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Blood, 15 March 2007, Vol. 109, No. 6, pp. 2399-2405. Prepublished online as a Blood First Edition Paper on November 7, 2006; DOI 10.1182/blood-2006-01-030643. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-01-030643v1 109/6/2399    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 Sloand, E. M. Articles by Young, N. S. Search for Related Content PubMed PubMed Citation Articles by Sloand, E. M. Articles by Young, N. S. Related Collections Hematopoiesis and Stem Cells Neoplasia Apoptosis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS CD34 cells from patients with trisomy 8 myelodysplastic syndrome (MDS) express early apoptotic markers but avoid programmed cell death by up-regulation of antiapoptotic proteins Elaine M. Sloand1, Loretta Pfannes1, Gubin Chen1, Simant Shah1, Elena E. Solomou1, John Barrett1, and Neal S. Young1 1 National Heart Lung and Blood Institute, Bethesda, MD CD34 cells from patients with trisomy 8 myelodysplastic syndrome (MDS) are distinguished from other MDS cells and from normal hematopoietic cells by their pronounced expression of apoptotic markers. Paradoxically, trisomy 8 clones can persist in patients with bone marrow failure and expand following immunosuppression. We previously demonstrated up-regulation of c-myc and CD1 by microarray analysis. Here, we confirmed these findings by real-time polymerase chain reaction (PCR), demonstrated up-regulation of survivin, c-myc, and CD1 protein expression, and documented comparable colony formation by annexin+ trisomy 8– CD34+ and annexin– CD34 cells. There were low levels of DNA degradation in annexin+ trisomy 8 CD34 cells, which were comparable with annexin– CD34 cells. Trisomy 8 cells were resistant to apoptosis induced by gamma irradiation. Knock-down of survivin by siRNA resulted in preferential loss of trisomy 8 cells. These results suggest that trisomy 8 cells undergo incomplete apoptosis and are nonetheless capable of colony formation and growth. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. J. Barrett and E. Sloand Autoimmune mechanisms in the pathophysiology of myelodysplastic syndromes and their clinical relevance Haematologica, April 1, 2009; 94(4): 449 - 451. [Full Text] [PDF] A. Shenoy, L. Pfannes, F. Wilhelm, M. Maniar, N. Young, and E. M Sloand Suppression of Cyclin D 1 (CD1) by on 01910.Na Is Associated with Decreased Survival or Trisomy 8 Myelodysplastic Bone Marrow: A Potential Targetted Therapy for Trisomy 8 MDS. Blood (ASH Annual Meeting Abstracts), November 16, 2008; 112(11): 1651 - 1651. [Abstract] [Full Text] E. M Sloand, H. Padilla-Nash, M. Furnari, R. Calado, L. Casey, T. Reid, and N. S Young Inflammation Caused by Allogeneic Lymphocytes Results in Aneuploidy in Bone Marrow Mononuclear Cells (BMMNC) Blood (ASH Annual Meeting Abstracts), November 16, 2008; 112(11): 3112 - 3112. [Abstract] [Full Text] G. C. Bagby and G. Meyers Bone Marrow Failure as a Risk Factor for Clonal Evolution: Prospects for Leukemia Prevention Hematology, January 1, 2007; 2007(1): 40 - 46. [Abstract] [Full Text] [PDF]

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