Overcoming adaptive resistance to KRAS inhibitors through vertical pathway targeting
Open accessAbstract
KRAS G12C inhibitors have shown promise in KRAS G12C–mutant lung cancer but intrinsic and acquired resistance are common. Cotreatment with inhibitors of the protein phosphatase SHP2 can abrogate the adaptive response of cancer cells to KRAS inhibitors resulting in greater suppression of MAPK signaling and enhanced tumor growth inhibition. See related article by Ryan et al., p. 1633
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Targeting common nodes downstream of multiple RTK signaling pathways may represent a feasible strategy to overcome adaptive Ras reactivation across heterogeneous KRAS mutant cancers.
“Given the individual-specific involvement of RTK, targeting common nodes downstream of multiple RTK signaling pathways may represent a feasible strategy to overcome adaptive Ras reactivation across heterogeneous KRAS mutant cancers.11,84”
From Overcoming Resistance to Drugs Targeting KRAS Mutation (2020) · cites this paper as [84]
Drug resistance to KRAS G12C inhibitors eventually develops with long-term treatment.
“Preclinical and clinical data have revealed that drug resistance to KRAS G12C inhibitors eventually develops with long‐term treatment.[ 6, 33, 41 ]”
From Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK–YAP Signaling (2021) · cites this paper as [41]
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References 5 · Cited by 39
- Authors
- Yaeger, R., & Solit, D. B.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Solit, David B.
- Venue
- Clinical Cancer Research
- Published
- 2020-04-01
- Volume
- 26
- Issue
- 7
- Pages
- 1538-1540
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- PMC
- PMC7453631
- OpenAlex
- W3003869816
- Cited by
- 39
- References
- 5
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 4 · 2023: 6 · 2022: 7 · 2021: 9 · 2020: 3
- FWCI
- 3.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (R01 CA233736)
- Cancer Center Core (P30 CA008748)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- KRAS G12C inhibitors, acquired drug resistance, adaptive resistance, SHP2 inhibition, MAPK signaling, lung cancer, combination therapy
- MeSH terms
- Feedback, Humans, Lung Neoplasms, Mutation, Proto-Oncogene Proteins p21(ras), Cell Line, Tumor
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