The DOI matches its Crossref record; 40 of the 41 references it cites were found in a registry or an index.
KRAS as a Therapeutic Target
Open accessAbstract
KRAS proteins play a major role in human cancer, but have not yielded to therapeutic attack. New technologies in drug discovery and insights into signaling pathways that KRAS controls have promoted renewed efforts to develop therapies through direct targeting of KRAS itself, new ways of blocking KRAS processing, or by identifying targets that KRAS cancers depend on for survival. Although drugs that block the well-established downstream pathways, RAF–MAPK and PI3K, are being tested in the clinic, new efforts are under way to exploit previously unrecognized vulnerabilities, such as altered metabolic networks, or novel pathways identified through synthetic lethal screens. Furthermore, new ways of suppressing KRAS gene expression and of harnessing the immune system offer further hope that new ways of treating KRAS are finally coming into view. These issues are discussed in this edition of CCR Focus. Clin Cancer Res; 21(8); 1797–801. ©2015 AACR. See all articles in this CCR Focus section, “Targeting RAS-Driven Cancers.”
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“It is the most dominant mutated subtype in the RAS family and is responsible for 85% of RAS gene-driven cancers, particularly in pancreatic, colorectal, and lung cancers.40–42”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [40]
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“Oncogenic KRAS can activate various downstream effector pathways, and the best characterized are phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinases (MAPK) (23–25).”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [23]
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Genetic Basis for Clinical Response to CTLA-4 Blockade in Melanoma
Snyder, A., Makarov, V., Merghoub, T., Yuan, J., Zaretsky, J. M., Desrichard, A., Walsh, L. A., Postow, M. A., Wong, P., Ho, T. S., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1406498 · Cited by 4,286
Discovery and saturation analysis of cancer genes across 21 tumour types
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K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
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A Comprehensive Survey of Ras Mutations in Cancer
Prior, I. A., Lewis, P. D., & Mattos, C. (2012) · Cancer Research · doi:10.1158/0008-5472.can-11-2612 · Cited by 2,063 · cited 1×
“In pancreatic cancer, KRAS mutations are detected in the earliest lesions and are retained in all metastases (17).”
BackgroundOncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism
Ying, H., Kimmelman, A. C., Lyssiotis, C. A., Hua, S., Chu, G. C., Fletcher-Sananikone, E., Locasale, J. W., Son, J., Zhang, H., Coloff, J. L., et al. (2012) · Cell · doi:10.1016/j.cell.2012.01.058 · Cited by 2,043
Drugging the undruggable RAS: Mission Possible?
Cox, A. D., Fesik, S. W., Kimmelman, A. C., Luo, J., & Der, C. J. (2014) · Nature Reviews Drug Discovery · doi:10.1038/nrd4389 · Cited by 1,997
Targeting RAF kinases for cancer therapy: BRAF-mutated melanoma and beyond
Holderfield, M. T., Deuker, M. M., McCormick, F. P., & McMahon, M. (2014) · Nature reviews. Cancer · doi:10.1038/nrc3760 · Cited by 850
Self-citationSingh, A., Greninger, P., Rhodes, D., Koopman, L., Violette, S., Bardeesy, N., & Settleman, J. (2009) · Cancer Cell · doi:10.1016/j.ccr.2009.03.022 · Cited by 841
Stephen, A. G., Esposito, D., Bagni, R. K., & McCormick, F. (2014) · Cancer Cell · doi:10.1016/j.ccr.2014.02.017 · Cited by 795
Self-citationKRAS and YAP1 Converge to Regulate EMT and Tumor Survival
Shao, D. D., Xue, W., Krall, E. B., Bhutkar, A., Piccioni, F., Wang, X., Schinzel, A. C., Sood, S., Rosenbluh, J., Kim, J. W., et al. (2014) · Cell · doi:10.1016/j.cell.2014.06.004 · Cited by 744
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BindingDB Entry 50017595: Efficient targeted oncogenic KRAS
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Bokhari, B. T. (2026) · Journal of Pharmaceutical Innovation · doi:10.1007/s12247-026-11139-z
Metadata
- Authors
- McCormick, F.
- Affiliations
- Frederick National Laboratory for Cancer Research (US)
- Corresponding author
- McCormick, Frank
- ORCID
- McCormick, Frank
- Venue
- Clinical Cancer Research
- Published
- 2015-04-14
- Volume
- 21
- Issue
- 8
- Pages
- 1797-1801
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- PMC
- PMC4407814
- OpenAlex
- W2062410054
- Cited by
- 320
- References
- 41
- Citations by year
- 2026: 10 · 2025: 22 · 2024: 18 · 2023: 35 · 2022: 26 · 2021: 32 · 2020: 45 · 2019: 35 · 2018: 31 · 2017: 29 · 2016: 26 · 2015: 10
- FWCI
- 3.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Cancer Institute (U01CA168370)
- 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, KRAS-targeted therapy, MAPK/ERK pathway, PI3K signaling, synthetic lethality, cancer metabolism, cancer immunotherapy, KRAS oncogenic signaling, drug discovery
- MeSH terms
- Animals, Antineoplastic Agents, Cell Transformation, Neoplastic, Humans, Immunity, Immunotherapy, Mutation, Neoplasms, Genetic Therapy, Signal Transduction, Proto-Oncogene Proteins p21(ras), Drug Resistance, Neoplasm, Protein Subunits, RNA Interference, RNA, Small Interfering, Protein Kinase Inhibitors, Molecular Targeted Therapy
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