Abstract
Constitutively active mutant RAS GTPases are key oncogenic drivers in many cancers. Targeting mutant KRAS has gained momentum as the first KRAS-G12C mutant specific inhibitor, sotorasib, has been approved for the treatment of NSCLC. Activity of sotorasib was demonstrated in patients with advanced lung cancers harboring KRAS-G12C mutations, however, resistance development via on-target and off-target mechanisms has been monitored. Mechanistic data and strategies to overcome resistance to targeted KRAS-G12C inhibitors are largely lacking.
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