Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumour
This analysis showed that the type of KIT mutation predicts response to imatinib: tumours with exon 11 mutations responded in over 80 percent of cases, exon 9 mutations in under half, and tumours without a KIT or PDGFRA mutation rarely responded.
Overview
Mutation analysis of tumours from 127 patients with advanced GIST treated with imatinib in the phase 2 B2222 trial, correlating KIT and PDGFRA genotype with response and progression-free survival.
Partial response was 83.5 percent in KIT exon 11-mutant tumours, 47.8 percent in exon 9-mutant tumours and 0 percent in tumours without a detectable KIT or PDGFRA mutation, with corresponding differences in event-free survival.
- Response 83.5 percent (exon 11) vs 47.8 percent (exon 9) vs 0 percent (no mutation).
- PDGFRA mutations found in a subset of KIT wild-type tumours.
Mutation testing is standard before imatinib in GIST: exon 11 tumours receive 400 mg, exon 9 tumours are dosed at 800 mg, and PDGFRA D842V tumours are given avapritinib instead.
- Retrospective analysis of a trial cohort.
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