Dean W. Felsher

Clinical Focus

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

Professional Education

Postdoctoral Advisees

Stacey Adam,  Stephanie Casey,  Stephanie Casey,  Bikul Das,  Yulin Li,  Emelyn Shroff,  Ling Tong,  Tahera Zabuawala

Graduate & Fellowship Program Affiliations

• Cancer Biology
• Immunology
• Medicine
• Pathology

Internet Links

• Felsher Laboratory

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

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?

Clinical Trials

• Phase II study of Atorvastatin safety and antitumor effects in non-Hodgkin's Lymphoma Recruiting
• Molecular Analysis of Thoracic Malignancies Recruiting

Publications

• Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction. Choi PS, van Riggelen J, Gentles AJ, Bachireddy P, Rakhra K, Adam SJ, Plevritis SK, Felsher DW. Proc Natl Acad Sci U S A. 2011; 108 (42): 17432-7
• Survival and death signals can predict tumor response to therapy after oncogene inactivation. Tran PT, Bendapudi PK, Lin HJ, Choi P, Koh S, Chen J, Horng G, Hughes NP, Schwartz LH, Miller VA, Kawashima T, Kitamura T, Paik D, Felsher DW. Sci Transl Med. 2011; 3 (103): 103ra99
• CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation. Rakhra K, Bachireddy P, Zabuawala T, Zeiser R, Xu L, Kopelman A, Fan AC, Yang Q, Braunstein L, Crosby E, Ryeom S, Felsher DW. Cancer Cell. 2010; 18 (5): 485-98
• MYC as a regulator of ribosome biogenesis and protein synthesis. van Riggelen J, Yetil A, Felsher DW. Nat Rev Cancer. 2010; 10 (4): 301-9
• The interaction between Myc and Miz1 is required to antagonize TGFbeta-dependent autocrine signaling during lymphoma formation and maintenance. van Riggelen J, Müller J, Otto T, Beuger V, Yetil A, Choi PS, Kosan C, Möröy T, Felsher DW, Eilers M. Genes Dev. 2010; 24 (12): 1281-94