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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4392-4398. Prepublished online as a Blood First Edition Paper on February 6, 2007; DOI 10.1182/blood-2006-03-012575. This Article Full Text (PDF) All Versions of this Article: blood-2006-03-012575v1 109/10/4392    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 Peterson, L. F. Articles by Zhang, D.-E. Search for Related Content PubMed PubMed Citation Articles by Peterson, L. F. Articles by Zhang, D.-E. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 24, 2006 Accepted January 27, 2007 The p21waf1 pathway is involved in blocking leukemogenesis by the t(8;21) fusion protein AML1-ETO Luke F. Peterson, Ming Yan, and Dong-Er Zhang* Dept of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA * Corresponding author; email: dzhang{at}scripps.edu. The 8;21 translocation is a major contributor to acute myeloid leukemia of the M2 classification occurring in approximately 40% of these cases. Multiple mouse models using this fusion protein demonstrate that AML1-ETO requires secondary mutagenic event(s) to promote leukemogenesis. Here, we show that the negative cell cycle regulator p21waf1 gene is up-regulated by AML1-ETO at the protein, RNA, and promoter levels. Retroviral transduction and hematopoietic cell transplantation experiments with p21waf1 deficient cells show that AML1-ETO is able to promote leukemogenesis in the absence of p21waf1. Thus loss of p21waf1 facilitates AML1-ETO induced leukemogenesis, suggesting that mutagenic event(s) in the p21waf1 pathway to bypass the growth inhibitory effect from AML1-ETO induced p21waf1 expression can be a significant factor in AML1-ETO associated acute myeloid leukemia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Salat, R. Liefke, J. Wiedenmann, T. Borggrefe, and F. Oswald ETO, but Not Leukemogenic Fusion Protein AML1/ETO, Augments RBP-J{kappa}/SHARP-Mediated Repression of Notch Target Genes Mol. Cell. Biol., May 15, 2008; 28(10): 3502 - 3512. [Abstract] [Full Text] [PDF] O. Krejci, M. Wunderlich, H. Geiger, F.-S. Chou, D. Schleimer, M. Jansen, P. R. Andreassen, and J. C. Mulloy p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death Blood, February 15, 2008; 111(4): 2190 - 2199. [Abstract] [Full Text] [PDF] L. F. Peterson, A. Boyapati, E.-Y. Ahn, J. R. Biggs, A. J. Okumura, M.-C. Lo, M. Yan, and D.-E. Zhang Acute myeloid leukemia with the 8q22;21q22 translocation: secondary mutational events and alternative t(8;21) transcripts Blood, August 1, 2007; 110(3): 799 - 805. [Abstract] [Full Text] [PDF]

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