Andrew Goldstein, Ph.D.

Andrew Goldstein, Ph.D., investigates the interplay between inflammation, epithelial progenitor cells and the formation of tumors. Epithelial progenitor cells give rise to the cells that make up epithelial tissues, which line all of the organs and cavities inside the body. Previous research has established that normal prostate epithelial progenitor cells and aggressive prostate cancer cells possess similar characteristics. Goldstein studies epithelial progenitor cells in order to uncover the cellular and molecular changes that initiate prostate cancer and cause cancer progression and resistance to treatment. His research goals are to inform the development of new drugs that inhibit these changes and stop progression of the disease, as well as increase early detection of prostate cancer through improved screening methods.

Prostate cancer is the second leading cause of cancer death in American men, behind only lung cancer. About one man in 39 will die of prostate cancer each year, and an estimated 180,000 new cases of the disease are reported annually in the United States. Goldstein’s research has always focused on prostate cancer; he completed his graduate work in the lab of Dr. Owen Witte, studying epithelial progenitor cells that can increase cancer risk. Goldstein and Witte’s work included the first demonstration of a cell-of-origin for human prostate cancer, a discovery that could lead to the development of better tools for prediction, diagnosis and treatment of the disease. Goldstein is expanding the research to address the effects of chronic prostate inflammation on epithelial progenitor cells that can initiate cancer.

Goldstein also seeks to define metabolic regulators of progenitor cells and prostate cancer. In particular, the lab is studying the role of a molecule called CD38, which may help to prevent aggressive prostate cancers. He is taking a number of approaches to understand why CD38 is present in non-aggressive prostate cancers and absent in most aggressive prostate cancers. Understanding how low CD38 levels affect the growth of prostate cancer tumors could lead to the development of improved screening methods. Goldstein believes that the CD38 molecule could be used as a biomarker to help clinicians predict which patients will have aggressive metastatic disease. Such early detection can reduce the number of unnecessary surgeries and inform specific treatment options.

Goldstein earned his doctorate degree in molecular biology at UCLA.