Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

The KRAS G12C mutation in NSCLC: from target to resistance

Version 1 : Received: 19 May 2021 / Approved: 20 May 2021 / Online: 20 May 2021 (10:05:40 CEST)

A peer-reviewed article of this Preprint also exists.

Addeo, A.; Banna, G.L.; Friedlaender, A. KRAS G12C Mutations in NSCLC: From Target to Resistance. Cancers 2021, 13, 2541. Addeo, A.; Banna, G.L.; Friedlaender, A. KRAS G12C Mutations in NSCLC: From Target to Resistance. Cancers 2021, 13, 2541.

Journal reference: Cancers 2021, 13, 2541
DOI: 10.3390/cancers13112541

Abstract

Lung cancer represents the most common form of cancer accounting for 1.8 million deaths globally in 2020.The 5-year relative survival rate for lung cancer is lower than many other leading cancer types. Over the last decade the treatment for advanced and metastatic non small cell lung cancer have dramatically improved due to the development of immune checkpoint inhibitors and the identification of targetable driver mutations. Recently, potentially effective inhibitors of a hitherto untargetable oncogenic driver mutation in NSCLC, Kirsten Rat Sarcoma (KRAS) have been developed. KRAS mutations are found in 20-25% of NSCLC and represent the most frequent mutation. The mutation is almost exclusively detected in adenocarcinoma and is found among smokers 90% of the time. Along with the development of new drugs that have been showing promising activity, resistance mechanisms have begun to be clarified. The aim of this review is to unwrap the biology of KRAS in NSCLC with a specific focus on primary and secondary resistance mechanisms and their possible clinical implications.

Keywords

KRAS; target therapies; NSCLC

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