Development of combination therapies to maximize the impact of KRAS-G12C inhibitors in lung cancer
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Combined targeting of KRAS-G12C, mTOR, and IGF1R enhances and extends the response to recently developed KRAS-G12C inhibitors in lung cancer models.
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Combination therapies to suppress adaptive feedback proved key to optimizing the frequency and durability of response in each tumor type.
“Still, in all cases, combination therapies to suppress adaptive feedback proved key to optimizing the frequency and durability of response in each tumor type (34,50,51).”
From Vertical Pathway Inhibition Overcomes Adaptive Feedback Resistance to KRASG12C Inhibition (2020) · cites this paper as [51]
The Results (page unavailable) report that adding IGF1R and mTOR inhibitors to a KRAS-G12C inhibitor produced durable regression in lung-cancer xenografts where inhibitor treatment alone led to progression. The Discussion (page unavailable) describes suppressing compensatory feedback, but cautions that resistance may still evolve. These preclinical lung-cancer findings do not establish that combination therapy proved key to response frequency and durability in every tumor type. (LLM, conf=0.88)
Experimental — accuracy not yet measuredOther combinatorial partners including PI3K, mTOR, and Aurora Kinase inhibitors have been shown to have higher efficacy than EGFR inhibition in combination with KRAS G12C inhibition in lung cancer.
“other combinatorial partners including PI3K, mTOR, and Aurora Kinase inhibitors have been shown to have higher efficacy than EGFR inhibition in combination with KRAS G12C inhibition in lung cancer(10, 12, 13).”
From EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer. (2020) · cites this paper as [12]
The Discussion (page unavailable) reports that adding an mTOR inhibitor improves responses to KRAS-G12C inhibition and notes reports of improved activity with PI3K inhibitors. It does not establish that those combinations are more effective than EGFR inhibition, and the passages found do not address Aurora kinase inhibitors. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRestoration of flux through the ERK pathway was similarly observed after ARS-1620 treatment, and feedback activation of Ras upstream RTKs has been raised as one of the key mechanisms of resistance to ARS-1620.
“Interestingly, the restoration of flux through the ERK pathway was similarly observed after ARS-1620 treatment, and the feedback activation of Ras upstream RTKs has been raised as one of the key mechanisms of resistance to ARS-1620.12,15”
From Overcoming Resistance to Drugs Targeting KRAS Mutation (2020) · cites this paper as [15]
Genetic and pharmacological screens identified RTK signaling to PI3K and mTOR, and autophagy, as collateral dependencies with KRAS and MAPK pathway inhibitors.
“These experiments have identified receptor tyrosine kinase (RTK) signaling to PI3K and mTOR (23, 37–40), as well as the autophagy pathway (30) as collateral dependencies with KRAS and MAPK pathway inhibitors.”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [38]
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- Authors
- Molina-Arcas, M., Moore, C., Rana, S., van Maldegem, F., Mugarza, E., Romero-Clavijo, P., Herbert, E., Horswell, S., Li, L.-S., Janes, M. R., Hancock, D. C., & Downward, J.
- Affiliations
- Oncogene Biology, Francis Crick Institute, London NW1 1AT, UK.
- The Francis Crick Institute (GB)
- Institute of Cancer Research (GB)
- Royal Veterinary College (GB)
- Wellspring Biosciences (United States) (US)
- Corresponding author
- Downward, Julian
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2019-09-18
- Volume
- 11
- Issue
- 510
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6764843
- OpenAlex
- W2973796265
- Semantic Scholar
- dca6223aaab20972c7583a0426e8b63dfc81d7f3
- Cited by
- 203
- References
- 55
- Citations by year
- 2026: 8 · 2025: 22 · 2024: 27 · 2023: 32 · 2022: 36 · 2021: 51 · 2020: 24 · 2019: 3
- FWCI
- 20.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RVC Research Online (Royal Veterinary College) (submittedVersion, cc-by)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Wellcome (103799/Z/14/Z, FC001070)
- H2020 European Research Council (RASTARGET)
- Medical Research Council (FC001070)
- Cancer Research UK (FC001070)
- 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 › Melanoma and MAPK Pathways
- Keywords
- KRAS G12C inhibitors, KRAS-mutant lung cancer, lung adenocarcinoma, combination therapy, MEK inhibition, IGF1R inhibition, mTOR inhibition, MAPK signaling, IGF1R signaling, tumor regression, mouse model
- MeSH terms
- Animals, Antineoplastic Combined Chemotherapy Protocols, Carcinoma, Non-Small-Cell Lung, Cell Survival, Imidazoles, Lung Neoplasms, Mice, Nude, Mutation, Pyrazines, Pyridones, Pyrimidinones, Signal Transduction, Proto-Oncogene Proteins p21(ras), Receptor, IGF Type 1, Phosphatidylinositol 3-Kinases, Mitogen-Activated Protein Kinase Kinases, RNA, Small Interfering, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases
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