Fig. 1.

KIT oncoproteins in GIST are differentially inhibited by sunitinib and regorafenib. Immunoblotting evaluations of phospho-KIT and downstream phospho-AKT were performed in GISTs belonging to four clinical-genotypic categories: (a) imatinib-sensitive GISTs contained only KIT primary mutations; (b) imatinib-resistant GISTs with ATP-binding pocket KIT secondary mutations; (c) imatinib-resistant GISTs with activation loop KIT secondary mutations; (d) KIT-negative GISTs. This figure also provides quantifications, relative to the DMSO-only controls (normalised to 1.0), of the (a–c) phosphoKIT and phosphoAKT responses in KIT-dependent GISTs