Show simple item record

dc.contributor.authorLarrosa-Garcia, M.
dc.contributor.authorBaer, M.R.
dc.date.accessioned2019-09-19T18:35:47Z
dc.date.available2019-09-19T18:35:47Z
dc.date.issued2017
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85020791678&doi=10.1158%2f1535-7163.MCT-16-0876&partnerID=40&md5=c6feea11cda543140b6a97ddb632115d
dc.identifier.urihttp://hdl.handle.net/10713/10968
dc.description.abstractThe 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.en_US
dc.description.urihttps://doi.org/10.1158/1535-7163.MCT-16-0876en_US
dc.language.isoen_USen_US
dc.publisherAmerican Association for Cancer Research Inc.en_US
dc.relation.ispartofMolecular Cancer Therapeutics
dc.subject.meshLeukemia, Myeloid, Acuteen_US
dc.subject.meshFLT3 protein, humanen_US
dc.titleFLT3 Inhibitors in acute myeloid leukemia: Current status & future directionsen_US
dc.typeArticleen_US
dc.identifier.doi10.1158/1535-7163.MCT-16-0876
dc.identifier.pmid28576946


This item appears in the following Collection(s)

Show simple item record