Abstract

The extraordinary success of imatinib in gastrointestinal stromal tumors (GIST) represents a model for molecularly targeted therapy for other solid tumors. Research is currently going to identify the molecular basis of mechanisms of action and drug resistance. In this article, we review recent advances in the clinical management of patients with GISTs treated with imatinib, but also of patients with dermatofibrosarcoma protuberans, chordoma, aggressive fibromatosis, and some other common solid tumors treated with this drug. We reviewed the knowledge of the molecular mechanisms that are basic to imatinib effects in these tumors.

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