Dean W. Felsher

Clinical Focus

• Cancer > Lymphoma
• Hodgkin's Disease
• Hodgkin's Disease - Hematology
• Hodgkin's Disease - Medical Oncology
• Lymphoma

Professional Education

• Fellowship: UCSF Medical Center, CA (1997)
• Residency: University of Pennsylvania, PA (1994)
• Medical Education: UCLA Medical Center, CA (1992)
• MD PhD, UCLA, Medicine/Molecular Biology (1992)
• BS, University of Chicago, Chemistry (1985)

Postdoctoral Advisees

Stacey Adam, David Bellovin, Zhongwei Cao, Yulin Li, Aleksey Yevtodiyenko, Jan van Riggelen

Graduate & Fellowship Program Affiliations

• Cancer Biology
• Immunology
• Medicine
• Pathology

Web Site Links

• Felsher Laboratory

Research Interests

My laboratory investigates how oncogenes initiate and sustain tumorigenesis. I have developed model systems whereby I can conditionally activate oncogenes in normal human and mouse cells in tissue culture or in specific tissues of transgenic mice. In particular using the tetracycline regulatory system, I have generated a conditional model system for MYC-induced tumors. I have shown that cancers caused by the conditional over-expression of the MYC proto-oncogene regress with its inactivation. Thus, even though cancer is a multi-step process, the inactivation of one oncogene can be sufficient to induce tumor regression. Now, I am using these model systems to address three questions:

1. How do oncogenes initiate tumorigenesis?
2. How does oncogene inactivation cause tumor regression?
3. How do tumors escape dependence on oncogenes?

Publications

• Combined analysis of murine and human microarrays and ChIP analysis reveals genes associated with the ability of MYC to maintain tumorigenesis. Wu CH, Sahoo D, Arvanitis C, Bradon N, Dill DL, Felsher DW "PLoS Genet" 2008 ; 6 (4) : e1000090
• Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivation. Wu CH, van Riggelen J, Yetil A, Fan AC, Bachireddy P, Felsher DW "Proc Natl Acad Sci U S A" 2007 ; 32 (104) : 13028-33
• Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch. Giuriato S, Ryeom S, Fan AC, Bachireddy P, Lynch RC, Rioth MJ, van Riggelen J, Kopelman AM, Passegué E, Tang F, Folkman J, Felsher DW "Proc Natl Acad Sci U S A" 2006 ; 44 (103) : 16266-71
• MYC can induce DNA breaks in vivo and in vitro independent of reactive oxygen species. Ray S, Atkuri KR, Deb-Basu D, Adler AS, Chang HY, Herzenberg LA, Felsher DW "Cancer Res" 2006 ; 13 (66) : 6598-605
• MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancer. Shachaf CM, Kopelman AM, Arvanitis C, Karlsson A, Beer S, Mandl S, Bachmann MH, Borowsky AD, Ruebner B, Cardiff RD, Yang Q, Bishop JM, Contag CH, Felsher DW "Nature" 2004 ; 7012 (431) : 1112-7