ArticleJournal of cancer research and clinical oncology2024
Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma.
Article in Journal of cancer research and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Understanding tumor adaptations and resistance to MET inhibitors in MET-altered non-small cell lung cancer.Neoplasia (New York, N.Y.) · 2026Article
- Research progress on resistance and mechanisms of c-Met inhibitors in treatingJournal of thoracic disease · 2026Review
- Nanotechnology-Enabled Precision Therapy for Lung Cancer in Never-Smokers.Pharmaceutics · 2026Review
- Natural products as kinase inhibitors in lung cancer: molecular mechanisms, therapeutic potential, and clinical trials.Frontiers in pharmacology · 2026Review
- Targeted Therapies Modulating Mesenchymal-Epithelial Transition-Linked Oncogenic Signaling in the Tumor Microenvironment: Comparative Profiling of Capmatinib, Bemcentinib, and Galunisertib.Journal of clinical medicine · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
Traditionally, the D1228 E/G/H/N mutation has been thought to cause Type I MET-TKI resistance. We reported a 75-year-old female with non-small cell lung cancer harboring MET exon 14 skipping mutation, who developed acquired MET D1228H mutation induced by capmatinib treatment. Interestingly, the patient demonstrated marked response to second-line savolitinib treatment with the duration of response of 19 months and several additional metastatic lesions appeared. Pathological assessment of rebiopsy sample showed adenocarcinoma and targeted next-generation sequencing revealed the loss of MET D1228H mutation and presence of MET p.Y1230N mutation. In response, the treatment regimen was amended to include a daily administration of 60 mg of cabozantinib, which resulted in moderate size reduction of the tumours. The switch of resistance mutations indicated that different type Ib MET inhibitors may exhibit distinct mechanisms of resistance. We call for futher studies on resistance based on patient-derived pre-clinical models including patient-derived tumor-like cell clusters, patient-derived organoids, and patient-derived xenografts.
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