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Blood, 15 September 2007, Vol. 110, No. 6, pp. 2027-2033. Prepublished online as a Blood First Edition Paper on April 12, 2007; DOI 10.1182/blood-2007-02-074203. This Article Full Text Full Text (PDF) Supplemental Methods, Tables, and Figures Additional Supplemental Figures All Versions of this Article: blood-2007-02-074203v1 110/6/2027    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 Gattenloehner, S. Articles by Marx, A. Search for Related Content PubMed PubMed Citation Articles by Gattenloehner, S. Articles by Marx, A. Related Collections Oncogenes and Tumor Suppressors Gene Expression Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Novel RUNX1 isoforms determine the fate of acute myeloid leukemia cells by controlling CD56 expression Stefan Gattenloehner1, Sergei Chuvpilo1, Claudia Langebrake2, Dirk Reinhardt2, Hans-Konrad Müller-Hermelink1, Edgar Serfling1, Angela Vincent3, and Alexander Marx4 1 Institute of Pathology, University of Wuerzburg, Wuerzburg, Germany; 2 University Children's Hospital Hannover, Department of Pediatric Hematology and Oncology, Hannover, Germany; 3 Neurosciences Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom; and 4 Institute of Pathology, University of Heidelberg, University Hospital Mannheim, Mannheim, Germany CD56high acute myeloid leukemias (AMLs) have a poor prognosis, but it has been unclear how CD56 expression is controlled and how it relates to clinical aggressiveness. We show that CD56 expression on AML cells correlates with an abnormal expression pattern of runt-related transcription factor 1 (RUNX1) isoforms. Whereas full-length p48 RUNX1 (p48) up-regulated CD56 in AML cells, 3 previously unknown shorter RUNX1 isoforms, p38a, p30, and p24, suppressed CD56 expression. Both p48 and CD56 induced nuclear translocation of nuclear factor (NF)–B and increased bcl2L12 expression, and inhibition of this pathway by small inhibitory RNA-mediated p48 knock down or NF-B blockade substantially increased apoptosis in CD56+ AML cell lines. These findings indicate the potential for new therapy of CD56high AML by suppression of the "overactive" RUNX1/CD56/NF-B signaling pathway(s). CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J.-H. Klusmann, U. Creutzig, M. Zimmermann, M. Dworzak, N. Jorch, C. Langebrake, A. Pekrun, K. Macakova-Reinhardt, and D. Reinhardt Treatment and prognostic impact of transient leukemia in neonates with Down syndrome Blood, March 15, 2008; 111(6): 2991 - 2998. [Abstract] [Full Text] [PDF] B. H. Lemster, J. J. Michel, D. T. Montag, J. J. Paat, S. A. Studenski, A. B. Newman, and A. N. Vallejo Induction of CD56 and TCR-Independent Activation of T Cells with Aging J. Immunol., February 1, 2008; 180(3): 1979 - 1990. [Abstract] [Full Text] [PDF]

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