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- W1972829319 endingPage "468" @default.
- W1972829319 startingPage "457" @default.
- W1972829319 abstract "With the discovery of gain-of-function mutations of KIT in a majority of gastrointestinal stromal tumours (GIST) and access to the tailored tyrosine kinase inhibitor (TKI) imatinib, a new era in cancer therapy started. The drug caused marked tumour responses in most patients with advanced GISTs, but could also be used in an adjuvant setting after radical surgery or as downstaging treatment before intentionally curative surgery. With prolonged treatment imatinib resistance can develop, most likely due to secondary KIT mutations. In this situation the second-line TKI sunitinib is well suited to patients with KIT exon 9 mutations, or for patients without KIT/PDGFRA mutations (wild-type GIST). New treatment is required to treat imatinib or sunitinib resistance. New-generation TKIs have broader target profiles and increased activity against certain targets; but also new principles have been proposed, for example dose escalation, inhibition of downstream signalling molecules, HSP90 chaperon inhibition, transcriptional repression, combination with chemotherapy or receptor-mediated therapy of highly expressed cell surface receptors. Targeting of cancer stem cells may be another option." @default.
- W1972829319 created "2016-06-24" @default.
- W1972829319 creator A5049655193 @default.
- W1972829319 creator A5056070577 @default.
- W1972829319 creator A5071626792 @default.
- W1972829319 date "2009-04-01" @default.
- W1972829319 modified "2023-10-16" @default.
- W1972829319 title "Treatment of gastrointestinal stromal tumours: imatinib, sunitinib – and then?" @default.
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