Figure 2.

Autophagy as part of the molecular profile in both untreated and imatinib treated GIST cells. In untreated GIST cells (A), autophagy controls tumor cell growth. In treated GIST cells, imatinib binds KIT-PDGFRA receptors, blocking their downstream signaling cascade (B); however, a portion of the cells undergoes quiescence and activates autophagy-related survival mechanisms, which, in turn, may promote growth of resistant subclones, characterized by additional, imatinib-resistant mutations (C).