期刊
CANCER GENE THERAPY
卷 29, 期 7, 页码 875-878出版社
SPRINGERNATURE
DOI: 10.1038/s41417-021-00383-9
关键词
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While drugs targeting the KRAS-G12C mutation have shown promising improvements in clinical trials for treating patients, the majority of patients do not respond to this therapy due to intrinsic or acquired resistance. Understanding drug response in the tumor microenvironment may further advance the design, testing, and clinical application of KRAS-G12C inhibitors.
Although it has long been deemed undruggable, with the development of drugs specifically binding the KRAS-G12C mutant protein, clinical trials that directly inhibit oncogenic RAS have recently made promising improvements. In particular, the covalent KRAS-G12C inhibitors sotorasib and adagrasib are used to treat patients with advanced non-small cell lung cancer (NSCLC) carrying KRAS-G12C mutations. Unfortunately, the vast majority of patients do not respond to KRAS-G12C inhibitor therapy, mainly due to intrinsic or acquired resistance caused by cellular, molecular, and genetic mechanisms. Improving the understanding of drug response in the tumor microenvironment may continue to promote the design, testing, and clinical application of KRAS-G12C inhibitors.
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