Advances in the treatment of gastrointestinal stromal tumours
Tài liệu tham khảo
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D’Amato, 2005, Update on the biology and therapy of gastrointestinal stromal tumors, Cancer Control, 12, 44, 10.1177/107327480501200106
Heinrich, 2003, PDGFRA activating mutations in gastrointestinal stromal tumors, Science, 299, 5708, 10.1126/science.1079666
Heinrich, 2003, Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor, J Clin Oncol, 21, 4342, 10.1200/JCO.2003.04.190
Demetri, 2002, Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors, N Engl J Med, 347, 472, 10.1056/NEJMoa020461
Rankin, 2004, Dose effect of imatinib (IM) in patients (pts) with metastatic GIST - phase III sarcoma group study S0033, J Clin Oncol, 22, 10.1200/jco.2004.22.14_suppl.9005
Verweij, 2004, Progression-free survival in gastrointestinal stromal tumours with high-dose imatinib: randomised trial, Lancet, 364, 1127, 10.1016/S0140-6736(04)17098-0
Zalcberg, 2005, Outcome of patients with advanced gastro-intestinal stromal tumours crossing over to a daily imatinib dose of 800mg after progression on 400mg, Eur J Cancer, 41, 1751, 10.1016/j.ejca.2005.04.034
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Debiec-Rychter, 2006, KIT mutations and dose selection for imatinib in patients with advanced gastrointestinal stromal tumours, Eur J Cancer, 42, 1093, 10.1016/j.ejca.2006.01.030
Heinrich, 2006, Molecular correlates of imatinib resistance in gastrointestinal stromal tumors
Abrams, 2003, SU11248 inhibits KIT and platelet-derived growth factor receptor beta in preclinical models of human small cell lung cancer, Mol Cancer Ther, 2, 471
Kim, 2006, An orally administered multitarget tyrosine kinase inhibitor, SU11248, is a novel potent inhibitor of thyroid oncogenic RET/papillary thyroid cancer kinases, J Clin Endocrinol Metab, 91, 4070, 10.1210/jc.2005-2845
Mendel, 2003, In vivo antitumor activity of SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor and platelet-derived growth factor receptors: determination of a pharmacokinetic/pharmacodynamic relationship, Clin Cancer Res, 9, 327
Murray, 2003, SU11248 inhibits tumor growth and CSF-1R-dependent osteolysis in an experimental breast cancer bone metastasis model, Clin Exp Metastasis, 20, 757, 10.1023/B:CLIN.0000006873.65590.68
O’Farrell, 2003, SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo, Blood, 101, 3597, 10.1182/blood-2002-07-2307
Osusky, 2004, The receptor tyrosine kinase inhibitor SU11248 impedes endothelial cell migration, tubule formation, and blood vessel formation in vivo, but has little effect on existing tumor vessels, Angiogenesis, 7, 225, 10.1007/s10456-004-3149-y
Schueneman, 2003, SU11248 maintenance therapy prevents tumor regrowth after fractionated irradiation of murine tumor models, Cancer Res, 63, 4009
Heinrich, 2006, Sunitinib (SU) response in imatinib-resistant (IM-R) GIST correlates with KIT and PDGFRA mutation status
Morgan, 2006, Durable responses to SU11248 (sunitinib malate) are observed across all genotypes of imatinib mesylateresistant GIST
Demetri, 2006, Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial, Lancet, 368, 1329, 10.1016/S0140-6736(06)69446-4
Judson, 2006, Updated results from a phase III trial of sunitinib in advanced gastrointestinal stromal tumuor (GIST), Ann Oncol, 17, 162
Casali, 2006, Updated results from a phase III trial of sunitinib in GIST patients (pts) for whom imatinib (IM) therapy has failed due to resistance or intolerance
Dileo, 2006, Updated results from a ‘‘treatment-use’’ trial of sunitinib in advanced gastrointestinal stromal tumor (GIST)
Blay, 2006, Clinical benefit of continuous daily dosing of sunitinib in patients (pts) with advanced gastrointestinal stromal tumor (GIST)