ArticleActa oncologica (Stockholm, Sweden)2013
Intermittent and continuous imatinib in a human GIST xenograft model carrying KIT exon 17 resistance mutation D816H.
Article in Acta oncologica (Stockholm, Sweden), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Gastrointestinal stromal tumors with an uncommon primary mutation responded well to imatinib.Cancer pathogenesis and therapy · 2025Article
- Glycolysis in gastrointestinal stromal tumor: a brief overview.Neoplasia (New York, N.Y.) · 2024Review
- Inactivity of imatinib in gastrointestinal stromal tumors (GISTs) harboring a KIT activation-loop domain mutation (exon 17 mutation pN822K).OncoTargets and therapy · 2015Article
- Generation of orthotopic patient-derived xenografts from gastrointestinal stromal tumor.Journal of translational medicine · 2014Article
- Durable response with a combination of imatinib and sorafenib in KIT exon 17 mutant gastrointestinal stromal tumor.Journal of gastrointestinal oncology · 2014Article
- Characterization and assessment of the sensitivity and resistance of a newly established human gastrointestinal stromal tumour xenograft model to treatment with tyrosine kinase inhibitors.Clinical sarcoma research · 2014Article
- Drug rechallenge and treatment beyond progression--implications for drug resistance.Nature reviews. Clinical oncology · 2013Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcquired resistance to imatinib is frequently caused by secondary KIT mutations. We have investigated the effects of imatinib in mice with human gastrointestinal stromal tumour (GIST) xenograft which harbours a primary exon 11 deletion mutation and a secondary imatinib resistance mutation D816H in exon 17. Such mutations are commonly present in imatinib-resistant GIST in humans. MATERIAL AND
methodsThe mice were randomly allocated to receive imatinib either continuously or intermittently. Dynamic (18)F-FDG PET was performed and blood volume fraction (vB), rate transfer constants (k1, k2, k3) and metabolic rate of (18)F-FDG (MRFDG) were computed using a three-compartment model. Tumours were evaluated for the mitotic rate and the expression of HIF-1α , caspase-3 and glucose transporters (GLUTs).
resultsBoth intermittent and continuous imatinib delayed tumour growth significantly compared to controls, significantly in favour of the latter. k1 (representing perfusion, vascular permeability and binding of (18)F-FDG to the GLUTs) was significantly higher in the intermittent group compared to the continuous group, as was tumour GLUT-3 expression. k3 (representing internalisation of (18)F-FDG to the cells) and MR(FDG) were significantly lower.
conclusionImatinib delays GIST xenograft growth despite the presence of the D816H resistance mutation. The schedule of imatinib administration may influence tumour glucose uptake rate and metabolic rate.
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