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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 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 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 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. Related Collections Neoplasia Oncogenes and Tumor Suppressors Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA The p21Waf1 pathway is involved in blocking leukemogenesis by the t(8;21) fusion protein AML1-ETO Luke F. Peterson1, Ming Yan1, and Dong-Er Zhang1 1 Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, CA The 8;21 translocation is a major contributor to acute myeloid leukemia (AML) 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 events 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 events 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: Y.-H. Kuo, S. K. Zaidi, S. Gornostaeva, T. Komori, G. S. Stein, and L. H. Castilla Runx2 induces acute myeloid leukemia in cooperation with Cbf{beta}-SMMHC in mice Blood, April 2, 2009; 113(14): 3323 - 3332. [Abstract] [Full Text] [PDF] B. Yin, R. Delwel, P. J. Valk, M. R. Wallace, M. L. Loh, K. M. Shannon, and D. A. Largaespada A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene Blood, January 29, 2009; 113(5): 1075 - 1085. [Abstract] [Full Text] [PDF] 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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