ArticleOncogene2014
Oncogenic K-Ras requires activation for enhanced activity.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
97 citing papers in PubMed.
- Unveiling the gut-pancreas axis: microbial influence on stemness and tumor microenvironment of PDAC.Stem cells (Dayton, Ohio) · 2026Review
- A Narrative Review on Unravelling Bacterial-Mediated Carcinogenesis and Possible Alternative Treatment Strategies.BioMed research international · 2026Review
- Pancreatic cancer-associated myofibroblasts: a review.International journal of biological sciences · 2026Review
- Gut microbiome and nutritional strategies in gastrointestinal cancers: Clinical implications and therapeutic perspectives.World journal of clinical oncology · 2025Review
- Firmicutes in gut microbiota: hormonal influence on breast cancer in obese individuals.Discover oncology · 2025Review
- Progress in Intestinal Homeostasis and Mechanisms of Pancreatic Cancer.Phenomics (Cham, Switzerland) · 2025Review
- Nuclear Galectin-1 promotesProceedings of the National Academy of Sciences of the United States of America · 2025Article
- The dual role of gut microbiota in pancreatic cancer: new insights into onset and treatment.Therapeutic advances in medical oncology · 2025Review
- The role of oral microbiota in digestive system diseases: current advances and perspectives.Journal of oral microbiology · 2025Review
- Coxsackievirus and adenovirus receptor expression facilitates enteroviral infections to drive the development of pancreatic cancer.Nature communications · 2024Article
- KRAS-Driven Tumorigenesis and KRAS-Driven Therapy in Pancreatic Adenocarcinoma.Molecular cancer therapeutics · 2024Review
- A Narrative Review: Immunometabolic Interactions of Host-Gut Microbiota and Botanical Active Ingredients in Gastrointestinal Cancers.International journal of molecular sciences · 2024Review
- Gut-Liver-Pancreas Axis Crosstalk in Health and Disease: From the Role of Microbial Metabolites to Innovative Microbiota Manipulating Strategies.Biomedicines · 2024Review
- Early elevations of RAS protein level and activity are critical for the development of PDAC in the context of inflammation.Cancer letters · 2024Article
- Article
- Hematopoietic progenitor kinase 1 inhibits the development and progression of pancreatic intraepithelial neoplasia.The Journal of clinical investigation · 2023Article
- The Role of Krüppel-like Factors in Pancreatic Physiology and Pathophysiology.International journal of molecular sciences · 2023Review
- The Expressions of NF-κB, COX-2, Sp1, and c-Jun in Pancreatic Ductal Adenocarcinoma and Their Associations with Patient Survival.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Article
- PPDPF Promotes the Development of Mutant KRAS-Driven Pancreatic Ductal Adenocarcinoma by Regulating the GEF Activity of SOS1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Microbiota in the Natural History of Pancreatic Cancer: From Predisposition to Therapy.Cancers · 2022Review
37 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
7 authors.
Funding
Abstract
Oncogenic Ras mutations are widely considered to be locked in a permanent 'On' state and 'constitutively active'. Yet, many healthy people have cells possessing mutant Ras without apparent harm, and in animal models mutant Ras causes transformation only after upregulation of Ras activity. Here, we demonstrate that oncogenic K-Ras is not constitutively active but can be readily activated by upstream stimulants to lead to prolonged strong Ras activity. These data indicate that in addition to targeting K-Ras downstream effectors, interventions to reduce K-Ras activation may have important cancer-preventive value, especially in patients with oncogenic Ras mutations. As other small G proteins are regulated in a similar manner, this concept is likely to apply broadly to the entire Ras family of molecules.
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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.