Gastrointestinal stromal tumors (GISTs), previously thought to arise from the smooth muscles of the gastrointestinal tract, have recently been identified as a separate clinicopathologic entity. This new entity was revealed when investigations using more refined techniques suggested that GISTs had neural rather than smooth muscle differentiation and expressed the cell surface receptor Kit (CD117). Ensuing research led to development of a new molecularly targeted therapy, imatinib mesylate, which showed significant response among GIST patients in initial clinical trials. This review describes treatment of GIST before and after imatinib and the significance of this accomplishment.
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