FLT3 targeting in the modern era: from clonal selection to combination therapies

Vanessa E Kennedy; Catherine C Smith

doi:10.1007/s12185-023-03681-0

FLT3 targeting in the modern era: from clonal selection to combination therapies

Int J Hematol. 2023 Dec 19. doi: 10.1007/s12185-023-03681-0. Online ahead of print.

Authors

Vanessa E Kennedy¹, Catherine C Smith^{2

3}

Affiliations

¹ Division of Hematology/Oncology, Department of Medicine, University of California San Francisco, 505 Parnassus Ave, Box 1270, San Francisco, CA, 94143, USA.
² Division of Hematology/Oncology, Department of Medicine, University of California San Francisco, 505 Parnassus Ave, Box 1270, San Francisco, CA, 94143, USA. catherine.smith@ucsf.edu.
³ Helen Diller Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, USA. catherine.smith@ucsf.edu.

PMID: 38112995
DOI: 10.1007/s12185-023-03681-0

Abstract

Fms-like tyrosine kinase 3 (FLT3) is the most frequently mutated gene in acute myeloid leukemia (AML). Modern targeting of FLT3 with inhibitors has improved clinical outcomes and FLT3 inhibitors have been incorporated into the treatment of AML in all phases of the disease, including the upfront, relapsed/refractory and maintenance settings. This review will discuss the current understanding of FLT3 biology, the clinical use of FLT3 inhibitors, resistance mechanisms and emerging combination treatment strategies.

Keywords: AML; Acute Myeloid Leukemia; Clonal Evolution; FLT3; FLT3 inhibitor.

Publication types

Review