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Abstract
This dissertation presents novel evidence that PTPN11 is activated by an upstream kinase, TNK2. PTPN11-mutant JMML and AML primary patient cells have displayed significant sensitivity to TNK2 inhibition by dasatinib. My research has revealed that PTPN11 and TNK2 interact directly, allowing for TNK2 dependent phosphorylation of PTPN11.