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Blood, 1 May 2006, Vol. 107, No. 9, pp. 3676-3682. Prepublished online as a Blood First Edition Paper on December 22, 2005; DOI 10.1182/blood-2005-09-3826. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-09-3826v1 2005-09-3826v2 107/9/3676    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 Passamonti, F. Articles by Cazzola, M. Search for Related Content PubMed PubMed Citation Articles by Passamonti, F. Articles by Cazzola, M. Related Collections Neoplasia Cell Adhesion and Motility Oncogenes and Tumor Suppressors Signal Transduction Free Research Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Relation between JAK2 (V617F) mutation status, granulocyte activation, and constitutive mobilization of CD34+ cells into peripheral blood in myeloproliferative disorders Francesco Passamonti, Elisa Rumi, Daniela Pietra, Matteo G. Della Porta, Emanuela Boveri, Cristiana Pascutto, Laura Vanelli, Luca Arcaini, Sara Burcheri, Luca Malcovati, Mario Lazzarino, and Mario Cazzola From the Department of Hematology and the Department of Pathology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Policlinico San Matteo and University of Pavia Medical School, Pavia, Italy. We studied the relationship between granulocyte JAK2 (V617F) mutation status, circulating CD34+ cells, and granulocyte activation in myeloproliferative disorders. Quantitative allele-specific polymerase chain reaction (PCR) showed significant differences between various disorders with respect to either the proportion of positive patients (53%-100%) or that of mutant alleles, which overall ranged from 1% to 100%. In polycythemia vera, JAK2 (V617F) was detected in 23 of 25 subjects at diagnosis and in 16 of 16 patients whose disease had evolved into myelofibrosis; median percentages of mutant alleles in these subgroups were significantly different (32% versus 95%, P < .001). Circulating CD34+ cell counts were variably elevated and associated with disease category and JAK2 (V617F) mutation status. Most patients had granulocyte activation patterns similar to those induced by administration of granulocyte colony-stimulating factor. A JAK2 (V617F) gene dosage effect on both CD34+ cell counts and granulocyte activation was clearly demonstrated in polycythemia vera, where abnormal patterns were mainly found in patients carrying more than 50% mutant alleles. These observations suggest that JAK2 (V617F) may constitutively activate granulocytes and by this means mobilize CD34+ cells. This exemplifies a novel paradigm in which a somatic gain-of-function mutation is initially responsible for clonal expansion of hematopoietic cells and later for their abnormal trafficking via an activated cell progeny. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Is bone marrow fibrosis the real problem? Ronald Hoffman and Mingjiang Xu Blood 2006 107: 3421-3422. [Full Text] [PDF] This article has been cited by other articles: G. Barosi, G. Birgegard, G. Finazzi, M. Griesshammer, C. Harrison, H. C. Hasselbalch, J.-J. Kiladjian, E. Lengfelder, M. F. McMullin, F. 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