한빛사 논문
DongsungKim1,5, Jenny YaohuaXue1,2,5, PiroLito1,2,3,4,*
1Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer, New York, NY, USA
2Weill Cornell/Rockefeller/Sloan Kettering Tri-Institutional MD-PhD Program, New York, NY, USA
3Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA
4Department of Medicine, Weill Cornell Medical College, New York, NY, USA
5These authors contributed equally
*Corresponding author
Abstract
KRAS mutations are among the most common genetic alterations in lung, colorectal, and pancreatic cancers. Direct inhibition of KRAS oncoproteins has been a long-standing pursuit in precision oncology, one established shortly after the discovery of RAS mutations in human cancer cells nearly 40 years ago. Recent advances in medicinal chemistry have established inhibitors targeting KRAS(G12C), a mutation found in ∼13% of lung adenocarcinomas and, at a lower frequency, in other cancers. Preclinical studies describing their discovery and mechanism of action, coupled with emerging clinical data from patients treated with these drugs, have sparked a renewed enthusiasm in the study of KRAS and its therapeutic potential. Here, we discuss how these advances are reshaping the fundamental aspects of KRAS oncoprotein biology and the strides being made toward improving patient outcomes in the clinic.
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