Setting the Benchmark for KRAS G12C -Mutated NSCLC

Activating mutations in the KRAS proto-oncogene were identified and characterized more than 40 years ago across several distinct human cancers, including pancreatic and colorectal cancers as well as non–small-cell lung cancer (NSCLC). KRAS somatic alterations are found in approximately 25 to 30% of lung adenocarcinomas and represent the most prevalent genomic driver event in NSCLC.1 Within KRAS variants in NSCLC, the KRAS p.G12C single-nucleotide mutation (glycine-to-cysteine substitution at codon 12) is found in approximately 13% of lung adenocarcinomas. KRAS-mutated NSCLCs are generally associated with smoking (current or former use), increased programmed death ligand 1 (PD-L1) expression on tumor cells, an . . .