellular signaling alterations and found that Rac1, a Rho GTPase (Ras-related small G protein), is hyperactive in the more malignant, hormone independent cancer cells. Rac1 inhibition increased levels of the cyclin dependent kinase inhibitor p21 and decreased proliferation, indicating an important a role for Rac1 in p21 regulation. Hyperactive Rac signaling, which has also been demonstrated in breast cancer, presents potentially important therapeutic targets for breast and prostate cancers. Dr. Burnstein's team have had a long term interest in signaling pathways that influence the activity of the androgen receptor (AR) in prostate cancer and the roles they play in mediating hormone independent cancer growth. They found that Vav3, a Rho GTPase guanine nucleotide exchange factor, increases during progression to hormone independence and enhances hormone receptor transcriptional activity. Because Vav3 is an activator of Rac1, mechanistic links between Rho GTPases, steroid receptors and cell cycle are being investigated.