Theranostics 2022; 12(13):5691-5709. doi:10.7150/thno.71260 This issue Cite
Review
1. Center for Cell Signaling, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA
2. Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School, Newark, New Jersey 07103, USA
3. Rutgers Cancer Institute of New Jersey, New Brunswick, NJ 08903, USA
4. Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
5. Lead contact
Aberrant activation of KRAS signaling is common in cancer, which has catalyzed heroic drug development efforts to target KRAS directly or its downstream signaling effectors. Recent works have yielded novel small molecule drugs with promising preclinical and clinical activities. Yet, no matter how a cancer is addicted to a specific target - cancer's genetic and biological plasticity fashions a variety of resistance mechanisms as a fait accompli, limiting clinical benefit of targeted interventions. Knowledge of these mechanisms may inform combination strategies to attack both oncogenic KRAS and subsequent bypass mechanisms.
Keywords: KRAS, RAF, MEK, targeted therapy resistance, cancer