کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2785550 1153975 2007 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
KIT Mutations in GIST
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شناسی تکاملی
پیش نمایش صفحه اول مقاله
KIT Mutations in GIST
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Current Opinion in Genetics & Development - Volume 17, Issue 1, February 2007, Pages 3–7
نویسندگان
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