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In studies of other receptor tyrosine kinases implicated inside the oncogenesis of GIST, nilotinib realized potent and selective inhibition of PDGFRα and PDGFRβ. As is the case with imatinib, nilotinib potently inhibited the autophosphorylation of A31 cells transformed by PDGFRASufferers resistant or intolerant to prior therapy that provided imat