The DOI matches its Crossref record; 109 of the 109 references it cites were found in a registry or an index.
KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer
Open accessAbstract
mutation frequency, pancreatic ductal adenocarcinoma (PDAC) is considered the most RAS-addicted of all cancers. We review the role of KRAS as a driver and therapeutic target in PDAC.
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“In pancreatic cancer, KRAS mutation is often the initiating genetic event leading to pancreatic intraepithelial neoplasms. Carcinogenesis and metastasis are stimulated by acquiring other mutations such as p53 (64%), SMAD4 (21%), and CDKN2A (17%) [63].”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [63]
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“This high prevalence is significant as it makes PDAC arguably the most RAS-addicted cancer, with substantial experimental evidence that mutant KRAS is essential for its growth [107].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [107]
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“In particular, the KRAS isoform is mutated in 84% of all RAS-mutant cancers, with a near 100% mutation frequency in PDAC.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [107]
In the citing paper
“The majority of KRAS mutations are at codon 12, with the highest prevalence of G12D mutation (35%), followed by G12V (20–30%), G12R (10–20%), Q61 (~5%), G12C (1–2%), and other rare muations9–12.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [9]
In the citing paper
“A number of highly selective and potent inhibitors have been developed against kinases in the Ras signaling network particularly those in the MAPK and PI3K/mTOR pathways (9, 12).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [12]
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“the KRASG12C allele occurs in only 1.6% of PDAC cases, whereas the KRASG12D allele is present in greater than 40%, followed in frequency by KRASG12V and KRASG12R mutations74.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [74]
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Citations
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“Further, wholeexome deep-sequencing data of pancreatic cancer patients shows that 93% of the rare PIK3CA mutations co-occur with aKRASmutation, suggesting activated KRAS alone is not sufficient to effectively activate PI3K (Jones et al. 2008; Biankin et al. 2012; Sausen et al. 2015; Waddell et al. 2015; Witkiewicz et…”
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BindingDB Entry 50018665: Targeting mutated GTPase KRAS in tumor therapies.
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BindingDB (2026) · UC San Diego · doi:10.7270/q26w9gxr
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BindingDB (2023) · UC San Diego · doi:10.7270/q2pc368t
BindingDB (2022) · UC San Diego · doi:10.7270/q27h1p69
BindingDB Entry 50018560: JDQ443, a Structurally Novel, Pyrazole-Based, Covalent Inhibitor of KRAS
BindingDB (2024) · UC San Diego · doi:10.7270/q2x92ghc
Metadata
- Authors
- Waters, A. M., & Der, C. J.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2017-12-11
- Volume
- 8
- Issue
- 9
- Pages
- a031435
- ISSN
- 2157-1422 (ISSN-L)
- PMC
- PMC5995645
- OpenAlex
- W2771729549
- Cited by
- 875
- References
- 109
- Citations by year
- 2026: 73 · 2025: 112 · 2024: 121 · 2023: 118 · 2022: 153 · 2021: 157 · 2020: 98 · 2019: 35 · 2018: 8
- Type
- posted content
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cold Spring Harbor Perspectives in Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- Funders
- U.S. Department of Defense
- American Association for Cancer Research
- Pancreatic Cancer Action Network
- Lustgarten Foundation
- National Science Council
- National Institutes of Health (5r01ca042978-30)
- National Cancer Institute (CA042978, CA203657, P01CA203657, R01CA175747, T32CA009156, P50CA196510, R01-CA042978, CA199235, U01CA199235, CA196510, P30CA016086)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- KRAS, pancreatic ductal adenocarcinoma, pancreatic cancer, driver mutations, therapeutic target, KRAS inhibitors
- MeSH terms
- Adenocarcinoma, Animals, Humans, Mutation, Signal Transduction, Proto-Oncogene Proteins p21(ras), Carcinoma, Pancreatic Ductal, Protein Kinase Inhibitors, Molecular Targeted Therapy
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