الفهرس 
Genetics and Pathogenesis of GISTOnly 14 pages are availabe for public view
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Abstract
Although, GIST patients harboring kit exon 13 mutation at codon 642 appear to benefit from imatinib therapy, mutation at codon 654 of the same exon within the kit gene is associated with resistance and poor rates of survival (McAuliffe et al., 2008). Thus, the phenotype that results from mutation of these codons is imatinib-sensitivity for 642 and imatinib-resistance for 654, despite the minimal 13 codons that separate these two amino acids. Therefore, not all mutations of exon 13 are alike, and a mutant codon 654 but not 642 appears to be critical in the molecular resistance to imatinib. On the other hand, inhibitors such as sorafenib and sunitinib have shown activity in patients whose tumors harbor these imatinib-resistant mutations. Thus, the identification of specific mutations in kit or PDGFR-α may allow selection of active therapies over ones that are inactive (Widmer et al., 2008).