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Division of Oncology, Departments of Medicine and Pathology Stanford University, Stanford, California
Requests for reprints: Dean W. Felsher, Division of Oncology, Departments of Medicine and Oncology, CCSR 1150, MC 5151 Stanford University, Stanford, CA, 94305. Phone: 650-498-5269; Fax: 650-725-1420; E-mail: dfelsher{at}stanford.edu.
Upon MYC inactivation, tumors variously undergo proliferative arrest, cellular differentiation, and apoptosis and in some cases, apparently permanently revoking tumorigenesis. In liver tumor cells, we recently showed that MYC inactivation uncovers stem cell properties and triggers differentiation, but in this case, their neoplastic properties are restorable by MYC reactivation. 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.
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D. W. Felsher, I. B. Weinstein, and A. Joe Oncogene Addiction versus Oncogene Amnesia: Perhaps More than Just a Bad Habit? Cancer Res., May 1, 2008; 68(9): 3081 - 3086. [Abstract] [Full Text] [PDF] |
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D. W. Felsher Validating Oncogenes as Therapeutic Targets Using Conditional Transgenic Models Am. Assoc. Cancer Res. Educ. Book, April 14, 2007; 2007(1): 27 - 36. [Full Text] [PDF] |
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C. Morrison, M. Radmacher, N. Mohammed, D. Suster, H. Auer, S. Jones, J. Riggenbach, N. Kelbick, G. Bos, and J. Mayerson MYC Amplification and Polysomy 8 in Chondrosarcoma: Array Comparative Genomic Hybridization, Fluorescent In Situ Hybridization, and Association With Outcome J. Clin. Oncol., December 20, 2005; 23(36): 9369 - 9376. [Abstract] [Full Text] [PDF] |
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