Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract and most frequently occurs in the stomach (60-70%). It originates from the interstitial cells of Cajal (or a common progenitor cell). It is characterized by gain-of-function mutations in KIT (CD117) or PDGFRA tyrosine kinase receptors. On imaging, it typically presents as a well-defined, round or oval, exophytic or endophytic submucosal mass. Central necrosis, hemorrhage, and cavitation are common in large tumors.
Age Range
40-80
Peak Age
55
Gender
Equal
Prevalence
Uncommon
GIST originates from the interstitial cells of Cajal (peristaltic pacemaker cells) located in the muscularis propria of the gastrointestinal wall, or from a common progenitor cell. Activating mutations in the KIT proto-oncogene (c-kit, chromosome 4q12) play a central role in pathogenesis; these mutations lead to ligand-independent tyrosine kinase activation and uncontrolled cell proliferation. PDGFRA mutations are found in the majority of KIT-negative cases. The tumor grows in a submucosal location and can develop exophytically (toward the serosal side) or endophytically (toward the luminal side); on imaging, this exophytic growth pattern is characteristic and the most important feature distinguishing it from intraluminal adenocarcinoma. In large tumors, central areas with insufficient blood supply become necrotic and appear as hypodense central areas on CT; these necrotic areas are prone to hemorrhage and form cavitation when communicating with the lumen.
The pathognomonic imaging finding of GIST is a well-defined exophytic submucosal mass originating from muscularis propria with intense arterial enhancement. In large tumors, central necrosis/cavitation and heterogeneous enhancement are observed. Preserved overlying mucosa is the most important finding distinguishing it from other gastric tumors.
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In the arterial phase, an intensely enhancing [X] cm mass with exophytic extension from the stomach is noted, consistent with GIST.
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In the portal venous phase, the mass retains enhancement, with central hypodense necrotic area and preserved perigastric fat planes noted.
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In the delayed phase, washout is noted in solid components of the mass, consistent with a hypervascular mesenchymal tumor.
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On MRI, a [X] cm mass related to the stomach, hyperintense on T2W with intense enhancement on dynamic contrast-enhanced sequences, is noted, consistent with GIST.
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On EUS, a [X] cm hypoechoic solid mass originating from the muscularis propria layer of the gastric wall is noted, consistent with GIST.
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On PET-CT, intense FDG uptake with SUVmax: [X] is noted in the mass related to the stomach, consistent with metabolically active GIST.
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On barium study, a smooth-bordered submucosal filling defect in the [location] gastric wall is noted, consistent with mesenchymal tumor (GIST?).
Criteria
Low-risk GIST is typically <5 cm in size with ≤5 mitoses/50 HPF mitotic index. On CT, it appears as a homogeneous, well-defined, intensely enhancing mass. Central necrosis is usually absent. Post-surgical recurrence risk is low (5-10%) and adjuvant imatinib therapy is generally not required. 5-year survival is >90%.
Distinct Features
Criteria
High-risk GIST has >5 cm (usually >10 cm) size and/or >5 mitoses/50 HPF mitotic index. On CT, it appears as a heterogeneous, large exophytic mass containing central necrosis/cavitation. Risk of liver and peritoneal metastasis is high (40-60%). Adjuvant imatinib for minimum 3 years is recommended after surgery. KIT exon 11 mutation is the best prognostic indicator for imatinib response.
Distinct Features
Criteria
GIST most commonly metastasizes to the liver (60%) and peritoneum (30%); lymph node metastasis is rare (5%), which distinguishes it from other GI malignancies. Liver metastases are hypervascular and enhance in the arterial phase. Long survival is possible even in metastatic disease with imatinib therapy. PET-CT is the gold standard for treatment response evaluation.
Distinct Features
Distinguishing Feature
Distinguishing Feature
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Urgency
Management
Biopsy
Not NeededFollow-up
GISTs respond to imatinib (tyrosine kinase inhibitor) therapy. Size and mitotic index determine malignant potential. Tumors >5 cm are high risk. Surgical resection is curative.