ReviewNature reviews. Cancer2018
A model for RAS mutation patterns in cancers: finding the sweet spot.
Review in Nature reviews. Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
240 citing papers in PubMed, 383 citations in OpenAlex.
- Codon-specific KRAS mutations predict survival benefit of trifluridine/tipiracil in metastatic colorectal cancer.Nature medicine · 2023Trial
- Clinical utility of circulating tumor DNA sequencing in advanced gastrointestinal cancer: SCRUM-Japan GI-SCREEN and GOZILA studies.Nature medicine · 2020Trial
- Reframing cancer therapy through tumor plasticity.Nature cancer · 2026Review
- Hyper-mutational processes provide a head-start for weak cancer drivers: Explaining atypical KRAS variants.PLoS computational biology · 2026Article
- Baseline cellular state shapes the molecular impact of mutant Kirsten rat sarcoma viral oncogene homologue (KRAS) alleles in reconstituted pancreatic cancer cells.Molecular omics · 2026Article
- Targeting non-small cell lung cancer: Molecular mechanisms and clinical studies (Review).Oncology letters · 2026Review
- Insights From Mutational and Transcriptomic Profiles in Epithelial-myoepithelial Carcinoma.The American journal of surgical pathology · 2026Article
- KRAS (G12D)-selective inhibitor MRTX1133 suppresses proliferation and differentially modulates chemosensitivity in ovarian mucinous carcinoma.Oncology letters · 2026Article
- Efficacy of dual KRASCell death & disease · 2026Article
- A catalogue of missense and nonsense mutation abundances for the U.S. cancer patient population.medRxiv : the preprint server for health sciences · 2026Article
- PTEN Oxidation Promotes Constitutive PI3K Signaling and Inducible Macropinocytosis in Pancreatic Cancer.Cancer research · 2026Article
- Small-molecule degraders for oncogenic KRASNature communications · 2026Article
- Article
- Prognostic Implications of Codon-SpecificJCO precision oncology · 2026Article
- Next-Generation Sequencing-Based Detection ofGenes · 2026Article
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Identification of Small-Molecule Inhibitors that Block the GTP-Binding Pocket of K-Ras and Other Members of the Ras Superfamily of Small GTPases.Molecular cancer therapeutics · 2026Article
- Novel Potential Markers of Metabolic Dysfunction-Associated Steatohepatitis Prone to Hepatocellular Carcinoma.Canadian journal of gastroenterology & hepatology · 2026Article
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- CAR-T cell therapy for pancreatic cancer: Translating emerging targets and dual-targeting strategies from solid tumors.Frontiers in immunology · 2026Review
180 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
The three RAS genes - HRAS, NRAS and KRAS - are collectively mutated in one-third of human cancers, where they act as prototypic oncogenes. Interestingly, there are rather distinct patterns to RAS mutations; the isoform mutated as well as the position and type of substitution vary between different cancers. As RAS genes are among the earliest, if not the first, genes mutated in a variety of cancers, understanding how these mutation patterns arise could inform on not only how cancer begins but also the factors influencing this event, which has implications for cancer prevention. To this end, we suggest that there is a narrow window or 'sweet spot' by which oncogenic RAS signalling can promote tumour initiation in normal cells. As a consequence, RAS mutation patterns in each normal cell are a product of the specific RAS isoform mutated, as well as the position of the mutation and type of substitution to achieve an ideal level of signalling.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.