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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.
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Submitted January 22, 2007
Accepted March 20, 2007
Different STAT-3 and STAT-5 phosphorylation discriminates among Ph-negative chronic myeloproliferative diseases and is independent of the V617F JAK-2 mutation
Luciana Teofili, Maurizio Martini, Tonia Cenci, Giovanna Petrucci, Lorenza Torti, Sergio Storti, Francesco Guidi, Giuseppe Leone, and Luigi Maria Larocca*
Department of Hematology, Catholic University, Rome, Italy
Department of Pathology, Catholic University, Rome, Italy
Department of Hematology, Catholic University, Campobasso, Italy
* Corresponding author; email: llarocca{at}rm.unicatt.it.
The V617F JAK2 mutation reported in Ph-negative myeloproliferative diseases (MPD) 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 pSTA-5) by immunostaining bone marrow biopsies. We found three 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 MPD, 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.
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