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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3374-3376. Prepublished online as a Blood First Edition Paper on August 4, 2005; DOI 10.1182/blood-2005-05-1889. This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: 2005-05-1889v1 106/10/3374    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 Kralovics, R. Articles by Skoda, R. C. Search for Related Content PubMed PubMed Citation Articles by Kralovics, R. Articles by Skoda, R. C. Related Collections Neoplasia Oncogenes and Tumor Suppressors Signal Transduction Free Research Articles Brief Reports Clinical Trials and Observations Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CLINICAL TRIALS AND OBSERVATIONS Brief report Altered gene expression in myeloproliferative disorders correlates with activation of signaling by the V617F mutation of Jak2 Robert Kralovics, Soon-Siong Teo, Andreas S. Buser, Martin Brutsche, Ralph Tiedt, Andre Tichelli, Francesco Passamonti, Daniela Pietra, Mario Cazzola, and Radek C. Skoda From the Experimental Hematology, Department of Research, Division of Clinical Hematology, Division of Pneumology, and Division of Diagnostic Hematology, Basel University Hospital, Basel, Switzerland; and Division of Hematology, University of Pavia Medical School and IRCCS Policlinico S. Matteo, Pavia, Italy. We identified 13 new gene expression markers that were elevated and one marker, ANKRD15, that was down-regulated in patients with polycythemia vera (PV). These 14 markers, as well as the previously described PRV1 and NF-E2, exhibited the same gene expression alterations also in patients with exogenously activated granulocytes due to sepsis or granulocyte colony-stimulating factor (G-CSF) treatment. The recently described V617F mutation in the Janus kinase 2 (JAK2) gene allows defining subclasses of patients with myeloproliferative disorders based on the JAK2 genotype. Patients with PV who were homozygous or heterozygous for JAK2-V617F exhibited higher levels of expression of the 13 new markers, PRV1, and NF-E2 than patients without JAK2-V617F, whereas ANKRD15 was down-regulated in these patients. Our results suggest that the alterations in expression of the markers studied are due to the activation of the Jak/signal transducer and activator of transcription (STAT) pathway through exogenous stimuli (sepsis or G-CSF treatment), or endogenously through the JAK2-V617F mutation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: V617F "JAKs" up myeloproliferative signal Ayalew Tefferi Blood 2005 106: 3335-3336. [Full Text] [PDF] This article has been cited by other articles: L. Pieri, C. Bogani, P. Guglielmelli, M. Zingariello, R. A. Rana, N. Bartalucci, A. Bosi, and A. M. Vannucchi The JAK2V617 mutation induces constitutive activation and agonist hypersensitivity in basophils from patients with polycythemia vera Haematologica, November 1, 2009; 94(11): 1537 - 1545. [Abstract] [Full Text] [PDF] N. Fourouclas, J. Li, D. C. Gilby, P. J. Campbell, P. A. Beer, E. M. Boyd, A. C. Goodeve, D. Bareford, C. N. Harrison, J. T. Reilly, et al. Methylation of the suppressor of cytokine signaling 3 gene (SOCS3) in myeloproliferative disorders Haematologica, November 1, 2008; 93(11): 1635 - 1644. [Abstract] [Full Text] [PDF] K. Liu, R. Kralovics, Z. Rudzki, B. Grabowska, A. S. Buser, D. Olcaydu, H. Gisslinger, R. Tiedt, P. Frank, K. Okon, et al. A de novo splice donor mutation in the thrombopoietin gene causes hereditary thrombocythemia in a Polish family Haematologica, May 1, 2008; 93(5): 706 - 714. [Abstract] [Full Text] [PDF] D. Pietra, S. Li, A. Brisci, F. Passamonti, E. Rumi, A. Theocharides, M. Ferrari, H. Gisslinger, R. Kralovics, L. Cremonesi, et al. Somatic mutations of JAK2 exon 12 in patients with JAK2 (V617F)-negative myeloproliferative disorders Blood, February 1, 2008; 111(3): 1686 - 1689. [Abstract] [Full Text] [PDF] E. Antonioli, P. Guglielmelli, G. Poli, C. Bogani, A. Pancrazzi, G. Longo, V. Ponziani, L. Tozzi, L. Pieri, V. Santini, et al. 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Masliah, V. Praloran, and S. Hermouet Latent myeloproliferative disorder revealed by the JAK2-V617F mutation and endogenous megakaryocytic colonies in patients with splanchnic vein thrombosis. Blood, November 1, 2006; 108(9): 3223 - 3224. [Full Text] [PDF] E. Lippert, M. Boissinot, R. Kralovics, F. Girodon, I. Dobo, V. Praloran, N. Boiret-Dupre, R. C. Skoda, and S. Hermouet The JAK2-V617F mutation is frequently present at diagnosis in patients with essential thrombocythemia and polycythemia vera Blood, September 15, 2006; 108(6): 1865 - 1867. [Abstract] [Full Text] [PDF] C. Bellanne-Chantelot, I. Chaumarel, M. Labopin, F. Bellanger, V. Barbu, C. De Toma, F. Delhommeau, N. Casadevall, W. Vainchenker, G. Thomas, et al. Genetic and clinical implications of the Val617Phe JAK2 mutation in 72 families with myeloproliferative disorders Blood, July 1, 2006; 108(1): 346 - 352. [Abstract] [Full Text] [PDF] A. I. 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