Abstract
Advances in the Treatment of FLT3-Mutated AML
Highlights
The Fms-Like Tyrosine kinase 3 (FLT3) gene is located on chromosome 13q12, and the resultant protein is a member of the class III Receptor Tyrosine Kinase (RTK) family
The FLT3 gene is located on chromosome 13q12, and the resultant protein is a member of the class III RTK family
The FLT3 RTK expression is normally limited to early myeloid progenitors and it appears to play a key role in the differentiation and maturation of hematopoietic precursors
Summary
The FLT3 gene is located on chromosome 13q12, and the resultant protein is a member of the class III RTK family. FLT3 mutations frequently co-occurred with NPM1 and DNMT3A mutations (39%) and chromatin or RNA splicing gene mutations (15%), and were associated with t(15;17) and t(6;9) translocations (35% and 80%, respectively).Patients with FLT3-ITD mutation are usually not cured with conventional chemotherapy [4] They have higher induction death rate, a lower CR rate, increased risk of relapse, and adverse DFS, event-free survival, and OS [5]. Amino acid substitutions within the FLT3-TKD (generally at position D835) decrease the affinity of TKI for their target receptors [3] These mechanisms activate intracellular signaling pathways such as ERK or STAT5 even in the presence of TKI, and AML cells escape from their cytotoxic effects [3]. Recovery of FLT3 activity during treatment breaks of cyclic drug administration
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