text: <unk><unk><unk> s (GISTs) are rare but the most common mesenchymal (nonepithelial)<unk> s of the<unk>  tract. GISTs are derived from the interstitial cells of Cajal or undifferen2tiated precursor cells that finally develop into interstitial cells of Cajal. GIST<unk> s can either be benign<unk> s or massive malignant<unk> s with widespread metastasis. They can occur in any part of the<unk>  tract with the most common location as stomach. GIST<unk> s) can grow as an endophytic or exophytic lesions. Genes involved in the pathogenesis of<unk><unk><unk> s include mutations in c-Kit gene and PDGFRA (platelet derived growth factor receptor-alpha) gene. Both Kit gene and PDGFRA are tyrosine kinase receptors and control cell proliferation. Mutation in c-Kit gene and PDGFRA leads to inhibition of apoptosis and uncontrolled cell proliferation. In some rare cases where the patient do not exhibit the typical mutation in c-Kit and PDGFRA, mutations in succinate dehydrogenase (SDH) have been reported. Conditions associated with GIST include urticaria pigmentosa, neurofibromatosis type 1, and Carney-Stratakis syndrome. On gross pathology, GISTs have a rounded appearance with areas of hemorrhage. On microscopic histopathological analysis, GISTs are cellular<unk> s arising from muscularis propria and composed of spindle cells (70%), epithelioid cells (20%) or either one of them.
option_0: Gastrointestinal stromal tumor pathophysiology
option_1: Mucoepidermoid carcinoma pathophysiology
option_2: Merkel cell cancer pathophysiology
option_3: Esthesioneuroblastoma pathophysiology
option_4: Basal cell carcinoma pathophysiology
option_5: Neurofibroma pathophysiology
option_6: Acinic cell carcinoma pathophysiology
option_7: Hamartoma pathophysiology