ArticleCancer research2012
Targeting eNOS in pancreatic cancer.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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Who cites it
48 citing papers in PubMed, 76 citations in OpenAlex.
- Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- The anticancer properties of the nanocomposite of low-nanoscale Ag nanoparticles obtained in SiOBMC pharmacology & toxicology · 2026Article
- Loss of inducible nitric oxide synthase promotes Kras/Pten-driven lung tumorigenesis.Frontiers in cell and developmental biology · 2026Article
- Long-term effects of sub-chronic exposure to L-NAME on reproductive system of male rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- In Vitro Cytotoxic Potential and In Vivo Antitumor Effects of NOS/PDK-Inhibitor T1084.International journal of molecular sciences · 2024Article
- Ionizable lipid nanoparticles for RAS protease delivery to inhibit cancer cell proliferation.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- Hypoxia-induced NOS1 as a therapeutic target in hypercholesterolemia-related colorectal cancer.Cancer & metabolism · 2024Article
- Analysis of single nuclear chromatin accessibility reveals unique myeloid populations in human pancreatic ductal adenocarcinoma.Clinical and translational medicine · 2024Article
- Mutant K-Ras in Pancreatic Cancer: An Insight on the Role of Wild-Type N-Ras and K-Ras-Dependent Cell Cycle Regulation.Current issues in molecular biology · 2023Article
- N-acetylcysteine improves the inhibitory effect of Quercetin-rich onion extract on HT-29 and HCT-116 colorectal cancer migration and invasion through iNOS suppression.International journal of medical sciences · 2023Article
- Oxidative Stress Markers Are Associated with a Poor Prognosis in Patients with Pancreatic Cancer.Antioxidants (Basel, Switzerland) · 2022Article
- Combination of NOS- and PDK-Inhibitory Activity: Possible Way to Enhance Antitumor Effects.International journal of molecular sciences · 2022Article
- Article
- Metastatic Melanoma Progression Is Associated with Endothelial Nitric Oxide Synthase Uncoupling Induced by Loss of eNOS:BH4 Stoichiometry.International journal of molecular sciences · 2021Article
- The molecular biology of pancreatic adenocarcinoma: translational challenges and clinical perspectives.Signal transduction and targeted therapy · 2021Review
- Engineering subtilisin proteases that specifically degrade active RAS.Communications biology · 2021Article
- Approaches to inhibiting oncogenic K-Ras.Small GTPases · 2021Review
- Pan-Cancer Analysis of NOS3 Identifies Its Expression and Clinical Relevance in Gastric Cancer.Frontiers in oncology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 2 countries.
Funding
Abstract
Mortality from pancreatic ductal adenocarcinoma cancer (PDAC) is among the highest of any cancer and frontline therapy has changed little in years. Activation of endothelial nitric oxide synthase (eNOS, NOS3, or NOS III) has been implicated recently in the pathogenesis of PDACs. In this study, we used genetically engineered mouse and human xenograft models to evaluate the consequences of targeting eNOS in PDACs. Genetic deficiency in eNOS limited the development of preinvasive pancreatic lesions and trended toward an extended lifespan in mice with advanced pancreatic cancer. These effects were also observed upon oral administration of the clinically evaluated NOS small molecule inhibitor N(G)-nitro-L-arginine methyl ester (l-NAME). Similarly, other transgenic models of oncogenic KRas-driven tumors responded to l-NAME treatment. Finally, these results were recapitulated in xenograft models of human pancreatic cancer, in which l-NAME was found to broadly inhibit tumorigenic growth. Taken together, our findings offer preclinical proof-of-principle to repurpose l-NAME for clinical investigations in treatment of PDACs and possibly other KRas-driven human cancers.
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.