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MET-Driven Resistance to Sotorasib in KRAS G12C–Mutant NSCLC and Response to Combined KRAS and MET Inhibition

Year: 2025
Type: article
Abstract: Introduction: amplification has been described as a putative off-target resistance mechanism, although its clinical relevance remains incompletely understood. Methods: fluorescence in situ hybridization. Results: amplification achieved a renewed partial response to the combination of sotorasib and tepotinib after progression on sotorasib monotherapy. Conclusion: amplification as a resistance mechanism and to define optimal therapeutic thresholds for combined KRAS and MET inhibition.
Language: English
Field: Medicine
Open Access status: gold
Estimated APC paid: $2,000
OpenAlex ID: W4415612293
FWCI: 0.595
Cites: 13
Cited by: 1
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