{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T08:36:44Z","timestamp":1790671004244,"version":"4.1.0"},"reference-count":20,"publisher":"American Society of Hematology","issue":"7","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2004,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>We recently identified the chimeric kinase FIP1L1-platelet-derived growth factor receptor \u03b1 (PDGFR\u03b1) 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\u2014imatinib (STI-571), PKC412, and SU5614\u2014inhibited 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\u03b1. (Blood. 2004;103:2802-2805)<\/jats:p>","DOI":"10.1182\/blood-2003-07-2479","type":"journal-article","created":{"date-parts":[[2003,11,25]],"date-time":"2003-11-25T01:14:27Z","timestamp":1069722867000},"page":"2802-2805","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":72,"title":["The EOL-1 cell line as an in vitro model for the study of FIP1L1-PDGFRA\u2013positive chronic eosinophilic leukemia"],"prefix":"10.1182","volume":"103","author":[{"given":"Jan","family":"Cools","sequence":"first","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hilmar","family":"Quentmeier","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian J. P.","family":"Huntly","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Marynen","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James D.","family":"Griffin","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans G.","family":"Drexler","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. Gary","family":"Gilliland","sequence":"additional","affiliation":[{"name":"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."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"key":"2020021218031444600_REF1","doi-asserted-by":"crossref","unstructured":"Chusid MJ, Dale DC, West BC, Wolff SM. The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore). 1975;54: 1-27.","DOI":"10.1097\/00005792-197501000-00001"},{"key":"2020021218031444600_REF2","doi-asserted-by":"crossref","unstructured":"Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood. 1994;83: 2759-2779.","DOI":"10.1182\/blood.V83.10.2759.2759"},{"key":"2020021218031444600_REF3","unstructured":"Bain BJ. Eosinophilic leukaemias and the idiopathic hypereosinophilic syndrome. Br J Haematol. 1996;95: 2-9."},{"key":"2020021218031444600_REF4","doi-asserted-by":"crossref","unstructured":"Cools J, DeAngelo DJ, Gotlib J, et al. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med. 2003;348: 1201-1214.","DOI":"10.1056\/NEJMoa025217"},{"key":"2020021218031444600_REF5","doi-asserted-by":"crossref","unstructured":"Drexler HG, Matsuo AY, MacLeod RA. Continuous hematopoietic cell lines as model systems for leukemia- lymphoma research. Leuk Res. 2000;24: 881-911.","DOI":"10.1016\/S0145-2126(00)00070-9"},{"key":"2020021218031444600_REF6","doi-asserted-by":"crossref","unstructured":"Quentmeier H, Reinhardt J, Zaborski M, Drexler HG. FLT3 mutations in acute myeloid leukemia cell lines. Leukemia. 2003;17: 120-124.","DOI":"10.1038\/sj.leu.2402740"},{"key":"2020021218031444600_REF7","doi-asserted-by":"crossref","unstructured":"Klion AD, Noel P, Akin C, et al. Elevated serum tryptase levels identify a subset of patients with a myeloproliferative variant of idiopathic hypereosinophilic syndrome associated with tissue fibrosis, poor prognosis, and imatinib responsiveness. Blood. 2003;101: 4660-4666.","DOI":"10.1182\/blood-2003-01-0006"},{"key":"2020021218031444600_REF8","doi-asserted-by":"crossref","unstructured":"Saito H, Bourinbaiar A, Ginsburg M, et al. Establishment and characterization of a new human eosinophilic leukemia cell line. Blood. 1985;66: 1233-1240.","DOI":"10.1182\/blood.V66.6.1233.1233"},{"key":"2020021218031444600_REF9","doi-asserted-by":"crossref","unstructured":"Quentmeier H, Reinhardt J, Zaborski M, Drexler HG. MLL partial tandem duplication in acute leukemia cell lines. Leukemia. 2003;17: 980-981.","DOI":"10.1038\/sj.leu.2402911"},{"key":"2020021218031444600_REF10","doi-asserted-by":"crossref","unstructured":"Ayton PM, Cleary ML. Molecular mechanisms of leukemogenesis mediated by MLL fusion proteins. Oncogene. 2001;20: 5695-5707.","DOI":"10.1038\/sj.onc.1204639"},{"key":"2020021218031444600_REF11","unstructured":"Caligiuri MA, Strout MP, Schichman SA, et al. Partial tandem duplication of ALL1 as a recurrent molecular defect in acute myeloid leukemia with trisomy 11. Cancer Res. 1996;56: 1418-1425."},{"key":"2020021218031444600_REF12","doi-asserted-by":"crossref","unstructured":"Kelly LM, Gilliland DG. Genetics of myeloid leukemias. Annu Rev Genomics Hum Genet. 2002;3: 179-198.","DOI":"10.1146\/annurev.genom.3.032802.115046"},{"key":"2020021218031444600_REF13","doi-asserted-by":"crossref","unstructured":"Capdeville R, Buchdunger E, Zimmermann J, Matter A. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug. Nat Rev Drug Discov. 2002;1: 493-502.","DOI":"10.1038\/nrd839"},{"key":"2020021218031444600_REF14","unstructured":"Andrejauskas-Buchdunger E, Regenass U. Differential inhibition of the epidermal growth factor-, platelet- derived growth factor-, and protein kinase C-mediated signal transduction pathways by the staurosporine derivative CGP 41251. Cancer Res. 1992;52: 5353-5358."},{"key":"2020021218031444600_REF15","doi-asserted-by":"crossref","unstructured":"Cools J, Stover EH, Boulton CL, et al. PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFR-induced myeloproliferative disease. Cancer Cell. 2003;3: 459-469.","DOI":"10.1016\/S1535-6108(03)00108-9"},{"key":"2020021218031444600_REF16","doi-asserted-by":"crossref","unstructured":"Sun L, Tran N, Tang F, et al. Synthesis and biological evaluations of 3-substituted indolin-2-ones: a novel class of tyrosine kinase inhibitors that exhibit selectivity toward particular receptor tyrosine kinases. J Med Chem. 1998;41: 2588-2603.","DOI":"10.1021\/jm980123i"},{"key":"2020021218031444600_REF17","doi-asserted-by":"crossref","unstructured":"Yee KW, O'Farrell AM, Smolich BD, et al. SU5416 and SU5614 inhibit kinase activity of wild-type and mutant FLT3 receptor tyrosine kinase. Blood. 2002;100: 2941-2949.","DOI":"10.1182\/blood-2002-02-0531"},{"key":"2020021218031444600_REF18","doi-asserted-by":"crossref","unstructured":"Spiekermann K, Dirschinger RJ, Schwab R, et al. The protein tyrosine kinase inhibitor SU5614 inhibits FLT3 and induces growth arrest and apoptosis in AML-derived cell lines expressing a constitutively activated FLT3. Blood. 2003;101: 1494-1504.","DOI":"10.1182\/blood-2002-04-1045"},{"key":"2020021218031444600_REF19","doi-asserted-by":"crossref","unstructured":"Griffin JH, Leung J, Bruner RJ, Caligiuri MA, Briesewitz R. Discovery of a fusion kinase in EOL-1 cells and idiopathic hypereosinophilic syndrome. Proc Natl Acad Sci U S A. 2003;100: 7830-7835.","DOI":"10.1073\/pnas.0932698100"},{"key":"2020021218031444600_REF20","doi-asserted-by":"crossref","unstructured":"Higuchi W, Koike T, Ihizumi T, Shibata A. Hyper-eosinophilic syndrome terminating in acute myelogenous leukemia. Acta Haematol. 1993;90: 165-166.","DOI":"10.1159\/000204402"}],"container-title":["Blood"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/ashpublications.org\/blood\/article-pdf\/103\/7\/2802\/1697160\/zh800704002802.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"http:\/\/ashpublications.org\/blood\/article-pdf\/103\/7\/2802\/1697160\/zh800704002802.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,2,13]],"date-time":"2020-02-13T00:02:14Z","timestamp":1581552134000},"score":1,"resource":{"primary":{"URL":"https:\/\/ashpublications.org\/blood\/article\/103\/7\/2802\/18262\/The-EOL1-cell-line-as-an-in-vitro-model-for-the"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2004,4,1]]},"references-count":20,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2004,4,1]]}},"URL":"https:\/\/doi.org\/10.1182\/blood-2003-07-2479","relation":{},"ISSN":["0006-4971","1528-0020"],"issn-type":[{"value":"0006-4971","type":"print"},{"value":"1528-0020","type":"electronic"}],"subject":[],"published":{"date-parts":[[2004,4,1]]}}}