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    FLT3 Inhibitors in acute myeloid leukemia: Current status & future directions

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    Author
    Larrosa-Garcia, M.
    Baer, M.R.
    Date
    2017
    Journal
    Molecular Cancer Therapeutics
    Publisher
    American Association for Cancer Research Inc.
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1158/1535-7163.MCT-16-0876
    Abstract
    The receptor tyrosine kinase fms-like tyrosine kinase 3 (FLT3), involved in regulating survival, proliferation, and differentiation of hematopoietic stem/progenitor cells, is expressed on acute myeloid leukemia (AML) cells in most patients. Mutations of FLT3 resulting in constitutive signaling are common in AML, including internal tandem duplication (ITD) in the juxtamembrane domain in 25% of patients and point mutations in the tyrosine kinase domain in 5%. Patients with AML with FLT3-ITD have a high relapse rate and short relapse-free and overall survival after chemotherapy and after transplant. A number of inhibitors of FLT3 signaling have been identified and are in clinical trials, both alone and with chemotherapy, with the goal of improving clinical outcomes in patients with AML with FLT3 mutations. While inhibitor monotherapy produces clinical responses, they are usually incomplete and transient, and resistance develops rapidly. Diverse combination therapies have been suggested to potentiate the efficacy of FLT3 inhibitors and to prevent development of resistance or overcome resistance. Combinations with epigenetic therapies, proteasome inhibitors, downstream kinase inhibitors, phosphatase activators, and other drugs that alter signaling are being explored. This review summarizes the current status of translational and clinical research on FLT3 inhibitors in AML, and discusses novel combination approaches.
    Keyword
    Leukemia, Myeloid, Acute
    FLT3 protein, human
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85020791678&doi=10.1158%2f1535-7163.MCT-16-0876&partnerID=40&md5=c6feea11cda543140b6a97ddb632115d; http://hdl.handle.net/10713/10968
    ae974a485f413a2113503eed53cd6c53
    10.1158/1535-7163.MCT-16-0876
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