Research Topics
Species | Dean FelsherSummaryAffiliation: Stanford University Country: USA Publications
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Publications
Sustained loss of a neoplastic phenotype by brief inactivation of MYCMeenakshi Jain
Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA 94305 5151, USA
Science 297:102-4. 2002..These results raise the possibility that transient inactivation of MYC may be an effective therapy for certain cancers...- CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivationKavya Rakhra
Division of Oncology, Departments of Medicine, Pathology and Molecular Imaging, Stanford University School of Medicine, Stanford, CA 94305, USA
Cancer Cell 18:485-98. 2010..Hence, CD4(+) T cells are required for the remodeling of the tumor microenvironment through the expression of chemokines, such as thrombospondins, in order to elicit oncogene addiction... - Developmental context determines latency of MYC-induced tumorigenesisShelly Beer
Division of Oncology, Department of Medicine, Stanford University, Stanford, California, USA
PLoS Biol 2:e332. 2004..Adult somatic cells have evolved mechanisms to prevent individual oncogenes from initiating cellular growth, DNA replication, and mitotic cellular division alone, thereby preventing any single genetic event from inducing tumorigenesis... - A quantitative PCR method to detect blood microRNAs associated with tumorigenesis in transgenic miceAlice C Fan
Stanford University, School of Medicine, Division of Oncology, Department of Medicine, Stanford, CA 94305 5151, USA
Mol Cancer 7:74. 2008..Our results suggest that specific changes in blood miRNA can be detected during tumorigenesis and tumor regression... - Putting oncogenes into a developmental contextDean W Felsher
Cancer Biol Ther 3:942-4. 2004..Cancer may generally be better thought of as a consequence of genetic events that occur in a permissive epigenetic state. Developmental context may be a critical determinant in the pathogenesis of neoplasia... - Tumor dormancy and oncogene addictionDean W Felsher
Division of Oncology, Department of Medicine, Stanford University, Palo Alto, CA, USA
APMIS 116:629-37. 2008..Hence, understanding when and how oncogene inactivation induces apoptosis, differentiation, and senescence within a tumor will be important when developing effective strategies for the treatment of cancer... - Myc and a Cdk2 senescence switchJan van Riggelen
Jan van Riggelen and Dean W Felsher are in the Division of Oncology, Departments of Medicine, Pathology and Molecular Imaging, Stanford University School of Medicine, Stanford University, CA 94305 5151, USA
Nat Cell Biol 12:7-9. 2010..This has implications for how c-Myc overcomes failsafe mechanisms to induce tumorigenesis and suggests that the inhibition of Cdk2 may have therapeutic efficacy in the treatment of cancer... - Oncogene addiction versus oncogene amnesia: perhaps more than just a bad habit?Dean W Felsher
Division of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA
Cancer Res 68:3081-6; discussion 3086. 2008..Thus, oncogenes induce cancer because they induce a cellular state of enforced oncogenic amnesia in which, only upon oncogene inactivation, the tumor becomes aware of its transgression... - Reversibility of oncogene-induced cancerDean W Felsher
Division of Oncology, Department of Medicine, Stanford University, CCSR 1105B, 269 Campus Drive, Stanford, CA 94305 5151, USA
Curr Opin Genet Dev 14:37-42. 2004..Understanding how and when oncogene inactivation reverses cancer will be important in both defining the molecular pathogenesis of cancer as well as developing new molecularly based treatments... - Reversing cancer from inside and out: oncogene addiction, cellular senescence, and the angiogenic switchDean W Felsher
Division of Oncology, Department of Medicine, Stanford University, Stanford, CA 94305, USA
Lymphat Res Biol 6:149-54. 2008..We have argued that the abatement of oncogenic activity within a cancer cell not only leads to the demise of a tumor from within but also through the instruction of the restoration of the microenvironment... - Tumor dormancy: death and resurrection of cancer as seen through transgenic mouse modelsDean W Felsher
Division of Oncology, Department of Medicine, Stanford University, Stanford, California 94305 5151, USA
Cell Cycle 5:1808-11. 2006..Understanding when and how oncogene inactivation induces sustained tumor regression will be important towards the development of successful therapeutic strategies for cancer... - Pharmacological inactivation of MYC for the treatment of cancerDean W Felsher
Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, California, USA
Drug News Perspect 16:370-4. 2003..Several different strategies have been employed to develop novel drugs that may be effective to target the inactivation of MYC for the treatment of cancer. Some of these strategies are discussed... - Cancer revoked: oncogenes as therapeutic targetsDean W Felsher
Division of Oncology, Department of Medicine, Stanford University, 269 Campus Drive, CCSR 1105, Stanford, California 94305 5151, USA
Nat Rev Cancer 3:375-80. 2003..So why does oncogene inactivation cause tumour regression and will this be a generally successful approach for the treatment of human neoplasia?.. - Tumor dormancy and MYC inactivation: pushing cancer to the brink of normalcyCatherine M Shachaf
Division of Oncology, Department of Medicine, Stanford University, Stanford, California 94305, USA
Cancer Res 65:4471-4. 2005..Thus, whereas oncogene inactivation can push cancer to the brink of normalcy, some cells retain the latent capacity to turn cancerous again, arguing that they may exist in a state of tumor dormancy... - How cancers escape their oncogene habitSylvie Giuriato
Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, California 94305-5151, USA
Cell Cycle 2:329-32. 2003..Thereby, more effective strategies will be developed to clinically treat cancer... - MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancerCatherine M Shachaf
Division of Medical Oncology, Department of Medicine, Stanford University, California 94305, USA
Nature 431:1112-7. 2004.... - Genomic and proteomic analysis reveals a threshold level of MYC required for tumor maintenanceCatherine M Shachaf
Department of Medicine and Pathology, Division of Medical Oncology, Stanford University School of Medicine, Stanford University, Stanford, California 94305, USA
Cancer Res 68:5132-42. 2008..Thus, at the MYC threshold, there is a loss of its ability to maintain tumorigenesis, with associated shifts in gene and protein expression that reestablish cell cycle checkpoints, halt protein translation, and promote apoptosis... - Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomasPhuoc T Tran
Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
PLoS ONE 3:e2125. 2008..quot; However, most cancers are caused by multiple genetic events making it difficult to determine which oncogenes or combination of oncogenes will be the most effective targets for their treatment... - Rehabilitation of cancer through oncogene inactivationCatherine M Shachaf
Division of Oncology, Departments of Medicine and Pathology, Stanford University, 269 Campus Drive, Stanford, CA 94305-5151, USA
Trends Mol Med 11:316-21. 2005..Future therapies to treat cancer will need to address the possibility that tumor cells can camouflage a normal phenotype following treatment, resting in a dormant, latently cancerous state... - Nanofluidic proteomic assay for serial analysis of oncoprotein activation in clinical specimensAlice C Fan
Stanford University, Departments of Medicine and Pathology, California, USA
Nat Med 15:566-71. 2009..Therefore, we have described a new and highly sensitive method for determining oncoprotein expression and phosphorylation in clinical specimens for the development of new therapeutics for cancer... - (18)F and (18)FDG PET imaging of osteosarcoma to non-invasively monitor in situ changes in cellular proliferation and bone differentiation upon MYC inactivationConstadina Arvanitis
Department of Chemical and Systems Biology, Stanford School of Medicine, Stanford, California 94403, USA
Cancer Biol Ther 7:1947-51. 2008.... - MYC as a regulator of ribosome biogenesis and protein synthesisJan van Riggelen
Division of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
Nat Rev Cancer 10:301-9. 2010..We discuss how the modulation of ribosome biogenesis by MYC may be essential to its physiological functions as well as its pathological role in tumorigenesis... - Combined analysis of murine and human microarrays and ChIP analysis reveals genes associated with the ability of MYC to maintain tumorigenesisChi Hwa Wu
Department of Medicine, Division of Oncology, Stanford University School of Medicine, Stanford, California, United States of America
PLoS Genet 4:e1000090. 2008..Hence, through our analysis of gene expression in murine tumor models and human lymphomas, we have identified a novel gene signature correlated with the ability of MYC to maintain tumorigenesis... - Hypoxia in models of lung cancer: implications for targeted therapeuticsEdward E Graves
Department of Radiation Oncology, Stanford University, California 94305 5847, USA
Clin Cancer Res 16:4843-52. 2010.... - Hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesisShelly Beer
Department of Medicine, Division of Oncology, School of Medicine, Center for Clinical Sciences Research, Stanford University, Stanford, California, United States of America
PLoS ONE 3:e2493. 2008.... - The interaction between Myc and Miz1 is required to antagonize TGFbeta-dependent autocrine signaling during lymphoma formation and maintenanceJan van Riggelen
Department of Medicine, Division of Oncology, Stanford University, School of Medicine, Stanford, California 94304, USA
Genes Dev 24:1281-94. 2010.... - Low-level shRNA cytotoxicity can contribute to MYC-induced hepatocellular carcinoma in adult miceShelly Beer
Department of Medicine, Division of Oncology, School of Medicine, Center for Clinical Sciences Research, Stanford University, Stanford, California 94305 5151, USA
Mol Ther 18:161-70. 2010..Our data warrant caution regarding the possible carcinogenic potential of shRNAs when used as clinical agent, particularly in circumstances where tissues are genetically predisposed to cellular transformation and proliferation... - Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivationChi Hwa Wu
Department of Medicine, Division of Oncology, Stanford University School of Medicine, CA 94305, USA
Proc Natl Acad Sci U S A 104:13028-33. 2007..Our results suggest that cellular senescence programs remain latently functional, even in established tumors, and can become reactivated, serving as a critical mechanism of oncogene addiction associated with MYC inactivation... - Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesisCatherine M Shachaf
Division of Medical Oncology, Department of Medicine, Stanford University, Stanford, CA 94305 5151, USA
Blood 110:2674-84. 2007..Thus, atorvastatin, by inhibiting HMGcoA reductase, induces changes in phosphoprotein signaling that in turn prevent MYC-induced lymphomagenesis... - Conditional transgenic models define how MYC initiates and maintains tumorigenesisConstadina Arvanitis
Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, CA 94305, USA
Semin Cancer Biol 16:313-7. 2006..In other cases, even brief MYC inactivation is sufficient to induce sustained tumor regression. Insights from conditional transgenic mouse models will be useful in the development of therapies that target MYC for the treatment of cancer... - Identifying critical signaling molecules for the treatment of cancerConstadina Arvanitis
Department of Medicine, Stanford University School of Medicine, CA 94305-5151, USA
Recent Results Cancer Res 172:5-24. 2007 - Getting at MYC through RASPavan Bachireddy
Division of Medical Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
Clin Cancer Res 11:4278-81. 2005 - Genomically complex lymphomas undergo sustained tumor regression upon MYC inactivation unless they acquire novel chromosomal translocationsAsa Karlsson
Division of Oncology, Department of Medicine, Stanford University, CA 94305, USA
Blood 101:2797-803. 2003..We conclude that even highly genetically complex cancers are reversible on the inactivation of MYC, unless they acquire novel genetic alterations that can sustain a neoplastic phenotype... - Conditional animal models: a strategy to define when oncogenes will be effective targets to treat cancerSylvie Giuriato
Division of Oncology, Stanford University, CCSR 1105, 269 Campus Drive, Stanford, CA 94305-5151, USA
Semin Cancer Biol 14:3-11. 2004..Thus, these animal models will be useful to define the specific genes that will be therapeutically useful to target for the treatment of particular human cancers... - MYC can induce DNA breaks in vivo and in vitro independent of reactive oxygen speciesSuma Ray
Division of Oncology, Department of Medicine and Pathology, Stanford University School of Medicine, 269 Campus Drive, Stanford, CA 94305, USA
Cancer Res 66:6598-605. 2006..Hence, MYC overexpression can induce ROS and SSBs under some conditions, but generally induces widespread DSBs in vivo and in vitro independent of ROS production... - PET imaging of tumor neovascularization in a transgenic mouse model with a novel 64Cu-DOTA-knottin peptideCarsten H Nielsen
Molecular Imaging Program at Stanford, Department of Radiology, Division of Oncology, Stanford University, Stanford, California 94305 5427, USA
Cancer Res 70:9022-30. 2010..Collectively, these results show 64Cu-DOTA-knottin 2.5F to be a promising candidate for clinical translation for earlier detection and improved characterization of lung cancer... - Enhanced NFATc1 nuclear occupancy causes T cell activation independent of CD28 costimulationMinggui Pan
Division of Oncology, Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA
J Immunol 178:4315-21. 2007..In addition, NFATc1(nuc) destabilizes a positive feedback loop in which NFATc1 activates its own transcription as well as its targets, such as CD40 ligand and Th1/Th2 cytokines... - Impact of hydrodynamic injection and phiC31 integrase on tumor latency in a mouse model of MYC-induced hepatocellular carcinomaLauren E Woodard
Department of Genetics, Stanford University School of Medicine, Stanford, California, United States of America
PLoS ONE 5:e11367. 2010..However, chromosomal aberrations have been associated with phiC31 integrase expression in tissue culture, leading to questions about safety... - Conditionally MYC: insights from novel transgenic modelsConstadina Arvanitis
Departments of Medicine and Pathology, Division of Oncology, School of Medicine, Stanford University, CCSR 1105B, 269 Campus Drive, Stanford, CA 94305-5151, USA
Cancer Lett 226:95-9. 2005..Here we review results from recent experimental model systems, which demonstrate that the inactivation of MYC may be a specific and effective treatment for many types of cancer... - Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switchSylvie Giuriato
Departments of Medicine and Pathology, Division of Oncology, Stanford University School of Medicine, CCSR Building, Room 1120, 269 Campus Drive, Stanford, CA 94305 5151, USA
Proc Natl Acad Sci U S A 103:16266-71. 2006..Therefore, the combined inactivation of oncogenes and angiogenesis may be a more clinically effective treatment of cancer. We conclude that angiogenesis is an essential component of oncogene addiction... - Defective double-strand DNA break repair and chromosomal translocations by MYC overexpressionAsa Karlsson
Department of Medicine, Division of Oncology, Stanford University, Stanford, CA 94305 5151, USA
Proc Natl Acad Sci U S A 100:9974-9. 2003..Hence, MYC overexpression may be a previously undescribed example of a dominant mutator that may fuel tumorigenesis by inducing chromosomal damage... - HIF-dependent antitumorigenic effect of antioxidants in vivoPing Gao
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cancer Cell 12:230-8. 2007..These findings challenge the paradigm that antioxidants diminish tumorigenesis primarily through decreasing DNA damage and mutations and provide significant support for a key antitumorigenic effect of diminishing HIF levels... - Comparative genomic hybridization on mouse cDNA microarrays and its application to a murine lymphoma modelSandrine Sander
Department of Pathology, Stanford University, Stanford, CA 94305-5176, USA
Oncogene 24:6101-7. 2005.... - Noninvasive molecular imaging of c-Myc activation in living miceHua Fan-Minogue
Department of Radiology, Stanford University School of Medicine, CA 94305 5427, USA
Proc Natl Acad Sci U S A 107:15892-7. 2010.... - Apoptosis-stimulating protein of p53 (ASPP2) heterozygous mice are tumor-prone and have attenuated cellular damage-response thresholdsKerstin M Kampa
Department of Medicine, Division of Hematology and Medical Oncology, Oregon Health and Science University, Portland, OR 97239, USA
Proc Natl Acad Sci U S A 106:4390-5. 2009.... - Development of a micro-computed tomography-based image-guided conformal radiotherapy system for small animalsHu Zhou
Department of Radiation Oncology, Stanford University, Stanford, CA 94305 5847, USA
Int J Radiat Oncol Biol Phys 78:297-305. 2010.... - 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/CDK2Debabrita Deb-Basu
Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, California, USA
Cell Cycle 5:1348-55. 2006..Our results have implications for the mechanisms by which MYC overexpression dysregulates cell cycle transit, causes genomic destabilization and is restrained from causing tumorigenesis... - CDK2 is required by MYC to induce apoptosisDebabrita Deb-Basu
Division of Oncology, Department of Medicine, Stanford University, Stanford, California 94305 5151, USA
Cell Cycle 5:1342-7. 2006..The inhibition of CDK2 did not prevent apoptosis induced by the DNA damaging agent etoposide. Our results surprisingly suggest that CDK2 defines whether MYC induction causes apoptosis... - Specific tumor suppressor function for E2F2 in Myc-induced T cell lymphomagenesisRene Opavsky
Human Cancer Genetics Program, Department of Molecular Virology, Immunology, and Medical Genetics, College of Medicine and Public Health, Ohio State University, Columbus, OH 43210, USA
Proc Natl Acad Sci U S A 104:15400-5. 2007..These results identify the E2f2 locus as a tumor suppressor through its ability to modulate apoptosis... - An efficient and versatile system for acute and chronic modulation of renal tubular function in transgenic miceMilena Traykova-Brauch
Department of Cellular and Molecular Pathology, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany
Nat Med 14:979-84. 2008..These experiments establish Pax8-rtTA mice as a powerful tool for modeling renal diseases in transgenic mice... - Lethal cutaneous disease in transgenic mice conditionally expressing type I human T cell leukemia virus TaxHakju Kwon
Gladstone Institute of Virology and Immunology, San Francisco, California 94158, USA
J Biol Chem 280:35713-22. 2005..Of note, this skin disease completely resolved when Tax transgene expression was suppressed by administration of doxycycline, emphasizing the key role played by this viral oncoprotein in the observed pathology... - Suppression of p53 by Notch in lymphomagenesis: implications for initiation and regressionLevi J Beverly
The Wistar Institute, Philadelphia, Pennsylvania 19104, USA
Cancer Res 65:7159-68. 2005..Furthermore, we propose that suppression of p53 by Notch is a key mechanism underlying the initiation of T-cell lymphoma... - The human BCL6 transgene promotes the development of lymphomas in the mouseBeverly W Baron
Department of Pathology, Section of Hematology Oncology, University of Chicago, Chicago, IL 60637, USA
Proc Natl Acad Sci U S A 101:14198-203. 2004..Because BCL6 expression has been reported in a number of T cell tumors as well as in the more commonly occurring B cell lymphomas in humans, our transgenic mice provide a model for the study of human lymphomas... - Oncogenes as therapeutic targetsDean W Felsher
Semin Cancer Biol 14:1. 2004 - Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapySylvie Giuriato
INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France
Cancer Biol Ther 6:1318-23. 2007....
Research Grants
- MYC's Role in the Initiation and Maintenance of CancerDean W Felsher; Fiscal Year: 2010..The results of these studies will provide novel insights into the mechanism of "oncogene addiction" and will be useful towards the development of new treatments for T-ALL/lymphoblastic lymphoma. ..
- Molecular and Cellular Basis of Oncogene AddictionDean Felsher; Fiscal Year: 2009..The results of our proposed experiments will have important implications for the mechanisms by which the MYC oncogene maintains tumorigenesis and the development of new therapies for the treatment of cancer. ..
- MYC's Role in the Initiation and Maintenance of CancerDean Felsher; Fiscal Year: 2006..The results obtained from these studies will be useful in determining how MYC causes tumorigenesis and defining when the inactivation of MYC is likely to be effective in the treatment of human neoplasia. ..
- MYC's Role in the Initiation and Maintenance of CancerDean Felsher; Fiscal Year: 2007..The results of these studies will provide novel insights into the mechanism of "oncogene addiction" and will be useful towards the development of new treatments for T-ALL/lymphoblastic lymphoma. ..
- Differentiation of Osteogenic Sarcoma by MYCDean Felsher; Fiscal Year: 2007..The results of our experiments may have important implications for how the state of differentiation of a cell influences the ability of MYC to induce gene expression and thereby initiate and sustain tumorigenesis. ..
- C-MYC INDUCED TUMORIGENESIS AND GENOMIC INSTABILITYDean Felsher; Fiscal Year: 2002....
- Molecular and Cellular Basis of Oncogene AddictionDean W Felsher; Fiscal Year: 2010..The results of our proposed experiments will have important implications for the mechanisms by which the MYC oncogene maintains tumorigenesis and the development of new therapies for the treatment of cancer. ..