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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
Treatment of Acute Myeloid Leukemia with the FLT3 Gene Mutation
Carlos Best-Aguilera1, O Rodrigo Gómez-Vázquez2, A Elizabeth Guzmán-Hernández2
1Department of Hematology, Hospital General de Occidente/ Universidad de Guadalajara, Av. Zoquipan 1050, 45170, Zapopan, Jal., Mexico. carlosbest@gmail.com.
Abstract:
In acute myeloid leukemia (AML), mutations of the Fms-like tyrosine kinase 3 receptor (FLT3) and its overexpression are related with hyperleukocytosis, higher risk of relapse, and decrease of both disease-free survival and overall survival. It has been suggested that this phenomenon confers proliferative and survival advantages to the malignant blast cells. As a consequence, it is an attractive therapeutic target. As the best treatment strategy for mutated FLT3 AML remains to be defined, the addition of FLT3 inhibitor drugs to chemotherapy or to the bone marrow transplant approach has become a growing strategy. With encouraging results, this combination seems to be an attractive option. Relevant data regarding the current treatment trends on mutated FLT3 AML is reviewed here.
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