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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 (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 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. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 16, 2007 Accepted April 1, 2007 Novel RUNX1 isoforms determine the fate of acute myeloid leukemia cells by controlling CD56 expression Stefan Gattenloehner*, Sergei Chuvpilo, Claudia Langebrake, Dirk Reinhardt, Hans-Konrad Muller-Hermelink, Edgar Serfling, Angela Vincent, and Alexander Marx Institute of Pathology, University of Wuerzburg, Wuerzburg, Germany Department of Pediatric Hematology and Oncology, University Children's Hospital Hannover, Hannover, Germany Neurosciences Group, Weatherall Inst. of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom Inst. of Pathology, University of Heidelberg, University Hospital Mannheim, Mannheim, Germany * Corresponding author; email: stefan.gattenloehner{at}mail.uni-wuerzburg.de. 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 here that CD56 expression on AML cells correlates with an abnormal expression pattern of RUNX1 isoforms. Whereas full-length p48 RUNX1 (p48) upregulated CD56 in AML cells, three previously unknown shorter RUNX1 isoforms, p38a, p30 and p24, suppressed CD56 expression. Both p48 and CD56 induced nuclear translocation of NF-B and increased bcl2L12 expression, and inhibition of this pathway by siRNA-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 signalling pathway(s). CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Gattenlohner, T. Stuhmer, E. Leich, M. Reinhard, B. Etschmann, H.-U. Volker, A. Rosenwald, E. Serfling, R. C. Bargou, G. Ertl, et al. Specific Detection of CD56 (NCAM) Isoforms for the Identification of Aggressive Malignant Neoplasms with Progressive Development Am. J. Pathol., April 1, 2009; 174(4): 1160 - 1171. [Abstract] [Full Text] [PDF] A. Zollinger, T. Stuhmer, M. Chatterjee, S. Gattenlohner, E. Haralambieva, H.-K. Muller-Hermelink, M. Andrulis, A. Greiner, C. Wesemeier, J. C. Rath, et al. Combined functional and molecular analysis of tumor cell signaling defines 2 distinct myeloma subgroups: Akt-dependent and Akt-independent multiple myeloma Blood, October 15, 2008; 112(8): 3403 - 3411. [Abstract] [Full Text] [PDF] 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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