Exact(1)
GIST are characterized by mutually exclusive KIT (85 %) or platelet-derived growth factor receptor alpha (PDGFRA) (5-105-10%ain ofunctionon mutations, leading to constitutive ligand-independent activation of receptor signalling [ 17– 17].
Similar(59)
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However, the KIT-negative cases were immunoreactive for PDGFRα, providing immunohistochemical confirmation that KIT and PDGFRα exhibit mutually exclusive expression, and not only mutually exclusive mutations [ 15].
These driver mutations may occur in different genes but are mutually exclusive: most affect the proto-oncogenes KIT 75-800 %) and PDGFRA (5 10 %), which encode for mutated proteins with ligand independent constitutive activation of tyrosine kinase receptor.
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