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Clinical use of FLT3 inhibitors in acute myeloid leukemia

Authors Sutamtewagul G, Vigil CE

Received 25 April 2018

Accepted for publication 15 June 2018

Published 16 October 2018 Volume 2018:11 Pages 7041—7052

DOI https://doi.org/10.2147/OTT.S171640

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Justinn Cochran

Peer reviewer comments 6

Editor who approved publication: Dr Arseniy Yuzhalin


Grerk Sutamtewagu, Carlos E Vigil

Division of Hematology, Oncology and Blood and Marrow Transplantation, University of Iowa Hospitals and Clinics, Iowa City, IA, USA

Abstract: Acute myeloid leukemia (AML) is a highly heterogeneous disease. Mutation with internal tandem duplication of fms-like tyrosine kinase-3 (FLT3-ITD) is one of the two most common driver mutations and the presence of FLT3-ITD delivers poor prognosis. A number of ongoing clinical efforts are focused on FLT3 inhibitor use to improve the outcomes of this otherwise difficult leukemia. Midostaurin has been shown to improve outcomes in FLT3-mutated AML in the frontline setting. Several FLT3 inhibitors, especially second-generation agents, have shown clinically meaningful activity in relapsed or refractory AML and in patients not amenable to intensive therapy. In this article, we briefly review the biology of FLT3 in the physiological state and its role in leukemogenesis. We present a detailed review of current clinical evidence of FLT3 inhibitors and their use in the induction, treatment of relapsed or refractory disease, and maintenance setting.

Keywords: fms-like tyrosine kinase 3, FLT3 inhibitor, FLT3-ITD mutation, leukemia, myeloid, acute, protein kinase inhibitors

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