title: [GIST refractory to imatinib treatment].
abstract: After the introduction of imatinib, the outcome for patients with advanced gastro-intestinal stromal tumor (GIST) was vastly improved. However, resistance to imatinib has become a new problem. The cause of resistance to imatinib is the low sensitivity of gene mutations in the KIT gene or PDGFRα, or an acquisition of additional mutations, and a low plasma level of imatinib. Sunitinib is the first drug that showed an effectiveness for treating GIST refractory to imatinib. New molecular target drugs for overcoming imatinib resistance are being developed now.
authors.affiliation: Division of Clinical Oncology, Shizuoka Cancer Center.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Onozawa
authors.forename: Masanori
authors.initials: M
authors.lastname: Terashima
mesh_terms: D000970:Antineoplastic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001549:Benzamides; D002986:Clinical Trials as Topic; D019008:Drug Resistance, Neoplasm; D046152:Gastrointestinal Stromal Tumors / Q000188:drug therapy* / Q000235:genetics; D006801:Humans; D000068877:Imatinib Mesylate; D009154:Mutation; D010879:Piperazines / Q000009:adverse effects / Q000627:therapeutic use*; D019009:Proto-Oncogene Proteins c-kit / Q000235:genetics; D011743:Pyrimidines / Q000009:adverse effects / Q000627:therapeutic use*; D020796:Receptor, Platelet-Derived Growth Factor alpha / Q000235:genetics
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D019009:Proto-Oncogene Proteins c-kit; D020796:Receptor, Platelet-Derived Growth Factor alpha