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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. Using mass cytometry, the Goldstein lab has recently defined immune cell heterogeneity in the mouse and human prostate (AJCEU). Working with colleagues from UCLA, Johns Hopkins and Weill-Cornell, the Goldstein lab has demonstrated that CD38 is methylated in prostate cancer and regulates extracellular NAD+ (Cancer & Metabolism). Most recently, the Goldstein Lab has determined that luminal progenitor cells are increased in the aging mouse and human prostate (Cell Reports). The lab continues to interrogate the mechanisms responsible for cancer initiation, progression and treatment-resistance.