Gastrointestinal stromal tumor pathophysiology: Difference between revisions
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[[Image:gist.jpg|thumb|left|Gastrointestinal stromal tumor of stomach. Courtesy of Ed Uthman, MD.]] | [[Image:gist.jpg|thumb|left|Gastrointestinal stromal tumor of stomach. Courtesy of Ed Uthman, MD.]] | ||
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[[Image:GIST 2.jpg|left|thumb|200px|[[Endoscopy|Endoscopic]] image of GIST in fundus of [[stomach]], seen on retroflexion.]] | |||
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[[Image:GIST 3.jpg|left|thumb|200px|Same GIST seen on forward view of the endoscope showing overlying clot.]] | |||
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==References== | ==References== | ||
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Revision as of 02:17, 18 January 2012
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Gastrointestinal stromal tumor Microchapters |
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Differentiating Gastrointestinal stromal tumor from other Diseases |
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Diagnosis |
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Gastrointestinal stromal tumor pathophysiology On the Web |
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Directions to Hospitals Treating Gastrointestinal stromal tumor |
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Risk calculators and risk factors for Gastrointestinal stromal tumor pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
GISTs are thought to arise from interstitial cells of Cajal (ICC),[1] that are normally part of the autonomic nervous system of the intestine. They serve a pacemaker function in controlling motility.
Most (50-80%) GISTs arise because of a mutation in a gene called c-kit. This gene encodes a transmembrane receptor for a growth factor termed scf (stem cell factor). The c-kit/CD117 receptor is expressed on ICCs and a large number of other cells, mainly bone marrow cells, mast cells, melanocytes and several others. In the gut, however, a mass staining positive for CD117 is likely to be a GIST, arising from ICC cells.
The c-kit molecule comprises a long extracellular domain, a transmembrane segment, and an intracellular part. Mutations generally occur in the DNA encoding the intracellular part (exon 11), which acts as a tyrosine kinase to activate other enzymes. Mutations make c-kit function independent of activation by scf, leading to a high cell division rate and possibly genomic instability. It is likely that additional mutations are "required" for a cell with a c-kit mutation to develop into a GIST, but the c-kit mutation is probably the first step of this process.
The tyrosine kinase function of c-kit is vital in the therapy for GISTs.
Histopathology
References
- ↑ Miettinen M, Lasota J (2006). "Gastrointestinal stromal tumors: review on morphology, molecular pathology, prognosis, and differential diagnosis". Arch Pathol Lab Med. 130 (10): 1466–78. PMID 17090188.