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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.
Submitted July 23, 2003
Accepted November 16, 2003
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
Division of Hematology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Center for Human Genetics - Flanders Interuniversity Institute of Biotechnology (VIB), University of Leuven, Leuven, Belgium
Department of Human and Animal Cell Cultures, DSMZ - German Collection of Microorganisms and Cell Cultures, Braunschweig, Germany
Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Howard Hughes Medical Institute, Boston, MA, USA
Division of Hematology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
* Corresponding author; email: jan.cools{at}med.kuleuven.ac.be.
We recently identified the chimeric kinase FIP1L1-PDGFR as a cause of the hypereosinophilic syndrome and 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. The growth of EOL-1 cells was inhibited by 3 structurally divergent kinase inhibitors: imatinib (STI-571), PKC412, and SU5614. These results indicate that fusion of FIP1L1 to PDGFRA occurs rarely in leukemia cell lines, but 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.
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