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Blood, 15 May 2005, Vol. 105, No. 10, pp. 3875-3878. Prepublished online as a Blood First Edition Paper on January 27, 2005; DOI 10.1182/blood-2004-10-3934. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-10-3934v1 105/10/3875    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 Lannutti, B. J. Articles by Drachman, J. G. Search for Related Content PubMed PubMed Citation Articles by Lannutti, B. J. Articles by Drachman, J. G. Related Collections Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Brief report Induction of polyploidization in leukemic cell lines and primary bone marrow by Src kinase inhibitor SU6656 Brian J. Lannutti, Noel Blake, Manish J. Gandhi, Jo Anna Reems, and Jonathan G. Drachman From the Puget Sound Blood Center, Seattle, WA; and the Division of Hematology, University of Washington Medical Center, Seattle, WA. Megakaryocytes (MKs) undergo successive rounds of endomitosis during differentiation, resulting in polyploidy (typically, 16-64N). Previous studies have demonstrated that this occurs through an interruption of normal cell cycle progression during anaphase. However, the molecular mechanism(s) controlling this unique process is undefined. In the present report, we examine the effect of an Src kinase inhibitor, SU6656, on thrombopoietin (TPO)-induced growth and differentiation. Remarkably, when SU6656 (2.5 µM) was added to a megakaryocytic cell line, UT-7/TPO, the cells ceased cell division but continued to accumulate DNA by endomitosis. During this interval, CD41 and CD61 expression on the cell surface increased. Similar effects on polyploidization and MK differentiation were seen with expanded primary MKs, bone marrow from 2 patients with myelodysplastic syndrome, and other cell lines with MK potential. Our data suggest that SU6656 might be useful as a differentiation-inducing agent for MKs and is an important tool for understanding the molecular basis of MK endomitosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. Wang and B. Damania Kaposi's Sarcoma-Associated Herpesvirus Confers a Survival Advantage to Endothelial Cells Cancer Res., June 15, 2008; 68(12): 4640 - 4648. [Abstract] [Full Text] [PDF] M. K. Larson and S. P. Watson Regulation of proplatelet formation and platelet release by integrin {alpha}IIbbeta3 Blood, September 1, 2006; 108(5): 1509 - 1514. [Abstract] [Full Text] [PDF] M. K. Larson and S. P. Watson Differential Effects of Extracellular Matrix Proteins on Proplatelet Formation: A Novel Role for Fibrinogen. Blood (ASH Annual Meeting Abstracts), November 16, 2005; 106(11): 2654 - 2654. [Abstract]

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