ReviewSeminars in cancer biology2019
KRAS, YAP, and obesity in pancreatic cancer: A signaling network with multiple loops.
Review in Seminars in cancer biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review.Signal transduction and targeted therapy · 2023Pooled it
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- The RASA2/RASA3 ortholog RasGAP1 modulates obesity-linked phenotypes and is associated with leptin-analog signaling inFrontiers in endocrinology · 2026Article
- The Hippo terminal effector YAP boosts enterovirus replication in type 1 diabetes.Nature communications · 2025Article
- The Hippo signaling pathway modulates pancreatic tissue homeostasis.Cell death discovery · 2025Review
- Advances in research on the carcinogenic mechanisms and therapeutic potential of YAP1 in bladder cancer (Review).Oncology reports · 2025Review
- Transcriptomic analysis on pancreatic adenocarcinoma patients uncovers KRAS-mediated PPAR pathway alteration.Frontiers in oncology · 2025Article
- Oncolytic viral therapy as a novel potential solution for treatment of pancreatic cancer.Gastroenterology and hepatology from bed to bench · 2025Review
- Correlation Between Antihypertensive Drugs and Survival Among Patients with Pancreatic Ductal Adenocarcinoma.Cancers · 2024Review
- GL-V9 Promotes Autophagy-Mediated YAP1 Degradation and Activates Mitochondrial Apoptosis in PDAC Cells.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Article
- Metformin: A Dual-Role Player in Cancer Treatment and Prevention.International journal of molecular sciences · 2024Review
- A stumbling block in pancreatic cancer treatment: drug resistance signaling networks.Frontiers in cell and developmental biology · 2024Review
- Advances in the mechanism of metformin with wide-ranging effects on regulation of the intestinal microbiota.Frontiers in microbiology · 2024Review
- LIPH contributes to glycolytic phenotype in pancreatic ductal adenocarcinoma by activating LPA/LPAR axis and maintaining ALDOA stability.Journal of translational medicine · 2023Article
- Low dosage combination treatment with metformin and simvastatin inhibits obesity-promoted pancreatic cancer development in male KrasG12D mice.Scientific reports · 2023Article
- Pancreatic Cancer and Detection Methods.Biomedicines · 2023Review
- Short-chain fatty acids in cancer pathogenesis.Cancer metastasis reviews · 2023Review
- New insights into the role of adipocytes in pancreatic cancer progression: paving the way towards novel therapeutic targets.Theranostics · 2023Review
- Intra-tumoral infiltration of adipocyte facilitates the activation of antitumor immune response in pancreatic ductal adenocarcinoma.Translational oncology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) continues to be a lethal disease with no efficacious treatment modalities. The incidence of PDAC is expected to increase, at least partially because of the obesity epidemic. Increased efforts to prevent or intercept this disease are clearly needed. Mutations in KRAS are initiating events in pancreatic carcinogenesis supported by genetically engineered mouse models of the disease. However, oncogenic KRAS is not entirely sufficient for the development of fully invasive PDAC. Additional genetic mutations and/or environmental, nutritional, and metabolic stressors, e.g. inflammation and obesity, are required for efficient PDAC formation with activation of KRAS downstream effectors. Multiple factors "upstream" of KRAS associated with obesity, including insulin resistance, inflammation, changes in gut microbiota and GI peptides, can enhance/modulate downstream signals. Multiple signaling networks and feedback loops "downstream" of KRAS have been described that respond to obesogenic diets. We propose that KRAS mutations potentiate a signaling network that is promoted by environmental factors. Specifically, we envisage that KRAS mutations increase the intensity and duration of the growth-promoting signaling network. As the transcriptional activator YAP plays a critical role in the network, we conclude that the rationale for targeting the network (at different points), e.g. with FDA approved drugs such as statins and metformin, is therefore compelling.
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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.