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Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 92 No. 10 (November 15), 1998: pp. 3829-3840 Bcr-Abl Efficiently Induces a Myeloproliferative Disease and Production of Excess Interleukin-3 and Granulocyte-Macrophage Colony-Stimulating Factor in Mice: A Novel Model for Chronic Myelogenous Leukemia Xiaowu Zhang and Ruibao Ren From the Rosenstiel Basic Medical Sciences Research Center, the Department of Biochemistry, and the Department of Biology, Brandeis University, Waltham, MA. The bcr-abl oncogene plays a critical role in causing chronic myelogenous leukemia (CML). Effective laboratory animal models of CML are needed to study the molecular mechanisms by which the bcr-abl oncogene acts in the disease progression of CML. We used a murine stem cell retroviral vector (MSCV) to transduce the bcr-abl/p210 oncogene into mouse bone marrow cells and found that expression of Bcr-Abl/p210 induced a myeloproliferative disorder that resembled the chronic phase of human CML in 100% of bone marrow transplanted mice in about 3 weeks. This CML-like disease was readily transplanted to secondary recipient mice. Multiple clones of infected cells were expanded in the primary recipients, but the leukemia was primarily monoclonal in the secondary recipient mice. Mutation analysis demonstrated that the protein tyrosine kinase activity of Bcr-Abl/p210 was essential for its leukemogenic potential in vivo. Interestingly, we found that the leukemic cells expressed excess interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in the diseased mice. These studies demonstrate that expression of Bcr-Abl can induce a CML-like leukemia in mice much more efficiently and reproducibly than in previously reported mouse CML models, probably due to efficient expression in the correct target cell(s). Our first use of this model for analysis of the molecular mechanisms involved in CML raises the possibility that excess expression of hematopoietic growth factors such as IL-3 and GM-CSF may contribute to the clinical phenotype of CML. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Mumprecht, C. Schurch, J. Schwaller, M. Solenthaler, and A. F. Ochsenbein Programmed death 1 signaling on chronic myeloid leukemia-specific T cells results in T-cell exhaustion and disease progression Blood, August 20, 2009; 114(8): 1528 - 1536. [Abstract] [Full Text] [PDF] Z. Jagani, K. Song, J. L. Kutok, M. R. Dewar, A. Melet, T. Santos, A. Grassian, S. Ghaffari, C. Wu, R. 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Neubauer Expression of nuclear transcription factor interferon consensus sequence binding protein in chronic myeloid leukemia correlates with pretreatment risk features and cytogenetic response to interferon-{alpha} Blood, June 1, 2001; 97(11): 3648 - 3650. [Abstract] [Full Text] [PDF] R. C. Zhao, Y. Jiang, and C. M. Verfaillie A model of human p210bcr/ABL-mediated chronic myelogenous leukemia by transduction of primary normal human CD34+ cells with a BCR/ABL-containing retroviral vector Blood, April 15, 2001; 97(8): 2406 - 2412. [Abstract] [Full Text] [PDF] M. H. Tomasson, I. R. Williams, S. Li, J. Kutok, D. Cain, S. Gillessen, G. Dranoff, R. A. Van Etten, and D. G. Gilliland Induction of myeloproliferative disease in mice by tyrosine kinase fusion oncogenes does not require granulocyte-macrophage colony-stimulating factor or interleukin-3 Blood, March 1, 2001; 97(5): 1435 - 1441. [Abstract] [Full Text] [PDF] S. Li, S. Gillessen, M. H. Tomasson, G. Dranoff, D. G. Gilliland, and R. A. 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Nucifora, and R. Ren Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: A model for human AML PNAS, February 15, 2000; 97(4): 1760 - 1765. [Abstract] [Full Text] [PDF]

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