GIST are stromal tumors and the gastrointestinal tract (GIT) and some other organs of spindle-cell or epithelioid-cell structure expressing CD117 (C-kit, KIT), as well as those at different rates and in different combinations, CD34, smooth muscle and/or neurogenic differentiation antigens. It should be taken into account that CD117 are also expressed by melanomas, vascular, and some other tumors. The c-kit gene mutations leading to the expression and autoactivation of the tyrosine kinase receptor KIT underlie the oncogenesis of GIST, which results in enhanced proliferative activity and inhibited apoptosis. This is supported by successful chemotherapy for GIST with a KIT receptor inhibitor. The histogenesis of GIST is associated with GIT somatic stem, the Cajal cell precursors. Many GISTs behave like sarcomas and they are characterized by an infiltrating growth, hematogenic (mainly into the liver) and implantational (along the peritoneum) cancer spread. There are opinions that all such neoplasms are potentially malignany and small-sized GISTs are benign and have the minimum mitotic activity.
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