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Blood, 1 April 2004, Vol. 103, No. 7, pp. 2802-2805.
Prepublished online as a Blood First Edition Paper on November 20, 2003; DOI 10.1182/blood-2003-07-2479.
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NEOPLASIA
Brief report
The EOL-1 cell line as an in vitro model for the study of FIP1L1-PDGFRA–positive chronic eosinophilic leukemia
Jan Cools,
Hilmar Quentmeier,
Brian J. P. Huntly,
Peter Marynen,
James D. Griffin,
Hans G. Drexler, and
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.
We recently identified the chimeric kinase FIP1L1-platelet-derived growth factor receptor  (PDGFR) 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-PDGFR. (Blood. 2004;103:2802-2805)
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