The EOL-1 cell line as an in vitro model for the study of FIP1L1-PDGFRA–positive chronic eosinophilic leukemia

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  • Jan Cools
    From the Division of Hematology and the Howard Hughes Medical Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; Center for Human Genetics-Flanders Interuniversity Institute of Biotechnology (VIB), University of Leuven, Belgium; and the DSMZ-German Collection of Microorganisms and Cell Cultures, Department of Human and Animal Cell Cultures, Braunschweig, Germany.
  • Hilmar Quentmeier
    From the Division of Hematology and the Howard Hughes Medical Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; Center for Human Genetics-Flanders Interuniversity Institute of Biotechnology (VIB), University of Leuven, Belgium; and the DSMZ-German Collection of Microorganisms and Cell Cultures, Department of Human and Animal Cell Cultures, Braunschweig, Germany.
  • Brian J. P. Huntly
    From the Division of Hematology and the Howard Hughes Medical Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; Center for Human Genetics-Flanders Interuniversity Institute of Biotechnology (VIB), University of Leuven, Belgium; and the DSMZ-German Collection of Microorganisms and Cell Cultures, Department of Human and Animal Cell Cultures, Braunschweig, Germany.
  • Peter Marynen
    From the Division of Hematology and the Howard Hughes Medical Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; Center for Human Genetics-Flanders Interuniversity Institute of Biotechnology (VIB), University of Leuven, Belgium; and the DSMZ-German Collection of Microorganisms and Cell Cultures, Department of Human and Animal Cell Cultures, Braunschweig, Germany.
  • James D. Griffin
    From the Division of Hematology and the Howard Hughes Medical Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; Center for Human Genetics-Flanders Interuniversity Institute of Biotechnology (VIB), University of Leuven, Belgium; and the DSMZ-German Collection of Microorganisms and Cell Cultures, Department of Human and Animal Cell Cultures, Braunschweig, Germany.
  • Hans G. Drexler
    From the Division of Hematology and the Howard Hughes Medical Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; Center for Human Genetics-Flanders Interuniversity Institute of Biotechnology (VIB), University of Leuven, Belgium; and the DSMZ-German Collection of Microorganisms and Cell Cultures, Department of Human and Animal Cell Cultures, Braunschweig, Germany.
  • D. Gary Gilliland
    From the Division of Hematology and the Howard Hughes Medical Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; Center for Human Genetics-Flanders Interuniversity Institute of Biotechnology (VIB), University of Leuven, Belgium; and the DSMZ-German Collection of Microorganisms and Cell Cultures, Department of Human and Animal Cell Cultures, Braunschweig, Germany.

抄録

<jats:title>Abstract</jats:title> <jats:p>We recently identified the chimeric kinase FIP1L1-platelet-derived growth factor receptor α (PDGFRα) as a cause of the hypereosinophilic syndrome and of chronic eosinophilic leukemia. To investigate the role of FIP1L1-PDGFRA in the pathogenesis of acute leukemia, we screened 87 leukemia cell lines for the presence of FIP1L1-PDGFRA. One cell line, EOL-1, expressed the FIP1L1-PDGFRA fusion. Three structurally divergent kinase inhibitors—imatinib (STI-571), PKC412, and SU5614—inhibited the growth of EOL-1 cells. These results indicate that the fusion of FIP1L1 to PDGFRA occurs rarely in leukemia cell lines, but they identify EOL-1 as an in vitro model for the study of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia and for the analysis of small molecule inhibitors of FIP1L1-PDGFRα. (Blood. 2004;103:2802-2805)</jats:p>

収録刊行物

  • Blood

    Blood 103 (7), 2802-2805, 2004-04-01

    American Society of Hematology

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