2005
DOI: 10.1007/s11864-005-0026-x
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Abstract: Imatinib mesylate (STI571) is an oral 2-phenylaminopyrimidine derivative that acts as a selective inhibitor against several receptor tyrosine kinases and has been viewed as one of the therapeutic success stories of the 21st century. Imatinib was first shown to inhibit the causative molecular translocation in chronic myelogenous leukemia, BCR-ABL. Because imatinib could also inhibit the activity of KIT, a 145-kD transmembrane glycoprotein, and because gastrointestinal stromal tumors (GISTs), the most common mes… Show more

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Cited by 26 publications
(14 citation statements)
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“…Molecularly targeted therapy has recently emerged as a new treatment paradigm that seeks to improve conventional systemic therapy by specifically and selectively targeting cancers while minimizing treatment-related morbidities. This approach has led to successful advances in several diseases, including gastrointestinal stromal tumor (2,3), an STS subtype. To use targeted therapy for STS, an increased knowledge of potential targets and their roles in STS progression and metastasis is needed (4,5).…”
Section: Introductionmentioning
confidence: 99%
“…Molecularly targeted therapy has recently emerged as a new treatment paradigm that seeks to improve conventional systemic therapy by specifically and selectively targeting cancers while minimizing treatment-related morbidities. This approach has led to successful advances in several diseases, including gastrointestinal stromal tumor (2,3), an STS subtype. To use targeted therapy for STS, an increased knowledge of potential targets and their roles in STS progression and metastasis is needed (4,5).…”
Section: Introductionmentioning
confidence: 99%
“…As discussed in the paper by Tarn and Godwin [32], varying kinases downstream from the cell surface receptors have been shown to be important. Therefore, there may be a benefit to combining imatinib with agents that affect these downstream pathways.…”
Section: Etiology Of Resistancementioning
confidence: 99%
“…It is clear that tumors with different types of mutations in KIT and PDGFR have varied response rates to imatinib, as is discussed in the study by Tarn and Godwin [32]. Other possible mechanisms include increased drug eff lux or other pharmacokinetic factors, which may be overcome by increasing the dose of imatinib.…”
Section: Etiology Of Resistancementioning
confidence: 99%
“…[25][26][27][28][29][30][31][32][33][34][35][36][37][38][39] However, misconceptions regarding such analysis are harbored by both clinicians and pathologists.…”
Section: Concepts and Procedures Concerning ''Targeted''mentioning
confidence: 99%