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References
Cools J, DeAngelo DJ, Gotlib J, Stover EH, Legare RD, Cortes 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.
Gotlib J, Cools J . Five years since the discovery of FIP1L1-PDGFRA: what we have learned about the fusion and other molecularly defined eosinophilias. Leukemia 2008; 22: 1999–2010.
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 USA 2003; 100: 7830–7835.
Lierman E, Michaux L, Beullens E, Pierre P, Marynen P, Cools J et al. FIP1L1-PDGFRalpha D842V, a novel panresistant mutant, emerging after treatment of FIP1L1-PDGFRalpha T674I eosinophilic leukemia with single agent sorafenib. Leukemia 2009; 23: 845–851.
Ohnishi H, Kandabashi K, Maeda Y, Kawamura M, Watanabe T . Chronic eosinophilic leukaemia with FIP1L1-PDGFRA fusion and T6741 mutation that evolved from Langerhans cell histiocytosis with eosinophilia after chemotherapy. Br J Haematol 2006; 134: 547–549.
Score J, Walz C, Jovanovic JV, Jones AV, Waghorn K, Hidalgo-Curtis C et al. Detection and molecular monitoring of FIP1L1-PDGFRA-positive disease by analysis of patient-specific genomic DNA fusion junctions. Leukemia 2009; 23: 332–339.
von Bubnoff N, Sandherr M, Schlimok G, Andreesen R, Peschel C, Duyster J . Myeloid blast crisis evolving during imatinib treatment of an FIP1L1-PDGFR alpha-positive chronic myeloproliferative disease with prominent eosinophilia. Leukemia 2005; 19: 286–287.
von Bubnoff N, Gorantla SP, Engh RA, Oliveira TM, Thone S, Aberg E et al. The low frequency of clinical resistance to PDGFR inhibitors in myeloid neoplasms with abnormalities of PDGFRA might be related to the limited repertoire of possible PDGFRA kinase domain mutations in vitro. Oncogene 2010; 30: 933–943.
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This work was supported by the ‘Deutsche José Carreras Leukämie-Stiftung e.V.’ (AR R09/29f), Germany.
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Metzgeroth, G., Erben, P., Martin, H. et al. Limited clinical activity of nilotinib and sorafenib in FIP1L1-PDGFRA positive chronic eosinophilic leukemia with imatinib-resistant T674I mutation. Leukemia 26, 162–164 (2012). https://doi.org/10.1038/leu.2011.181
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DOI: https://doi.org/10.1038/leu.2011.181
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