Reinforcing the need to look beyond genomic alterations to understand the complexity of cancer, researchers from Dana-Farber/Boston Children's Cancer and Blood Disorders Center report that a normal enzyme called SYK pairs with FLT3, the most commonly mutated enzyme found in acute myelogenous leukemia (AML), to promote progression of the disease. This molecular partnership also promotes AML cells' resistance to treatment with FLT3-blocking drugs, potentially explaining the relatively poor showing of FLT3 inhibitors in multiple clinical studies. In an animal model of AML, treatment with a combination of FLT3- and SYK-inhibiting drugs was significantly more effective than treatment with either drug alone.
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