期刊
BLOOD
卷 118, 期 8, 页码 2239-2242出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2011-03-343426
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资金
- German branch of the Jose Carreras Leukemia Foundation (Jose Carreras Leukamie-Stiftung e.V.) [DJCLS R06/02, R09/29f, H03/01]
- Leukaemia and Lymphoma Research, London, United Kingdom
- German Federal Ministry for Education and Research (Bundesministerium fur Bildung und Forschung
- Projekttrager Gesundheitsforschung) [DLR e.V.-01GI9980/6]
- European Community
Imatinib-resistant tyrosine kinase (TK) fusions involving FGFR1, JAK2, or FLT3 are rare but recurrent in patients with eosinophilia-associated neoplasms. We report here 2 male patients with ETV6-FLT3(+) myeloid/lymphoid neoplasms with eosinophilia who were treated with the multitargeted TK inhibitors sunitinib and sorafenib. Patient 1 achieved rapid complete hematologic response and complete cytogenetic response after 3 months of taking sunitinib. A secondary blast phase caused by clonal evolution was diagnosed after 6 months. He achieved a second complete hematologic response after taking sorafenib but relapsed 2 months later. An N841K point mutation within the TK domain of FLT3, previously reported in acute myeloid leukemia and potentially conferring resistance to sorafenib, was subsequently identified. Patient 2 was heavily pretreated according to the initial diagnosis of T-lymphoblastic lymphoma and died in sunitinib-induced pancytopenia. This report highlights the importance of a careful diagnostic workup for eosinophilia-associated neoplasms to evaluate the possibility of TK inhibitor therapy. (Blood. 2011; 118(8): 2239-2242)
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