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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

KIT Mutations in GIST.

Most gastrointestinal stromal tumors (GISTs) contain oncogenic KIT or PDGFRA receptor tyrosine kinase mutations. These rare neoplasms are remarkably sensitive to the KIT and PDGFRA kinase inhibitors imatinib (also known as Gleevec) and sunitinib (Sutent), which have recently been approved as the standard therapeutic courses for patients with inoperable GIST. However, most GIST patients eventually develop clinical resistance to imatinib and sunitinib. Imatinib and sunitinib resistance generally result from secondary mutations in the KIT and/or PDGFRA kinase domains. Preclinical studies suggest that imatinib and sunitinib resistant mutations can be treated using more potent kinase inhibitors, such as nilotinib, which inactivate the mutant kinase proteins. Alternately, the mutant kinase proteins can be targeted using HSP90 inhibitors, which result in degradation of activated KIT and/or PDGFRA, or using KIT transcriptional repressors, such as flavopiridol.[1]


  1. KIT Mutations in GIST. Fletcher, J.A., Rubin, B.P. Curr. Opin. Genet. Dev. (2007) [Pubmed]
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