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• W2321286988 abstract "Gastrointestinal stromal tumors (GIST) appear to originate from interstitial cells of Cajal (ICC) or their stem cell-like precursors.1 ICC are pacemaker-like intermediates between the GI autonomic nervous system and smooth muscle cells regulating GI motility and autonomic nerve function. Approximately 95% of GIST are positive for the CD117 antigen, an epitope of KIT receptor tyrosine kinase expressed by ICC.2 KIT-positive and KIT-dependent, ICC are located around the myenteric plexus and the muscularis propria throughout the GI tract. CD 117 is not a specific marker of GIST but may be expressed by other mesenchymal tumors too. DOG1 (Discovered on GIST) is a protein of unknown function that is expressed strongly on GIST and is rarely expressed on other soft tissue tumors.3 Around 85% of GIST possess oncogenic mutation in any two of the tyrosine kinase receptors the C KIT and the platelet derived growth factor receptor alpha (PDGFRA). Activation of either of these receptors plays a central role in the pathogenesis of GIST.1 The proper identification of GIST with genotyping is very important because of the availability of specific, molecular-targeted therapy with KIT/PDGFRA tyrosine kinase inhibitors (TKI), such as imatinib mesylate or, in the case of imatinib-resistant GIST, sunitinib malate.4" @default.
• W2321286988 created "2016-06-24" @default.
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• W2321286988 date "2014-04-01" @default.
• W2321286988 modified "2023-09-28" @default.
• W2321286988 title "EXON 11, C KIT mutation in a ‘CD 117’ & ‘DOG 1’ negative colonic gastrointestinal tumor" @default.
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• W2321286988 doi "https://doi.org/10.1016/j.mjafi.2013.07.011" @default.
• W2321286988 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4066891" @default.
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