Dean W. Felsher
Academic Appointments
- Associate Professor, Medicine - Oncology
- Associate Professor, Pathology
- Member, Bio-X
- Member, Cancer Center
Contact Information
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Clinical Offices
Lymphoma Clinic 875 Blake Wilbur Dr Clinic C Stanford, CA 94305-5820 Tel Work (650) 498-6000
- Academic Offices
Administrative Contact Leslie Quiroz Email Tel Work 650-725-6454Not for medical emergencies or patient use
Professional Snapshot
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 , Bikul Das , Yulin Li , Emelyn Shroff , Aleksey Yevtodiyenko , Jan van Riggelen
Graduate & Fellowship Program Affiliations
Web Site Links
Industry Relationships
Stanford is committed to ethical and transparent interactions with our industry partners. It is our policy to disclose payments of $5,000 or more, equity valued at $5,000 or more in a publicly traded company, or any equity in a privately held company, to physicians and scientists employed by Stanford University from companies or other commercial entities with which they interact as part of their professional activities. View Full Information
| Consulting: | Cell BioSciences |
Scientific Focus
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?
Clinical Trials
Publications
- Nanofluidic proteomic assay for serial analysis of oncoprotein activation in clinical specimens. Nat Med. 2009; (5): 566-71
- Combined analysis of murine and human microarrays and ChIP analysis reveals genes associated with the ability of MYC to maintain tumorigenesis. PLoS Genet. 2008; (6): e1000090
- Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivation. Proc Natl Acad Sci U S A. 2007; (32): 13028-33
- Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch. Proc Natl Acad Sci U S A. 2006; (44): 16266-71
- MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancer. Nature. 2004; (7012): 1112-7
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