Abstract

Treatment for advanced non-small cell lung cancer (NSCLC) has been revolutionized by the development of both immunotherapeutic and genomic based therapies. There is increasing appreciation for the interplay between genomic alterations and response to immune checkpoint blockade (ICB), as exhibited by alterations in driver mutations (e.g. EGFR/ALK) and non-driver co-mutations (e.g. STK11/KEAP1). Special attention has been paid to the most common oncogenic driver, KRAS, which is mutated in approximately 30% of NSCLC.

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