Abstract
Due to the remarkable advances in the understanding of the biology of gastrointestinal stromal tumors (GIST), tyrosine kinase inhibition has become the mainstay of therapy for patients with advanced GIST. Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3. Sunitinib has demonstrated benefit in patients with advanced GIST who have progressed on primary therapy with imatinib. The objectives of this review are to discuss the role of sunitinib in the current management of GIST, to review the unique side effect profile of the agent, and to discuss future trends in the use of the drug as the understanding of the mechanism of GIST evolves.
MeSH terms
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Antineoplastic Agents / adverse effects
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Antineoplastic Agents / therapeutic use*
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Drug Administration Schedule
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Gastrointestinal Stromal Tumors / drug therapy*
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Gastrointestinal Stromal Tumors / genetics
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Genotype
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Humans
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Indoles / adverse effects
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Indoles / therapeutic use*
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Protein Kinase Inhibitors / adverse effects
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Protein Kinase Inhibitors / therapeutic use*
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Proto-Oncogene Proteins c-kit / genetics
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Proto-Oncogene Proteins c-kit / metabolism
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Pyrroles / adverse effects
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Pyrroles / therapeutic use*
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Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors
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Receptors, Platelet-Derived Growth Factor / genetics
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Sunitinib
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Survival Rate
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Vascular Endothelial Growth Factor A / antagonists & inhibitors
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fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
Substances
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Antineoplastic Agents
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Indoles
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Protein Kinase Inhibitors
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Pyrroles
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Vascular Endothelial Growth Factor A
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FLT3 protein, human
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Proto-Oncogene Proteins c-kit
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Receptors, Platelet-Derived Growth Factor
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fms-Like Tyrosine Kinase 3
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Sunitinib