Dean W. Felsher, MD, PhD
Photo: Dean Felsher

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650-498-5269

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Elected 2005
Dr. Dean W. Felsher is currently a Professor in the Division of Oncology, Departments of Medicine and Pathology at Stanford University. Dr. Felsher obtained his B.A. in Chemistry at the University of Chicago and his MD PhD from the University of California, Los Angeles, He conducted his Oncology Fellowship training at the University of California San Francisco. Dr. Felsher's laboratory pursues both basic science and translational research studies investigating how oncogenes initiate and sustain tumorigenesis and using these insights towards the development of new therapies for cancer. He has pioneered strategies utilizing the Tetracycline regulatory System to develop conditional transgenic mouse model systems of tumorigenesis to address three questions: How does oncogene activation initiate tumorigenesis? When does oncogene inactivation reverse tumorigenesis? What are the mechanisms by which tumors escape dependence upon oncogenes? To date, he established a paradigm suggesting that the inactivation of a the single oncogene, MYC, can be sufficient to reverse the process of tumorigenesis, in lymphoma, leukemia, osteogenic sarcoma and hepatocellular carcinoma. Even genomically complex tumors were found to regress upon MCY inactivation. Moreover, he has shown that MYC oncogene inactivation uncovers pluripotent differentiation of tumor cells into normal cellular lineages. In some cases, this differentiation results in the permanent loss of a neoplastic phenotype and even brief MYC inactivation induces sustained tumor regression. In other cases, some of the tumor cells appear to retain the capacity for neoplastic features upon oncogene reactivation, hence existing in a state of tumor dormancy. The experimental model system that he has developed has contributed to several new principles of tumor biology, including the notion of the reversibility of cancer, the idea that oncogene inactivation can result in the uncovering of stem cell features of tumors, the idea that oncogene inactivation can either revoke tumorigenesis or induce a state of tumor dormancy, the notion that cellular senescence programs and angiogenic pathways play a important role in the mechanism of oncogene addiction, and finally, the role of the immune system in contributing to many of these mechanisms of oncogene addiction. Dr. Felsher's work has led to major contributions to our understanding of the molecular basis of cancer and useful towards the rational development of new therapeutics to treat cancer.