Journal
CELL
Volume 183, Issue 4, Pages 850-859Publisher
CELL PRESS
DOI: 10.1016/j.cell.2020.09.044
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Funding
- NIH/NCI [1R01CA23074501, 1R01CA23026701A1, K08CA191082-01A1, F30CA232549]
- Pew Charitable Trusts
- Damon Runyon Cancer Research Foundation
- American Lung Association
- Medical Scientist Training Program [T32GM007739]
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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 similar to 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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