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Blood, 15 October 2005, Vol. 106, No. 8, pp. 2862-2864. Prepublished online as a Blood First Edition Paper on June 28, 2005; DOI 10.1182/blood-2005-04-1515. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-04-1515v1 106/8/2862    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 Goerttler, P. S. Articles by Pahl, H. L. Search for Related Content PubMed PubMed Citation Articles by Goerttler, P. S. Articles by Pahl, H. L. Related Collections Neoplasia Oncogenes and Tumor Suppressors 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  NEOPLASIA Brief report The Jak2V617F mutation, PRV-1 overexpression, and EEC formation define a similar cohort of MPD patients Philipp S. Goerttler, Cordula Steimle, Edith März, Peter L. Johansson, Björn Andreasson, Martin Griesshammer, Heinz Gisslinger, Hermann Heimpel, and Heike L. Pahl From the Departments of Experimental Anaesthesiology and Biology, University Hospital Freiburg, Freiburg, Germany; Haematology Section, Department of Medicine, Sahlgrenska University Hospital, University of Göteborg, Göteborg, Sweden; Department of Medicine III, Hematology, Oncology, Rheumatology, and Infectious Diseases, University Hospital Ulm, Ulm, Germany; and Department of Internal Medicine I, Division of Hematology and Blood Coagulation, Medical University of Vienna, Vienna, Austria. Recently, a Jak2V617F mutation has been described in the vast majority of patients with polycythemia vera (PV) as well as in subsets of patients with essential thrombocythemia (ET) and idiopathic myelofibrosis (IMF). The question arises whether this mutation is observed in those patients with ET and IMF who have also displayed previously described molecular markers, notably the ability to form endogenous erythroid colonies (EECs), overexpression of polycythemia rubra vera 1 (PRV-1), and decreased c-Mpl expression. We therefore analyzed the Janus kinase 2 (Jak2) DNA sequence, EEC growth, PRV-1 expression, and c-Mpl (myeloproliferative) levels in a cohort of 78 myeloproliferative disorder (MPD) patients (42 ET, 22 PV, and 14 IMF). Presence of the Jak2V617F mutation was very highly correlated with PRV-1 overexpression and the ability to form EECs in all 3 subtypes of MPDs (P < .001). (Blood. 2005;106:2862-2864) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Let's not get too JAKed up! Ronald Hoffman Blood 2005 106: 2599. [Full Text] [PDF] This article has been cited by other articles: L. Teofili, F. Giona, M. Martini, T. Cenci, F. 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[Abstract] [Full Text] [PDF] G. Wernig, T. Mercher, R. Okabe, R. L. Levine, B. H. Lee, and D. G. Gilliland Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model Blood, June 1, 2006; 107(11): 4274 - 4281. [Abstract] [Full Text] [PDF] R. L. Levine, C. Belisle, M. Wadleigh, D. Zahrieh, S. Lee, P. Chagnon, D. G. Gilliland, and L. Busque X-inactivation-based clonality analysis and quantitative JAK2V617F assessment reveal a strong association between clonality and JAK2V617F in PV but not ET/MMM, and identifies a subset of JAK2V617F-negative ET and MMM patients with clonal hematopoiesis Blood, May 15, 2006; 107(10): 4139 - 4141. [Abstract] [Full Text] [PDF] A. V. Jones, R. T. Silver, K. Waghorn, C. Curtis, S. Kreil, K. Zoi, A. Hochhaus, D. Oscier, G. Metzgeroth, E. Lengfelder, et al. 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