Acquired resistance to imatinib is a significant problem for the clinical management of gastrointestinal stromal tumor (GIST) patients, and second-line small molecules have shown limited efficacy in this setting. We have recently demonstrated that a monoclonal antibody targeting KIT could potentially bypass imatinib resistance in preclinical models of GIST.
Keywords: CD117; KIT; gastrointestinal stromal tumor; imatinib; monoclonal antibody-based cancer therapy; receptor tyrosine kinase.