Profiles

The research in the Goldstein laboratory is focused on understanding the role of prostate epithelial cells in development, reproduction, aging and tumorigenesis. Dr. Goldstein described the isolation of epithelial progenitor cells from mouse and human prostate tissue and demonstrated the capacity of progenitor cells to initiate prostate cancer in response to oncogenic transformation. Following up on this work, Dr. Goldstein and colleagues determined that prostate cancer can evolve from a basal cell of origin to a luminal-like tumor-propagating cell population. The Goldstein lab has demonstrated that chronic inflammation in the human prostate is associated with an expansion of rare progenitor-like luminal cells marked by low CD38 expression that can initiate aggressive prostate cancer. These findings help to explain why chronic inflammation increases prostate cancer risk. The lab has determined that luminal progenitor cells are increased in the aging mouse and human prostate and that aging signatures indicate age-related metabolic reprogramming of prostate epithelial cells. Most recently, the lab has defined a role for MYC in treatment-induced metabolic reprogramming in prostate cancer and found that prostate lineage-specific metabolism governs luminal differentiation and response to antiandrogen treatment. The lab continues to interrogate the mechanisms responsible for prostate development, aging, and cancer initiation.