Abstract
Activating mutations in KRAS are a frequent source of oncogenesis but have lacked clinical targeted therapies despite being first identified four decades ago. Selective drugs for the G12C KRAS mutation have recently been approved for use in the United States, and have been granted conditional marketing authorization in the EU. Pre-clinical data indicate that tumors harboring KRAS mutations can rapidly develop resistance to targeted inhibition, and non-durable responses have been observed in clinical use.
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