| Summary: | Recent advances in molecular biology and the resultant identification of driver oncogenes have achieved major progress in precision medicine for non-small-cell lung cancer (NSCLC). v-Ki-ras2 Kirsten rat sarcoma viral oncogene (<i>KRAS</i>) is the most common driver in NSCLC, and targeting KRAS is considerably important. The recent discovery of covalent KRAS G12C inhibitors offers hope for improving the prognosis of NSCLC patients, but the development of combination therapies corresponding to tumor characteristics is still required given the vast heterogeneity of <i>KRAS</i>-mutated NSCLC. In this review, we summarize the current understanding of <i>KRAS</i> mutations regarding the involvement of malignant transformation and describe the preclinical and clinical evidence for targeting <i>KRAS</i>-mutated NSCLC. We also discuss the mechanisms of resistance to KRAS G12C inhibitors and possible combination treatment strategies to overcome this drug resistance.
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