# Current Therapeutic Strategies for FLT3-Mutated Acute Myeloid Leukemia: A Narrative Review

## TL;DR

This review discusses current treatments for a type of leukemia caused by mutations in the FLT3 gene and summarizes how these treatments affect cancer cell lines.

## Contribution

The paper provides a comprehensive overview of FLT3-mutated AML cell lines and their response to FDA-approved and investigational drugs.

## Key findings

- Only four human AML cell lines express an internal duplication in FLT3.
- Three FDA-approved drugs target mutated FLT3, but many others are under investigation.
- FLT3 mutations are associated with poor prognosis in AML patients.

## Abstract

Patients with acute myeloid leukemia (AML) typically present with unexplained weight loss, fatigue, and other nonspecific and varied symptoms, and are diagnosed by the aggressive onset of symptoms and a peripheral blood smear with a high proportion of myeloblasts. Patients with AML may have a variety of mutations, but mutations in FMS-like tyrosine kinase 3 (FLT3) are prognostic of outcomes. Notably, only four human AML cell lines express an internal duplication in FLT3, while two human AML cell lines contain an activating mutation in the juxtamembrane domain. A variety of other cell lines express mutated FLT3, including lymphoid leukemia cell lines. Several drugs have been developed to target mutated FLT3, but only three have been FDA-approved. In this review, we summarize the human myeloid leukemia cell lines that express mutated FLT3 and the effect of several drugs on these cell lines. Our aim in this review is to provide clinicians with a basic science understanding of human myeloid leukemia cell lines and to provide scientific researchers with the clinical implications of FLT3 signaling inhibition.