Related Experiment Video
Updated: Nov 4, 2025

04:36
Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors
Published on: October 17, 2025
391
FLT3 mutated acute myeloid leukemia: 2021 treatment algorithm
Naval Daver1, Sangeetha Venugopal2, Farhad Ravandi2
1Department of Leukemia, The University of Texas - MD Anderson Cancer Center, Houston, TX, USA. ndaver@mdanderson.org.
Blood Cancer Journal
|May 28, 2021
Summary
Approximately 30% of acute myeloid leukemia (AML) patients have FLT3 gene mutations. New FLT3 inhibitors improve outcomes, but resistance necessitates combination therapies for better AML treatment.
Area of Science:
- Hematology
- Oncology
- Molecular Biology
Background:
- About 30% of newly diagnosed acute myeloid leukemia (AML) patients harbor fms-like tyrosine kinase 3 (FLT3) gene mutations.
- While FLT3-ITD mutations clearly indicate a poor prognosis in AML, the prognostic value of FLT3-TKD mutations is still uncertain.
- Current guidelines advocate for prompt FLT3 mutation testing at diagnosis to guide treatment decisions and consider allogeneic stem cell transplant (ASCT).
Purpose of the Study:
- To review the current landscape of FLT3 mutations in AML, including their prognostic impact and the evolving role of targeted therapies.
- To highlight the challenges posed by resistance mechanisms and limited treatment options in relapsed/refractory FLT3-mutated AML.
- To emphasize the need for developing and implementing novel combination or sequential therapies for FLT3-mutated AML.
Main Methods:
- Literature review of studies on FLT3 mutations in AML.
- Analysis of current treatment guidelines and clinical trial data for FLT3 inhibitors.
- Discussion of resistance mechanisms and future therapeutic strategies.
Main Results:
- FLT3 mutations are common in AML and impact prognosis, with FLT3-ITD being particularly adverse.
- FLT3 inhibitors like midostaurin and gilteritinib have improved outcomes in newly diagnosed and relapsed/refractory FLT3-mutated AML, respectively.
- Resistance to single-agent FLT3 inhibitors and limited options for refractory disease remain significant challenges.
Conclusions:
- FLT3 mutation testing is crucial at diagnosis and relapse for guiding AML treatment.
- While FLT3 inhibitors have advanced AML therapy, achieving durable remissions, especially in relapsed/refractory settings without ASCT, remains difficult.
- Multi-agent combinatorial or sequential therapies are essential for overcoming resistance and improving outcomes in FLT3-mutated AML.

