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Blood, 1 November 2006, Vol. 108, No. 9, pp. 3128-3134. Prepublished online as a Blood First Edition Paper on June 6, 2006; DOI 10.1182/blood-2006-04-017392. This Article Full Text (PDF) Supplemental Table All Versions of this Article: blood-2006-04-017392v1 108/9/3128    most recent Alert me when this article is cited Alert me if a correction is posted 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 Ishii, T. Articles by Xu, M. Search for Related Content PubMed PubMed Citation Articles by Ishii, T. Articles by Xu, M. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 3, 2005 Accepted May 18, 2006 Involvement of various hematopoietic cell lineages by the JAK2V617F mutation in polycythemia vera Takefumi Ishii, Edward Bruno, Ronald Hoffman, and Mingjiang Xu* Section of Hematology/Oncology, Department of Medicine, University of Illinois College of Medicine * Corresponding author; email: mxu16{at}uic.edu. The JAK2V617F mutation has been shown to occur in the overwhelming majority of patients with polycythemia vera (PV). In order to study the role of the mutation in the excessive production of differentiated hematopoietic cells in PV, CD19+, CD3+, CD34+, CD33+, glycophorin A+ cells and granulocytes were isolated from the peripheral blood (PB) of 8 patients with PV and 3 normal donors mobilized with G-CSF and the percent of JAK2V617F mutant allele determined by quantitative real-time PCR. The JAK2V617F mutation was present in cells belonging to each of the myeloid lineages and was also present in B- and T-lymphocytes in a subpopulation of patients with PV. The proportion of hematopoietic cells expressing the JAK2V617F mutation decreased after differentiation of CD34+ cells in vitro in the presence of optimal concentrations of SCF, IL-3, IL-6 and Epo. These data suggest that the JAK2V617F mutation may not provide a proliferative and/or survival advantage for the abnormal PV clone. While the JAK2V617F mutation plays an important role in the biological origins of PV, it is likely not the sole event leading to PV. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: X. Wang, W. Zhang, T. Ishii, S. Sozer, J. Wang, M. Xu, and R. 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