Dean Felsher

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi request reprint Sustained loss of a neoplastic phenotype by brief inactivation of MYC
    Meenakshi Jain
    Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA 94305 5151, USA
    Science 297:102-4. 2002
  2. pmc CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation
    Kavya 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
  3. pmc Combined analysis of murine and human microarrays and ChIP analysis reveals genes associated with the ability of MYC to maintain tumorigenesis
    Chi Hwa Wu
    Department of Medicine, Division of Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS Genet 4:e1000090. 2008
  4. pmc Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas
    Phuoc T Tran
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 3:e2125. 2008
  5. pmc Hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesis
    Shelly 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
  6. pmc Developmental context determines latency of MYC-induced tumorigenesis
    Shelly Beer
    Division of Oncology, Department of Medicine, Stanford University, Stanford, California, USA
    PLoS Biol 2:e332. 2004
  7. pmc A quantitative PCR method to detect blood microRNAs associated with tumorigenesis in transgenic mice
    Alice C Fan
    Stanford University, School of Medicine, Division of Oncology, Department of Medicine, Stanford, CA 94305 5151, USA
    Mol Cancer 7:74. 2008
  8. doi request reprint Reversing cancer from inside and out: oncogene addiction, cellular senescence, and the angiogenic switch
    Dean W Felsher
    Division of Oncology, Department of Medicine, Stanford University, Stanford, CA 94305, USA
    Lymphat Res Biol 6:149-54. 2008
  9. ncbi request reprint Tumor dormancy: death and resurrection of cancer as seen through transgenic mouse models
    Dean W Felsher
    Division of Oncology, Department of Medicine, Stanford University, Stanford, California 94305 5151, USA
    Cell Cycle 5:1808-11. 2006
  10. doi request reprint 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

Detail Information

Publications57

  1. ncbi request reprint Sustained loss of a neoplastic phenotype by brief inactivation of MYC
    Meenakshi 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...
  2. pmc CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation
    Kavya 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...
  3. pmc Combined analysis of murine and human microarrays and ChIP analysis reveals genes associated with the ability of MYC to maintain tumorigenesis
    Chi 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...
  4. pmc Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas
    Phuoc T Tran
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 3:e2125. 2008
    ..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...
  5. pmc Hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesis
    Shelly 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
    ....
  6. pmc Developmental context determines latency of MYC-induced tumorigenesis
    Shelly 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...
  7. pmc A quantitative PCR method to detect blood microRNAs associated with tumorigenesis in transgenic mice
    Alice 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...
  8. doi request reprint Reversing cancer from inside and out: oncogene addiction, cellular senescence, and the angiogenic switch
    Dean 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...
  9. ncbi request reprint Tumor dormancy: death and resurrection of cancer as seen through transgenic mouse models
    Dean 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...
  10. doi request reprint 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...
  11. ncbi request reprint Myc and a Cdk2 senescence switch
    Jan 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...
  12. ncbi request reprint Cancer revoked: oncogenes as therapeutic targets
    Dean 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?..
  13. ncbi request reprint Putting oncogenes into a developmental context
    Dean 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...
  14. ncbi request reprint Pharmacological inactivation of MYC for the treatment of cancer
    Dean 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...
  15. doi request reprint Tumor dormancy and oncogene addiction
    Dean 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...
  16. ncbi request reprint Reversibility of oncogene-induced cancer
    Dean 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...
  17. ncbi request reprint MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancer
    Catherine M Shachaf
    Division of Medical Oncology, Department of Medicine, Stanford University, California 94305, USA
    Nature 431:1112-7. 2004
    ....
  18. ncbi request reprint Genomic and proteomic analysis reveals a threshold level of MYC required for tumor maintenance
    Catherine 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...
  19. ncbi request reprint Tumor dormancy and MYC inactivation: pushing cancer to the brink of normalcy
    Catherine 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...
  20. ncbi request reprint How cancers escape their oncogene habit
    Sylvie 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...
  21. pmc In vivo imaging-based mathematical modeling techniques that enhance the understanding of oncogene addiction in relation to tumor growth
    Chinyere Nwabugwu
    Department of Electrical Engineering, Stanford University School of Medicine, Stanford, CA 94305, USA
    Comput Math Methods Med 2013:802512. 2013
    ..Finally, delay differential equations were used to accurately model the tumor growth kinetics that we have observed. We use this to model oncogene addiction in MYC-induced lymphoma, osteosarcoma, and hepatocellular carcinoma...
  22. ncbi request reprint Rehabilitation of cancer through oncogene inactivation
    Catherine 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...
  23. pmc PET imaging of tumor neovascularization in a transgenic mouse model with a novel 64Cu-DOTA-knottin peptide
    Carsten 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...
  24. pmc Hypoxia in models of lung cancer: implications for targeted therapeutics
    Edward E Graves
    Department of Radiation Oncology, Stanford University, California 94305 5847, USA
    Clin Cancer Res 16:4843-52. 2010
    ....
  25. ncbi request reprint (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
    Constadina Arvanitis
    Department of Chemical and Systems Biology, Stanford School of Medicine, Stanford, California 94403, USA
    Cancer Biol Ther 7:1947-51. 2008
    ....
  26. ncbi request reprint Nanofluidic proteomic assay for serial analysis of oncoprotein activation in clinical specimens
    Alice 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...
  27. doi request reprint MYC as a regulator of ribosome biogenesis and protein synthesis
    Jan 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...
  28. pmc Low-level shRNA cytotoxicity can contribute to MYC-induced hepatocellular carcinoma in adult mice
    Shelly 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...
  29. ncbi request reprint Getting at MYC through RAS
    Pavan Bachireddy
    Division of Medical Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    Clin Cancer Res 11:4278-81. 2005
  30. ncbi request reprint Conditional animal models: a strategy to define when oncogenes will be effective targets to treat cancer
    Sylvie 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...
  31. pmc The interaction between Myc and Miz1 is required to antagonize TGFbeta-dependent autocrine signaling during lymphoma formation and maintenance
    Jan van Riggelen
    Department of Medicine, Division of Oncology, Stanford University, School of Medicine, Stanford, California 94304, USA
    Genes Dev 24:1281-94. 2010
    ....
  32. ncbi request reprint Genomically complex lymphomas undergo sustained tumor regression upon MYC inactivation unless they acquire novel chromosomal translocations
    Asa 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...
  33. pmc Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivation
    Chi 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...
  34. ncbi request reprint Identifying critical signaling molecules for the treatment of cancer
    Constadina Arvanitis
    Department of Medicine, Stanford University School of Medicine, CA 94305 5151, USA
    Recent Results Cancer Res 172:5-24. 2007
  35. ncbi request reprint Conditional transgenic models define how MYC initiates and maintains tumorigenesis
    Constadina 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...
  36. ncbi request reprint MYC can induce DNA breaks in vivo and in vitro independent of reactive oxygen species
    Suma 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...
  37. pmc Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesis
    Catherine 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...
  38. doi request reprint SPECT and PET imaging of EGF receptors with site-specifically labeled EGF and dimeric EGF
    Zoya Levashova
    Department of Radiology MIPS, Stanford University School of Medicine, California 94305, USA
    Bioconjug Chem 20:742-9. 2009
    ..We expect that nuclear imaging of EGF receptors with these tracers will be useful for clinical diagnosis, therapeutic monitoring, and development of new drugs and treatment regimens...
  39. ncbi request reprint Enhanced NFATc1 nuclear occupancy causes T cell activation independent of CD28 costimulation
    Minggui 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...
  40. pmc Defective double-strand DNA break repair and chromosomal translocations by MYC overexpression
    Asa 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...
  41. pmc Impact of hydrodynamic injection and phiC31 integrase on tumor latency in a mouse model of MYC-induced hepatocellular carcinoma
    Lauren 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...
  42. ncbi request reprint Comparative genomic hybridization on mouse cDNA microarrays and its application to a murine lymphoma model
    Sandrine Sander
    Department of Pathology, Stanford University, Stanford, CA 94305 5176, USA
    Oncogene 24:6101-7. 2005
    ....
  43. ncbi request reprint Conditionally MYC: insights from novel transgenic models
    Constadina 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...
  44. pmc HIF-dependent antitumorigenic effect of antioxidants in vivo
    Ping 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...
  45. pmc Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch
    Sylvie 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...
  46. pmc Noninvasive molecular imaging of c-Myc activation in living mice
    Hua 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
    ....
  47. ncbi request reprint CDK2 is required by MYC to induce apoptosis
    Debabrita 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...
  48. pmc Apoptosis-stimulating protein of p53 (ASPP2) heterozygous mice are tumor-prone and have attenuated cellular damage-response thresholds
    Kerstin 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
    ....
  49. pmc Development of a micro-computed tomography-based image-guided conformal radiotherapy system for small animals
    Hu Zhou
    Department of Radiation Oncology, Stanford University, Stanford, CA 94305 5847, USA
    Int J Radiat Oncol Biol Phys 78:297-305. 2010
    ....
  50. ncbi request reprint 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
    Debabrita 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...
  51. pmc Specific tumor suppressor function for E2F2 in Myc-induced T cell lymphomagenesis
    Rene 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...
  52. pmc An efficient and versatile system for acute and chronic modulation of renal tubular function in transgenic mice
    Milena 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...
  53. ncbi request reprint Oncogenes as therapeutic targets
    Dean W Felsher
    Semin Cancer Biol 14:1. 2004
  54. ncbi request reprint Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy
    Sylvie Giuriato
    INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France
    Cancer Biol Ther 6:1318-23. 2007
    ....
  55. ncbi request reprint Suppression of p53 by Notch in lymphomagenesis: implications for initiation and regression
    Levi 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...
  56. ncbi request reprint Lethal cutaneous disease in transgenic mice conditionally expressing type I human T cell leukemia virus Tax
    Hakju 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...
  57. pmc The human BCL6 transgene promotes the development of lymphomas in the mouse
    Beverly 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...

Research Grants19

  1. MYC's Role in the Initiation and Maintenance of Cancer
    Dean Felsher; Fiscal Year: 2001
    ..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. ..
  2. MYC's Role in the Initiation and Maintenance of Cancer
    Dean 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. ..
  3. Molecular and Cellular Basis of Oncogene Addiction
    Dean 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. ..
  4. MYC's Role in the Initiation and Maintenance of Cancer
    Dean Felsher; Fiscal Year: 2009
    ..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. ..
  5. MYC's Role in the Initiation and Maintenance of Cancer
    Dean 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. ..
  6. MYC's Role in the Initiation and Maintenance of Cancer
    Dean 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. ..
  7. Differentiation of Osteogenic Sarcoma by MYC
    Dean 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. ..
  8. Molecular and Cellular Basis of Oncogene Addiction
    Dean 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. ..
  9. MYC's Role in the Initiation and Maintenance of Cancer
    Dean Felsher; Fiscal Year: 2005
    ..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. ..
  10. Differentiation of Osteogenic Sarcoma by MYC
    Dean Felsher; Fiscal Year: 2005
    ..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. ..
  11. MYC's Role in the Initiation and Maintenance of Cancer
    Dean Felsher; Fiscal Year: 2003
    ..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. ..
  12. MYC's Role in the Initiation and Maintenance of Cancer
    Dean Felsher; Fiscal Year: 2004
    ..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. ..
  13. Differentiation of Osteogenic Sarcoma by MYC
    Dean Felsher; Fiscal Year: 2004
    ..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. ..
  14. MYC's Role in the Initiation and Maintenance of Cancer
    Dean Felsher; Fiscal Year: 2003
    ..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. ..
  15. C-MYC INDUCED TUMORIGENESIS AND GENOMIC INSTABILITY
    Dean Felsher; Fiscal Year: 2002
    ....
  16. MYC's Role in the Initiation and Maintenance of Cancer
    Dean Felsher; Fiscal Year: 2002
    ..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. ..
  17. Differentiation of Osteogenic Sarcoma by MYC
    Dean Felsher; Fiscal Year: 2006
    ..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. ..