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Blood, 1 July 2007, Vol. 110, No. 1, pp. 354-359. Prepublished online as a Blood First Edition Paper on March 21, 2007; DOI 10.1182/blood-2007-01-069237. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-01-069237v1 110/1/354    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 Teofili, L. Articles by Larocca, L. M. Search for Related Content PubMed PubMed Citation Articles by Teofili, L. Articles by Larocca, L. M. Related Collections Oncogenes and Tumor Suppressors Signal Transduction Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Different STAT-3 and STAT-5 phosphorylation discriminates among Ph-negative chronic myeloproliferative diseases and is independent of the V617F JAK-2 mutation Luciana Teofili1, Maurizio Martini2, Tonia Cenci1, Giovanna Petrucci2, Lorenza Torti1, Sergio Storti3, Francesco Guidi3, Giuseppe Leone1, and Luigi Maria Larocca2 Departments of1 Hematology and 2 Pathology of the Catholic University of Rome, Italy, and the 3 Department of Hematology of the Catholic University of Campobasso, Italy The V617F JAK2 mutation reported in Ph-negative myeloproliferative diseases (MPDs) induces the constitutive activation of JAK2, which produces an increased phosphorylation of signal transducer activator of transcription (STAT). In this study, we have analyzed a series of 114 patients (54 with polycythemia vera [PV], 44 with essential thrombocythemia [ET], 12 with idiopathic myelofibrosis [IM], and 4 with myelofibrosis secondary to MPD) for the expression pattern of phosphorylated STAT-3 and STAT-5 (pSTAT-3 and pSTAT-5, respectively) by immunostaining bone marrow biopsies. We found 3 specific patterns of pSTAT-3 and pSTAT-5 expression, significantly different from the normal staining pattern: uniformly increased pSTAT-3 and pSTAT-5 expression in PV, increased pSTAT-3 and reduced pSTAT-5 expression in ET, and uniformly reduced pSTAT-3 and pSTAT-5 expression in IM. A moderate increase of pSTAT-3 and pSTAT-5 expression was observed in secondary forms of erythrocytosis and thrombocytosis. In all evaluated MPDs, the pSTAT-5 and pSTAT-3 expression pattern was not influenced by the presence of V617F JAK2 mutation. These findings underline the importance of bone marrow histology in the differential diagnosis of Ph-negative MPD and support the hypothesis that V617F mutation simply contributes with other molecular defects in allowing the PV, ET, or IM phenotype to emerge. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. Teofili, F. Giona, M. Martini, T. Cenci, F. Guidi, L. Torti, G. Palumbo, A. Amendola, G. Leone, R. Foa, et al. The revised WHO diagnostic criteria for Ph-negative myeloproliferative diseases are not appropriate for the diagnostic screening of childhood polycythemia vera and essential thrombocythemia Blood, November 1, 2007; 110(9): 3384 - 3386. [Abstract] [Full Text] [PDF]

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