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Key Documents

Dean W. Felsher

Associate Professor, Medicine - Oncology
Associate Professor, Pathology
Member, Bio-X
Member, Cancer Center

Contact Information

Clinical Offices

Lymphoma Clinic 875 Blake Wilbur Dr Clinic C Stanford, CA 94305-5820
Telephone Work (650) 498-6000 Fax
Academic Offices

Personal Information

Administrative Contact
Leslie Quiroz Email lquiroz@stanford.edu Tel Work 650-725-6454

Not for medical emergencies or patient use

Clinical Focus

Cancer > Lymphoma
Hodgkin's Disease
Hodgkin's Disease - Hematology
Hodgkin's Disease - Medical Oncology
Lymphoma
Oncology
Oncology (Cancer)

Professional Education

UCSF Medical Center (1997) CA
University of Pennsylvania (1994) PA
UCLA Medical Center (1992) CA
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

Felsher Laboratory

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.

Consulting: Cell BioSciences

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. Fan AC, Deb-Basu D, Orban MW, Gotlib JR, Natkunam Y, O'Neill R, Padua RA, Xu L, Taketa D, Shirer AE, Beer S, Yee AX, Voehringer DW, Felsher DW. Nat Med. 2009; 15 (5): 566-71
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; 4 (6): 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; 104 (32): 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; 103 (44): 16266-71
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; 431 (7012): 1112-7
Developmental context determines latency of MYC-induced tumorigenesis. Beer S, Zetterberg A, Ihrie RA, McTaggart RA, Yang Q, Bradon N, Arvanitis C, Attardi LD, Feng S, Ruebner B, Cardiff RD, Felsher DW. PLoS Biol. 2004; 2 (11): e332
Cancer revoked: oncogenes as therapeutic targets. Felsher DW, Nat Rev Cancer. 2003; 3 (5): 375-80
Defective double-strand DNA break repair and chromosomal translocations by MYC overexpression. Karlsson A, Deb-Basu D, Cherry A, Turner S, Ford J, Felsher DW. Proc Natl Acad Sci U S A. 2003; 100 (17): 9974-9
Sustained loss of a neoplastic phenotype by brief inactivation of MYC. Jain M, Arvanitis C, Chu K, Dewey W, Leonhardt E, Trinh M, Sundberg CD, Bishop JM, Felsher DW. Science. 2002; 297 (5578): 102-4
Autochthonous liver tumors induce systemic T cell tolerance associated with T cell receptor down-modulation. Ney JT, Schmidt T, Kurts C, Zhou Q, Eckert D, Felsher DW, Schorle H, Knolle P, Tüting T, Barchet W, Büttner R, Limmer A, Gütgemann I. Hepatology. 2009; 49 (2): 471-81
The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouse. Lee HG, Casadesus G, Nunomura A, Zhu X, Castellani RJ, Richardson SL, Perry G, Felsher DW, Petersen RB, Smith MA. Am J Pathol. 2009; 174 (3): 891-7
Apoptosis-stimulating protein of p53 (ASPP2) heterozygous mice are tumor-prone and have attenuated cellular damage-response thresholds. Kampa KM, Acoba JD, Chen D, Gay J, Lee H, Beemer K, Padiernos E, Boonmark N, Zhu Z, Fan AC, Bailey AS, Fleming WH, Corless C, Felsher DW, Naumovski L, Lopez CD. Proc Natl Acad Sci U S A. 2009; 106 (11): 4390-5
SPECT and PET imaging of EGF receptors with site-specifically labeled EGF and dimeric EGF. Levashova Z, Backer MV, Horng G, Felsher D, Backer JM, Blankenberg FG. Bioconjug Chem. 2009; 20 (4): 742-9
Supramolecular stacking of doxorubicin on carbon nanotubes for in vivo cancer therapy. Liu Z, Fan AC, Rakhra K, Sherlock S, Goodwin A, Chen X, Yang Q, Felsher DW, Dai H. Angew Chem Int Ed Engl. 2009; 48 (41): 7668-72
Cell cycle re-entry and mitochondrial defects in myc-mediated hypertrophic cardiomyopathy and heart failure. Lee HG, Chen Q, Wolfram JA, Richardson SL, Liner A, Siedlak SL, Zhu X, Ziats NP, Fujioka H, Felsher DW, Castellani RJ, Valencik ML, McDonald JA, Hoit BD, Lesnefsky EJ, Smith MA. PLoS One. 2009; 4 (9): e7172
Low-level shRNA Cytotoxicity Can Contribute to MYC-induced Hepatocellular Carcinoma in Adult Mice. Beer S, Bellovin DI, Lee JS, Komatsubara K, Wang LS, Koh H, Börner K, Storm TA, Davis CR, Kay MA, Felsher DW, Grimm D. Mol Ther. 2009;
Tumor dormancy and oncogene addiction. Felsher DW, APMIS. 2008 Jul-Aug; 116 (7-8): 629-37
The current STATe of biomarkers to predict the response to anti-angiogenic therapies. Tran PT, Felsher DW. Cancer Biol Ther. 2008; 7 (12): 2004-6
A quantitative PCR method to detect blood microRNAs associated with tumorigenesis in transgenic mice. Fan AC, Goldrick MM, Ho J, Liang Y, Bachireddy P, Felsher DW. Mol Cancer. 2008; 7 74
An efficient and versatile system for acute and chronic modulation of renal tubular function in transgenic mice. Traykova-Brauch M, Schönig K, Greiner O, Miloud T, Jauch A, Bode M, Felsher DW, Glick AB, Kwiatkowski DJ, Bujard H, Horst J, von Knebel Doeberitz M, Niggli FK, Kriz W, Gröne HJ, Koesters R. Nat Med. 2008; 14 (9): 979-84
Genomic and proteomic analysis reveals a threshold level of MYC required for tumor maintenance. Shachaf CM, Gentles AJ, Elchuri S, Sahoo D, Soen Y, Sharpe O, Perez OD, Chang M, Mitchel D, Robinson WH, Dill D, Nolan GP, Plevritis SK, Felsher DW. Cancer Res. 2008; 68 (13): 5132-42
Hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesis. Beer S, Komatsubara K, Bellovin DI, Kurobe M, Sylvester K, Felsher DW. PLoS One. 2008; 3 (6): e2493
Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas. Tran PT, Fan AC, Bendapudi PK, Koh S, Komatsubara K, Chen J, Horng G, Bellovin DI, Giuriato S, Wang CS, Whitsett JA, Felsher DW. PLoS One. 2008; 3 (5): e2125
Oncogene addiction versus oncogene amnesia: perhaps more than just a bad habit? Felsher DW, Cancer Res. 2008; 68 (9): 3081-6; discussion 3086
Reversing cancer from inside and out: oncogene addiction, cellular senescence, and the angiogenic switch. Felsher DW, Lymphat Res Biol. 2008; 6 (3-4): 149-54
(18)F and (18)FDG PET imaging of osteosarcoma to non-invasively monitor in situ changes in cellular proliferation and bone differentiation upon MYC inactivation. Arvanitis C, Bendapudi PK, Tseng JR, Gambhir SS, Felsher DW. Cancer Biol Ther. 2008; 7 (12): 1947-51
HIF-dependent antitumorigenic effect of antioxidants in vivo. Gao P, Zhang H, Dinavahi R, Li F, Xiang Y, Raman V, Bhujwalla ZM, Felsher DW, Cheng L, Pevsner J, Lee LA, Semenza GL, Dang CV. Cancer Cell. 2007; 12 (3): 230-8
Specific tumor suppressor function for E2F2 in Myc-induced T cell lymphomagenesis. Opavsky R, Tsai SY, Guimond M, Arora A, Opavska J, Becknell B, Kaufmann M, Walton NA, Stephens JA, Fernandez SA, Muthusamy N, Felsher DW, Porcu P, Caligiuri MA, Leone G. Proc Natl Acad Sci U S A. 2007; 104 (39): 15400-5
CpG island methylation in a mouse model of lymphoma is driven by the genetic configuration of tumor cells. Opavsky R, Wang SH, Trikha P, Raval A, Huang Y, Wu YZ, Rodriguez B, Keller B, Liyanarachchi S, Wei G, Davuluri RV, Weinstein M, Felsher D, Ostrowski M, Leone G, Plass C. PLoS Genet. 2007; 3 (9): 1757-69
BCL-2 and mutant NRAS interact physically and functionally in a mouse model of progressive myelodysplasia. Omidvar N, Kogan S, Beurlet S, le Pogam C, Janin A, West R, Noguera ME, Reboul M, Soulie A, Leboeuf C, Setterblad N, Felsher D, Lagasse E, Mohamedali A, Thomas NS, Fenaux P, Fontenay M, Pla M, Mufti GJ, Weissman I, Chomienne C, Padua RA. Cancer Res. 2007; 67 (24): 11657-67
Enhanced NFATc1 nuclear occupancy causes T cell activation independent of CD28 costimulation. Pan M, Winslow MM, Chen L, Kuo A, Felsher D, Crabtree GR. J Immunol. 2007; 178 (7): 4315-21
Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesis. Shachaf CM, Perez OD, Youssef S, Fan AC, Elchuri S, Goldstein MJ, Shirer AE, Sharpe O, Chen J, Mitchell DJ, Chang M, Nolan GP, Steinman L, Felsher DW. Blood. 2007; 110 (7): 2674-84
Identifying critical signaling molecules for the treatment of cancer. Arvanitis C, Bendapudi PK, Bachireddy P, Felsher DW. Recent Results Cancer Res. 2007; 172 5-24
Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy. Giuriato S, Faumont N, Bousquet E, Foisseau M, Bibonne A, Moreau M, Al Saati T, Felsher DW, Delsol G, Meggetto F. Cancer Biol Ther. 2007; 6 (8): 1318-23
CDK2 is required by MYC to induce apoptosis. Deb-Basu D, Aleem E, Kaldis P, Felsher DW. Cell Cycle. 2006; 5 (12): 1342-7
c-Myc is an important direct target of Notch1 in T-cell acute lymphoblastic leukemia/lymphoma. Weng AP, Millholland JM, Yashiro-Ohtani Y, Arcangeli ML, Lau A, Wai C, Del Bianco C, Rodriguez CG, Sai H, Tobias J, Li Y, Wolfe MS, Shachaf C, Felsher D, Blacklow SC, Pear WS, Aster JC. Genes Dev. 2006; 20 (15): 2096-109
Tumor dormancy: death and resurrection of cancer as seen through transgenic mouse models. Felsher DW, Cell Cycle. 2006; 5 (16): 1808-11
Conditional transgenic models define how MYC initiates and maintains tumorigenesis. Arvanitis C, Felsher DW. Semin Cancer Biol. 2006; 16 (4): 313-7
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; 66 (13): 6598-605
MYC can enforce cell cycle transit from G1 to S and G2 to S, but not mitotic cellular division, independent of p27-mediated inihibition of cyclin E/CDK2. Deb-Basu D, Karlsson A, Li Q, Dang CV, Felsher DW. Cell Cycle. 2006; 5 (12): 1348-55
Getting at MYC through RAS. Bachireddy P, Bendapudi PK, Felsher DW. Clin Cancer Res. 2005; 11 (12): 4278-81
Lethal cutaneous disease in transgenic mice conditionally expressing type I human T cell leukemia virus Tax. Kwon H, Ogle L, Benitez B, Bohuslav J, Montano M, Felsher DW, Greene WC. J Biol Chem. 2005; 280 (42): 35713-22
Suppression of p53 by Notch in lymphomagenesis: implications for initiation and regression. Beverly LJ, Felsher DW, Capobianco AJ. Cancer Res. 2005; 65 (16): 7159-68
Rehabilitation of cancer through oncogene inactivation. Shachaf CM, Felsher DW. Trends Mol Med. 2005; 11 (7): 316-21
Tumor dormancy and MYC inactivation: pushing cancer to the brink of normalcy. Shachaf CM, Felsher DW. Cancer Res. 2005; 65 (11): 4471-4
Comparative genomic hybridization on mouse cDNA microarrays and its application to a murine lymphoma model. Sander S, Bullinger L, Karlsson A, Giuriato S, Hernandez-Boussard T, Felsher DW, Pollack JR. Oncogene. 2005; 24 (40): 6101-7
Conditionally MYC: insights from novel transgenic models. Arvanitis C, Felsher DW. Cancer Lett. 2005; 226 (2): 95-9
The E47 transcription factor negatively regulates CD5 expression during thymocyte development. Yang Y, Contag CH, Felsher D, Shachaf CM, Cao Y, Herzenberg LA, Herzenberg LA, Tung JW. Proc Natl Acad Sci U S A. 2004; 101 (11): 3898-902
Reversibility of oncogene-induced cancer. Felsher DW, Curr Opin Genet Dev. 2004; 14 (1): 37-42
Conditional animal models: a strategy to define when oncogenes will be effective targets to treat cancer. Giuriato S, Rabin K, Fan AC, Shachaf CM, Felsher DW. Semin Cancer Biol. 2004; 14 (1): 3-11
The human BCL6 transgene promotes the development of lymphomas in the mouse. Baron BW, Anastasi J, Montag A, Huo D, Baron RM, Karrison T, Thirman MJ, Subudhi SK, Chin RK, Felsher DW, Fu YX, McKeithan TW, Baron JM. Proc Natl Acad Sci U S A. 2004; 101 (39): 14198-203
Putting oncogenes into a developmental context. Felsher DW, Cancer Biol Ther. 2004; 3 (10): 942-4
Oncogenes as therapeutic targets. Felsher DW, Semin Cancer Biol. 2004; 14 (1): 1
How cancers escape their oncogene habit. Giuriato S, Felsher DW. Cell Cycle. 2003 Jul-Aug; 2 (4): 329-32
Pharmacological inactivation of MYC for the treatment of cancer. Felsher DW, Bradon N. Drug News Perspect. 2003 Jul-Aug; 16 (6): 370-4
Genomically complex lymphomas undergo sustained tumor regression upon MYC inactivation unless they acquire novel chromosomal translocations. Karlsson A, Giuriato S, Tang F, Fung-Weier J, Levan G, Felsher DW. Blood. 2003; 101 (7): 2797-803
c-Myc is a critical target for c/EBPalpha in granulopoiesis. Johansen LM, Iwama A, Lodie TA, Sasaki K, Felsher DW, Golub TR, Tenen DG. Mol Cell Biol. 2001; 21 (11): 3789-806
Overexpression of MYC causes p53-dependent G2 arrest of normal fibroblasts. Felsher DW, Zetterberg A, Zhu J, Tlsty T, Bishop JM. Proc Natl Acad Sci U S A. 2000; 97 (19): 10544-8
Transient excess of MYC activity can elicit genomic instability and tumorigenesis. Felsher DW, Bishop JM. Proc Natl Acad Sci U S A. 1999; 96 (7): 3940-4
Reversible tumorigenesis by MYC in hematopoietic lineages. Felsher DW, Bishop JM. Mol Cell. 1999; 4 (2): 199-207
A novel octamer regulatory element in the VH11 leader exon of B-1 cells. Goodglick L, Felsher DW, Neshat MS, Braun J. J Immunol. 1995; 154 (9): 4546-56
c-myc, MHCI, and NK resistance in immunodeficiency lymphomas. Braun J, Felsher DW, Goodglick LA. Ann N Y Acad Sci. 1992; 651 467-9
Independent rearrangement of Ig lambda genes in tissue culture-derived murine B cell lines. Felsher DW, Ando DT, Braun J. Int Immunol. 1991; 3 (7): 711-8
A murine model for B-cell lymphomagenesis in immunocompromised hosts: natural killer cells are an important component of host resistance to premalignant B-cell lines. Felsher DW, Rhim SH, Braun J. Cancer Res. 1990; 50 (21): 7050-6
A murine model for B-cell lymphomagenesis in immunocompromised hosts: c-myc-rearranged B-cell lines with a premalignant phenotype. Felsher DW, Denis KA, Weiss D, Ando DT, Braun J. Cancer Res. 1990; 50 (21): 7042-9
A rapid method for the purification of monomeric and/or dimeric phospholipases A2 in crotalid snake venoms. Welches W, Felsher D, Landshulz W, Maraganore JM. Toxicon. 1985; 23 (5): 747-54