Mutations in FLT3 receptor tyrosine kinase are the most frequently identified genetic event in acute myeloid leukemia (AML) that results in constitutive activation of survival and proliferation pathways including JAK/STAT, PI3K and RAS/MAPK pathways. The two major activating mutations in FLT3 gene are the internal tandem duplications (ITDs) of the juxtamembrane domain and the activation loop mutations of the tyrosine kinase domain . Thus, tyrosine kinases such as FLT3 represent an attractive therapeutic target for cancer therapies in AML. Several FLT3 tyrosine kinase inhibitors (TKIs) are currently under investigation including PKC-412.
Citation: Al-jamal HAN, Jusoh SAM, Sidek MR, Hassan R, Johan MF (2015) Restoration of PRG2 Expression by 5-Azacytidine Involves in Sensitivity of PKC-412 (Midostaurin) Resistant FLT3-ITD Positive Acute Myeloid Leukaemia Cells. J Hematol Thrombo Dis 3:186 doi:10.4172/2329-8790.1000186