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EditorialFree Preview

Setting the Benchmark for KRASG12C-Mutated NSCLC

List of authors.
  • Antonio Passaro, M.D., Ph.D.,
  • and Solange Peters, M.D., Ph.D.

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 . . .

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Funding and Disclosures

Disclosure forms provided by the authors are available with the full text of this editorial at NEJM.org.

Author Affiliations

From the Division of Thoracic Oncology, European Institute of Oncology IRCCS, Milan (A.P.); and Lausanne University Hospital, Lausanne, Switzerland (S.P.).

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