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

Introduction: KRAS G12C mutations define a molecularly distinct subset of NSCLC for which targeted therapy with sotorasib has exhibited clinical efficacy. However, acquired resistance is inevitable. MET amplification has been described as a putative off-target resistance mechanism, although its clin...

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Автори: Richard Riedel, MD, Lea Ruge, MD, Malte Verheyen, MD, Felix John, MD, Heather Scharpenseel, MD, Lucia Nogova, MD, PhD, Sebastian Michels, MD, Rieke N. Fischer, MD, Anna Eisert, MD, Carolin Jakob, MD, Emanuel Niesen, MD, Jana Fassunke, MD, Janna Siemanowski-Hrach, MD, Carina Heydt, MD, Anne Bunck, MD, Udo Siebolts, MD, PhD, Sabine Merkelbach-Bruse, MD, PhD, Reinhard Buettner, MD, PhD, Jürgen Wolf, MD, PhD, Matthias Scheffler, MD, PhD
Формат: Artigo
Мова:Inglês
Опубліковано: Elsevier 2026-03-01
Серія:JTO Clinical and Research Reports
Предмети:
NSCLC
KRAS G12C
Sotorasib
MET amplification
Tyrosine kinase inhibitor resistance
Онлайн доступ:http://www.sciencedirect.com/science/article/pii/S2666364325001432
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