Document Type

Article

Peer Reviewed

1

Publication Date

10-16-2018

Journal/Book/Conference Title

OncoTargets and Therapy

DOI of Published Version

10.2147/OTT.S171640

Start Page

7041

End Page

7052

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

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

Journal Article Version

Version of Record

Published Article/Book Citation

OncoTargets and Therapy 2018:11 7041-7052 https://doi.org/10.2147/OTT.S171640

Rights

© 2018 Sutamtewagul and Vigil

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License

Share

COinS
 

URL

https://ir.uiowa.edu/internalmedicine_pubs/30