SEARCH:   Advanced

Blood, 15 March 2006, Vol. 107, No. 6, pp. 2525-2530. Prepublished online as a Blood First Edition Paper on November 29, 2005; DOI 10.1182/blood-2005-06-2552. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-06-2552v1 107/6/2525    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 Corazza, F. Articles by Sariban, E. Search for Related Content PubMed PubMed Citation Articles by Corazza, F. Articles by Sariban, E. Related Collections Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Neoplasia Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Circulating thrombopoietin as an in vivo growth factor for blast cells in acute myeloid leukemia Francis Corazza, Christophe Hermans, Stéphanie D'Hondt, Alina Ferster, Alain Kentos, Yves Benoît, and Eric Sariban From the Laboratory of Hematology, Brugmann University Hospital, Brussels; the Laboratory of Pediatric Oncology and Hematology-Oncology Unit, Hôpital Universitaire des Enfants, Brussels; the Hematology Department, Erasme University Hospital, Brussels; and the Pediatric Oncology Department UZ-Ghent, Belgium. Thrombopoietin (TPO), the major growth factor for cells of the megakaryocytic lineage, is removed from circulation by binding to c-mpl receptors present on platelets and megakaryocytes. We studied patients with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia (AML) and used TPO-induced c-fos protein up-regulation as a marker of c-mpl functionality and observed that c-mpl-presenting blast cells were present in 62% (37 of 60) of patients with ALL but that c-mpl was nonfunctional in 0 of 28 patients and that they were present in 56% (22 of 39) of patients with AML and were functional in 43% (12 of 28). Adequate increases in serum TPO level in response to thrombocytopenia were seen in patients with ALL and with c-mpl-deficient (c-mpl-) AML. In contrast, in patients with c-mpl-proficient (c-mpl+) AML, TPO levels were found to be inappropriately low but increased to expected values during induction chemotherapy as blasts disappeared. In vitro significant TPO-associated blast cell proliferation or decreased apoptosis was observed only in patients with c-mpl+ AML compared with ALL or c-mpl- AML and was highly correlated with low in vivo TPO levels (P < .001). These data suggest that, in patients with AML, inadequate TPO levels are secondary to TPO clearing by functional c-mpl receptor myeloid blast cells and that TPO may serve as an in vivo myeloid leukemic growth factor in a significant number of patients. (Blood. 2006; 107:2525-2530) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Perreault and J. Burzynski Romiplostim: A novel thrombopoiesis-stimulating agent Am. J. Health Syst. Pharm., May 1, 2009; 66(9): 817 - 824. [Abstract] [Full Text] [PDF]

	Copyright © 2006 by American Society of Hematology         Online ISSN: 1528-0020