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Prepublished online as a Blood First Edition Paper on November 27, 2002; DOI 10.1182/blood-2002-10-3091. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-10-3091v1 101/7/2797    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Karlsson, A. Articles by Felsher, D. W. Search for Related Content PubMed PubMed Citation Articles by Karlsson, A. Articles by Felsher, D. W. Related Collections Neoplasia Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 April 2003, Vol. 101, No. 7, pp. 2797-2803 NEOPLASIA Genomically complex lymphomas undergo sustained tumor regression upon MYC inactivation unless they acquire novel chromosomal translocations Åsa Karlsson, Sylvie Giuriato, Flora Tang, Jingly Fung-Weier, Göran Levan, and Dean W. Felsher From the Division of Oncology, Departments of Medicine and Pathology, Stanford University, CA; Reproductive Genetics Unit, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco; and the Department of Cellular and Molecular BiologyGenetics, Göteborg University, Sweden. The targeted inactivation of oncogenes may be a specific and effective treatment for cancer. However, because human cancers are the consequence of multiple genetic changes, the inactivation of one oncogene may not be sufficient to cause sustained tumor regression. Moreover, cancers are genomically unstable and may readily compensate for the inactivation of a single oncogene. Here we confirm by spectral karyotypic analysis that MYC-induced hematopoietic tumors are highly genetically complex and genomically unstable. Nevertheless, the inactivation of MYC alone was found to be sufficient to induce sustained tumor regression. After prolonged MYC inactivation, some tumors exhibited a distinct propensity to relapse. When tumors relapsed, they no longer required the overexpression of MYC but instead acquired novel chromosomal translocations. 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. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. J. Horton, V. Walf-Vorderwulbecke, S. J. Chatters, N. J. Sebire, J. de Boer, and O. Williams Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities Blood, May 14, 2009; 113(20): 4922 - 4929. [Abstract] [Full Text] [PDF] X. Li, F. Gounari, A. Protopopov, K. Khazaie, and H. von Boehmer Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1 J. Exp. Med., November 24, 2008; 205(12): 2851 - 2861. [Abstract] [Full Text] [PDF] M. Eilers and R. N. Eisenman Myc's broad reach Genes & Dev., October 15, 2008; 22(20): 2755 - 2766. 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