ArticleeLife2021
Signaling levels mold the RAS mutation tropism of urethane.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 14 citations in OpenAlex.
- Evaluating the implications of K-Ras, KEAP1/NRF2-mediated signaling pathways and metabolic alterations in urethane-induced lung cancer.Journal of molecular histology · 2026Article
- Targeting chemical carcinogenesis: α-pinene and D-limonene as chemopreventive agents against NNK/TCDD- and urethane-induced lung tumorigenesis.Journal of food and drug analysis · 2025Article
- Article
- Wild-type RAS signaling is an essential therapeutic target inScience signaling · 2025Article
- Different Oncogenes and Reproductive Histories Shape the Progression of Distinct Premalignant Clones in Multistage Mouse Breast Cancer Models.The American journal of pathology · 2024Article
- Transfer RNAs as dynamic and critical regulators of cancer progression.Nature reviews. Cancer · 2023Review
- Navigating the ERK1/2 MAPK Cascade.Biomolecules · 2023Review
- Article
- Article
- Heterogeneity in RAS mutations: One size does not fit all.Science signaling · 2022Article
- An ultra-sensitive method to detect mutations in humanSmall GTPases · 2022Article
- Article
- Danger zone.eLife · 2021Article
Corrections and comments
- Commented on byDanger zone.2021
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
RAS genes are commonly mutated in human cancer. Despite many possible mutations, individual cancer types often have a 'tropism' towards a specific subset of RAS mutations. As driver mutations, these patterns ostensibly originate from normal cells. High oncogenic RAS activity causes oncogenic stress and different oncogenic mutations can impart different levels of activity, suggesting a relationship between oncoprotein activity and RAS mutation tropism. Here, we show that changing rare codons to common in the murine
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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.