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The Next Generation of KRAS Targeting: Reasons for Excitement and Concern
Open accessAbstract
The development of selective KRASG12C inhibitors that directly inhibit KRAS, an oncogene historically thought to be “undruggable,” represents a watershed moment in oncology and developmental therapeutics. Now, as KRAS-targeted therapy moves into its second phase, there is significant excitement and anticipation for durable disease control in tumor types where options remain limited, with clinical trials testing combination therapies, indirect pan-RAS/MAP kinase pathway inhibitors, and active-state RAS(on) inhibitors. However, there is also reason for caution regarding the safety and tolerability of expanded RAS inhibition. This is evidenced by the intolerability of some combination therapies with selective KRASG12C inhibitors and foreshadowed by prior failures of combination therapies in other oncogene-driven tumors. Herein, we review the landscape of and outlook for KRAS-targeted therapies. We specifically focus upon strategies to combat resistance to KRAS-targeted therapies, and discuss the possibility of off-target or unanticipated on-target effects that may limit clinical use.
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The findings support a critical role of crosstalk of RTKs and mutant KRAS in resistance to targeted therapies in CRC and provide a strong rationale for their co-targeting.
“The above findings support a critical role of crosstalk of RTKs and mutant KRAS in resistance to targeted therapies in CRC and provide a strong rationale in their co-targeting [86].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [86]
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Differential Response and Resistance to KRAS-Targeted Therapy
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Metadata
- Authors
- Akhave, N. S., Biter, A. B., & Hong, D. S.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Hong, David S.
- Venue
- Molecular Cancer Therapeutics
- Published
- 2022-10-24
- Volume
- 21
- Issue
- 11
- Pages
- 1645-1651
- ISSN
- 1535-7163 (ISSN-L)
- 1538-8514
- PMC
- PMC9633538
- OpenAlex
- W4307240054
- Cited by
- 17
- References
- 66
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 5 · 2023: 4
- FWCI
- 0.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Cancer Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Texas MD Anderson Cancer Center (600850 30 111244 13)
- Topics
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- KRAS G12C inhibitors, KRAS-targeted therapy, oncogenic Ras, combination therapy, drug resistance, off-target effects, on-target toxicity, oncogene-driven tumors, durable disease control
- MeSH terms
- Antineoplastic Agents, Humans, Mutation, Oncogenes, Proto-Oncogene Proteins p21(ras), Mitogen-Activated Protein Kinases
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