Dean W. Felsher
Academic Appointments
- Professor, Medicine - Oncology
- Member, Bio-X
- Member, Stanford Cancer Institute
- Professor, Pathology
Key Documents
Contact Information
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Clinical Offices
Lymphoma Clinic 875 Blake Wilbur Dr Clinic C Stanford, CA 94305 Tel Work (650) 498-6000 Fax (650) 725-9113
- Academic Offices
Alternate Contact Leslie Quiroz Email Tel Work 650-725-6454Not for medical emergencies or patient use
Professional Overview
Clinical Focus
- Lymphoma
- Hodgkin's Disease
- Hodgkin's Disease - Hematology
- Hodgkin's Disease - Medical Oncology
- Lymphoma
- Oncology (Cancer)
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
Stephanie Casey, Bikul Das, Meital Gabay, Daniel Koch, Emelyn Shroff, Ling Tong
Graduate & Fellowship Program Affiliations
Internet Links
Industry Relationships
Stanford is committed to ethical and transparent interactions with our industrial and other commercial partners. It is our policy to disclose payments (exclusive of travel support) from, and/or equity in, companies or other commercial entities to Stanford faculty of $5,000 or more in total value, as well as any equity in a privately held company, when the faculty member also has institutional responsibilities related to his or her interactions with the company. View Full Information
Scientific Focus
Current 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
- CD271(+) bone marrow mesenchymal stem cells may provide a niche for dormant Mycobacterium tuberculosis. Sci Transl Med. 2013; (170): 170ra13
- "Picolog," a synthetically-available bryostatin analog, inhibits growth of MYC-induced lymphoma in vivo. Oncotarget. 2012; (1): 58-66
- Immunology in the clinic review series; focus on cancer: multiple roles for the immune system in oncogene addiction. Clin Exp Immunol. 2012; (2): 188-94
- Twist1 suppresses senescence programs and thereby accelerates and maintains mutant Kras-induced lung tumorigenesis. PLoS Genet. 2012; (5): e1002650
- Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction. Proc Natl Acad Sci U S A. 2011; (42): 17432-7
- Survival and death signals can predict tumor response to therapy after oncogene inactivation. Sci Transl Med. 2011; (103): 103ra99
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