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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.

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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)–{kappa}B and increased bcl2L12 expression, and inhibition of this pathway by small inhibitory RNA-mediated p48 knock down or NF-{kappa}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-{kappa}B signaling pathway(s).


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