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References
Cortes JE, Perl AE, Dombret H, Kayser S, Steffen B, Rousselot P et al. Final results of a phase 2 open-label, monotherapy efficacy and safety study of quizartinib (AC220) in patients >=60 years of age with FLT3 ITD positive or negative relapsed/refractory acute myeloid leukemia. Blood 2012; 120: 48.
Cheson BD, Bennett JM, Kopecky KJ, Buchner T, Willman CL, Estey EH et al. Revised recommendations of the International Working Group for Diagnosis, Standardization of Response Criteria, Treatment Outcomes, and Reporting Standards for Therapeutic Trials in Acute Myeloid Leukemia. J Clin Oncol 2003; 21: 4642–4649.
Smith CC, Wang Q, Chin CS, Salerno S, Damon LE, Levis MJ et al. Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia. Nature 2012; 485: 260–263.
Levis M, Allebach J, Tse KF, Zheng R, Baldwin BR, Smith BD et al. A FLT3-targeted tyrosine kinase inhibitor is cytotoxic to leukemia cells in vitro and in vivo. Blood 2002; 99: 3885–3891.
Fathi AT, Le L, Hasserjian RP, Sadrzadeh H, Levis M, Chen YB . FLT3 inhibitor-induced neutrophilic dermatosis. Blood 2013; 122: 239–242.
Sexauer A, Perl A, Yang X, Borowitz M, Gocke C, Rajkhowa T et al. Terminal myeloid differentiation in vivo is induced by FLT3 inhibition in FLT3/ITD AML. Blood 2012; 120: 4205–4214.
Cloos J, Goemans BF, Hess CJ, van Oostveen JW, Waisfisz Q, Corthals S et al. Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples. Leukemia 2006; 20: 1217–1220.
Piloto O, Wright M, Brown P, Kim KT, Levis M, Small D . Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways. Blood 2007; 109: 1643–1652.
Miller CA, Wilson RK, Ley TJ . Genomic landscapes and clonality of de novo AML. N Engl J Med 2013; 369: 1473.
Challen GA, Sun D, Jeong M, Luo M, Jelinek J, Berg JS et al. Dnmt3a is essential for hematopoietic stem cell differentiation. Nat Genet 2012; 44: 23–31.
Shlush LI, Zandi S, Mitchell A, Chen WC, Brandwein JM, Gupta V et al. Identification of pre-leukaemic haematopoietic stem cells in acute leukaemia. Nature 2014; 506: 328–333.
Falini B, Bolli N, Liso A, Martelli MP, Mannucci R, Pileri S et al. Altered nucleophosmin transport in acute myeloid leukaemia with mutated NPM1: molecular basis and clinical implications. Leukemia 2009; 23: 1731–1743.
Grisendi S, Bernardi R, Rossi M, Cheng K, Khandker L, Manova K et al. Role of nucleophosmin in embryonic development and tumorigenesis. Nature 2005; 437: 147–153.
Galanis A, Levis M . Inhibition of c-Kit by tyrosine kinase inhibitors. Haematologica 2015; 100: e77–e79.
Sehgal AR, Gimotty PA, Zhao J, Hsu JM, Daber R, Morrissette JD et al. DNMT3A mutational status affects the results of dose-escalated induction therapy in acute myelogenous leukemia. Clin Cancer Res 2015; 21: 1614–1620.
Acknowledgements
This study was supported by the National Institutes of Health, the National Cancer Institute (NCI; grant 1K23CA141054 to AEP) and the Leukemia and Lymphoma Society (NPS, CCS and AEP). NPS was supported by a grant from the National Cancer Institute (1R01 CA166616-01) and MC is supported by R21CA198621 also from the NCI. We thank Cezary Swider, PhD for technical expertise and assistance with cell processing.
Author contributions
GEN designed research, collected data, performed research, performed histopathologic analysis of clinical samples and wrote the paper; JC analyzed data and wrote the paper; DR collected data; JDM and CDW performed research NPS and CCS performed research; AB performed histopathologic analysis of clinical samples; MC and AEP designed research, analyzed data and wrote the paper. All authors provided critical review of the paper and approved the submission.
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AEP has served as a consultant to Ambit Biosciences, Astellas Pharmaceuticals and Arog Pharmaceuticals. CCS received clinical trial grant funding from Astellas. The remaining authors declare no conflict of interest.
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Results were presented in part at the 54th annual meeting of the American Society of Hematology meeting.
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Nybakken, G., Canaani, J., Roy, D. et al. Quizartinib elicits differential responses that correlate with karyotype and genotype of the leukemic clone. Leukemia 30, 1422–1425 (2016). https://doi.org/10.1038/leu.2015.320
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DOI: https://doi.org/10.1038/leu.2015.320
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