Therapeutic applications of miRNAs in FLT3+ Acute Myeloid Leukemia

Acute Myeloid Leukemia (AML) is a blood cancer characterized by genetic and epigenetic aberrations leading to abnormal proliferation and survival of immature myeloid cells. FLT3 is a protein that plays a central role in hematopoiesis, and mutations in FLT3 have been well-identified and characterized in 30% of patients with AML. FLT3+ AML is associated with poor prognosis and short survival rate due to disease relapse and acquired therapy resistance during the treatment. Several attempts to target FLT3 in AML have shown modest effect and therefore developing new strategies to overcome therapy resistance and maintain long-lasting remission is greatly needed. Understanding how FLT3 is regulated transcriptionally is key to developing gene-targeted therapy.