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Blood, 15 January 2007, Vol. 109, No. 2, pp. 792-794. Prepublished online as a Blood First Edition Paper on September 12, 2006; DOI 10.1182/blood-2006-07-033985. This Article Full Text (PDF) All Versions of this Article: blood-2006-07-033985v1 109/2/792    most recent Alert me when this article is cited Alert me if a correction is posted 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 Bertwistle, D. Articles by Sherr, C. J Search for Related Content PubMed PubMed Citation Articles by Bertwistle, D. Articles by Sherr, C. J Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 6, 2006 Accepted August 18, 2006 Regulation of the Arf tumor suppressor in Eµ-Myc transgenic mice: longitudinal study of Myc-induced lymphomagenesis David Bertwistle and Charles J Sherr* HHMI/St. Jude Children's Research Hospital, Memphis, TN, USA * Corresponding author; email: sherr{at}stjude.org. Lymphomagenesis in Eµ-Myc mice is opposed by the Arf tumor suppressor, whose inactivation compromises p53 function and accelerates disease. Finding nascent Eµ-Myc-induced tumors in which p19Arf causes cell cycle arrest or apoptosis is problematic, since such cells will be eliminated until Arf or p53 function is lost. " Knock-in" mice expressing a green fluorescent protein (GFP) in lieu of Arf coding sequences allow analysis of Arf promoter regulation uncoupled from p19Arf action. Prior to frank lymphoma development, unexpectedly low levels of Eµ-Myc-induced p19Arf or GFP were expressed. However, as lymphomas arose in Arf+/GFP heterozygotes, additional oncogenic events synergized with Eµ-Myc to further induce the functionally null Arf-GFP allele. Concomitant up-regulation of p19Arf was not observed; instead, the wild type allele was inactivated. We infer that very low levels of Arf are tumor suppressive, and that further induction provides the selective pressure for the emergence of tumors that have inactivated the gene. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. E. Freeman-Anderson, Y. Zheng, A. C. McCalla-Martin, L. M. Treanor, Y. D. Zhao, P. M. Garfin, T.-C. He, M. N. Mary, J. D. Thornton, C. Anderson, et al. Expression of the Arf tumor suppressor gene is controlled by Tgf{beta}2 during development Development, June 15, 2009; 136(12): 2081 - 2089. [Abstract] [Full Text] [PDF] A. Gromley, M. L. Churchman, F. Zindy, and C. J. Sherr Transient expression of the Arf tumor suppressor during male germ cell and eye development in Arf-Cre reporter mice PNAS, April 14, 2009; 106(15): 6285 - 6290. [Abstract] [Full Text] [PDF] Z. Li, D. Boone, and S. R. Hann Nucleophosmin interacts directly with c-Myc and controls c-Myc-induced hyperproliferation and transformation PNAS, December 2, 2008; 105(48): 18794 - 18799. [Abstract] [Full Text] [PDF] J. A. Benanti, M. L. Wang, H. E. Myers, K. L. Robinson, C. Grandori, and D. A. Galloway Epigenetic Down-Regulation of ARF Expression Is a Selection Step in Immortalization of Human Fibroblasts by c-Myc Mol. Cancer Res., November 1, 2007; 5(11): 1181 - 1189. [Abstract] [Full Text] [PDF] M. Reimann, C. Loddenkemper, C. Rudolph, I. Schildhauer, B. Teichmann, H. Stein, B. Schlegelberger, B. Dorken, and C. A. Schmitt The Myc-evoked DNA damage response accounts for treatment resistance in primary lymphomas in vivo Blood, October 15, 2007; 110(8): 2996 - 3004. [Abstract] [Full Text] [PDF]

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