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In studies of other receptor tyrosine kinases implicated inside the oncogenesis of GIST, nilotinib attained strong and selective inhibition of PDGFRα and PDGFRβ. As is the case with imatinib, nilotinib potently inhibited the autophosphorylation of A31 cells transformed by PDGFRAIndividuals resistant or intolerant to prior cure that included imati

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