C-kit, GIST, and Imatinib
| Autor: | Eckhard Thiel, J. M. Siehl |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Oncology
medicine.medical_specialty biology GiST business.industry Sunitinib medicine.drug_class Standard treatment Imatinib Sunitinib malate Pharmacology digestive system diseases Tyrosine-kinase inhibitor Receptor tyrosine kinase Imatinib mesylate Internal medicine biology.protein Medicine business neoplasms medicine.drug |
| Zdroj: | Targeted Therapies in Cancer ISBN: 9783540460909 |
| DOI: | 10.1007/978-3-540-46091-6_12 |
| Popis: | A gain-of-function mutation of c-kit is the crucial step in tumorigenesis of gastrointestinal stromal tumors (GIST). Imatinib can block the activated receptor tyrosine kinase activity of c-kit. These findings made GIST an ideal candidate for evaluation of new targeted therapeutic approaches. Clinical studies demonstrated that, with imatinib, objective responses can be reached in more than 50% of patients with advanced GIST. Furthermore, even in those patients with stable disease, long-term tumor control could be achieved. Therefore imatinib at a dose of 400 mg/day is now the standard treatment of advanced GIST in which RO-resection cannot be reached. As imatinib resistance in GIST occurs at a median of 18 to 26 months, further targeted therapies have been explored. Sunitinib, another tyrosine kinase inhibitor, seems to be useful especially in patients with exon 9 mutations of c-kit, who usually have a worse response to imatinib. This might indicate that more exactly targeted therapies in GIST might improve clinical outcomes in the future. |
| Databáze: | OpenAIRE |
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