Abstract
Gastrointestinal stromal tumors (GISTs), the most common submucosal tumor in the gut, express the KIT protein. Gain-of-function mutations in the KIT or PDGF-R alpha gene is involved in oncogenesis and growth of GISTs. Although the first-line therapy of resectable GISTs is surgery, imatinib mesylate, a target-based molecule against KIT and PDGF-R alpha proteins, showed remarkable clinical effects and good tolerability for non-resectable GISTs. Now, imatinib is in the first-line for non-resectable GISTs. Resistance against imatinib, however, is proved after long-standing use of the drug.
MeSH terms
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Antineoplastic Agents / therapeutic use
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Benzamides
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Gastrointestinal Neoplasms / diagnosis
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Gastrointestinal Neoplasms / genetics*
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Gastrointestinal Neoplasms / therapy
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Humans
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Imatinib Mesylate
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Mutation
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Piperazines / therapeutic use
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Protein-Tyrosine Kinases / antagonists & inhibitors
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Proto-Oncogene Proteins c-kit / biosynthesis*
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Proto-Oncogene Proteins c-kit / genetics*
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Pyrimidines / therapeutic use
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Receptor, Platelet-Derived Growth Factor alpha / genetics
Substances
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Antineoplastic Agents
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Benzamides
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Piperazines
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Pyrimidines
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Imatinib Mesylate
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Protein-Tyrosine Kinases
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Proto-Oncogene Proteins c-kit
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Receptor, Platelet-Derived Growth Factor alpha