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The research in the Goldstein laboratory is focused on the intersection between cancer biology, stem cell biology and metabolism. During his graduate work, Dr. Goldstein described the isolation of epithelial progenitor cells from mouse and human prostate tissue (PNAS) and demonstrated the capacity of progenitor cells to initiate prostate cancer in response to oncogenic transformation (Science). 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 (PNAS). The Goldstein lab has demonstrated that chronic inflammation in the human prostate is associated with an expansion of rare luminal progenitor cells marked by low CD38 expression that can initiate aggressive prostate cancer (Cell Reports). These findings help to explain why chronic inflammation increases prostate cancer risk. More recently, the Goldstein lab has worked with colleagues from UCLA, Johns Hopkins and Weill-Cornell to demonstrate that CD38 is methylated in prostate cancer and regulates extracellular NAD+ (Cancer & Metabolism). The lab continues to interrogate the mechanisms responsible for cancer initiation, progression and treatment-resistance.