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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The authors wish to thank Dr. Mónica Vazquez del Mercado (CUCS, Universidad de Guadalajara) for her invaluable support in English grammar review.
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Carlos Best-Aguilera has received compensation from Avillion Development 1, Ltd., Novartis, AbbVie Farmacéuticos S.A. de C.V., and Celgene for service as a consultant.
O Rodrigo Gómez-Vázquez declares that he has no conflict of interest.
A. Elizabeth Guzmán-Hernández declares that she has no conflict of interest.
R. Monserrat Rojas-Sotelo has received compensation from Janssen and Avillion Development 1, Ltd. for service as a consultant.
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Best-Aguilera, C., Rodrigo Gómez-Vázquez, O., Elizabeth Guzmán-Hernández, A. et al. Treatment of Acute Myeloid Leukemia with the FLT3 Gene Mutation. Curr Oncol Rep 19, 21 (2017). https://doi.org/10.1007/s11912-017-0573-x
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DOI: https://doi.org/10.1007/s11912-017-0573-x