Abstract
KRAS mutations are detected in approximately 20-25% of lung adenocarcinomas and are the most common oncogenic alteration in all of human cancers. In non-small cell lung cancer (NSCLC), KRAS mutations are detected in tumors from patients with and without a prior smoking history. The most common KRAS mutation is KRAS G12C, which accounts for approximately 50% of KRAS mutations in NSCLC. Until recently, there were no effective therapies for KRAS mutant cancers. Much of the therapeutic approaches had focused on targeting KRAS effector pathways including the PI3K/AKT and MAPK pathways.
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