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Cells 2018, 7(1), 4; doi:10.3390/cells7010004

Targeting FLT3 Mutations in Acute Myeloid Leukemia

King Faisal Specialist Hospital and Research Center Riyadh, Riyadh 11211, Saudi Arabia
Author to whom correspondence should be addressed.
Received: 30 October 2017 / Revised: 19 December 2017 / Accepted: 4 January 2018 / Published: 8 January 2018
(This article belongs to the Special Issue Receptor Tyrosine Kinases in Health and Disease)
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The FMS-like tyrosine kinase 3 (FLT3) pathway has an important role in cellular proliferation, survival, and differentiation. Acute myeloid leukemia (AML) patients with mutated FLT3 have a large disease burden at presentation and a dismal prognosis. A number of FLT3 inhibitors have been developed over the years. The first-generation inhibitors are largely non-specific, while the second-generation inhibitors are more specific and more potent. These inhibitors are used to treat patients with FLT3-mutated AML in virtually all disease settings including induction, consolidation, maintenance, relapse, and after hematopoietic cell transplantation (HCT). In this article, we will review the use of FLT3 inhibitors in AML. View Full-Text
Keywords: FMS-like tyrosine kinase 3; acute myeloid leukemia; Midostaurine FMS-like tyrosine kinase 3; acute myeloid leukemia; Midostaurine

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

El Fakih, R.; Rasheed, W.; Hawsawi, Y.; Alsermani, M.; Hassanein, M. Targeting FLT3 Mutations in Acute Myeloid Leukemia. Cells 2018, 7, 4.

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