GSE121272
Gene expression profile of a FLT3-ITD acute myeloid leukemia cell line treated with FLT3 inhibitors for six and twelve hours
Adaptive resistance is an important mechanism of resistance to tyrokine kinase inhibitors in cancer. With this study we aimed to determine which signaling pathways may contribute to adaptive resistance by examining the mRNA profiles of FLT3-ITD AML cells treated with the FLT3 inhibitor, AC220. We also aimed to determine whether our novel inhibitor, NCGC1481, would inhibit the activation of these pathways. We concluded that AC220 induces activation of innate immune signaling and NCGC1481 prevents this activation. Overall design: mRNA profiles of a FLT3-ITD AML cell line treated with AC220 or novel compound, NCGC1481, compared to DMSO control at 6 and 12 hours of treatment