ArticleNature2008
Tumour maintenance is mediated by eNOS.
Article in Nature, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers, 2 of them syntheses that pooled it.
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
172 citing papers in PubMed, 2 syntheses or guidelines pooled it, 318 citations in OpenAlex.
- Association between endothelial nitric oxide synthase 894G>T polymorphism and prostate cancer risk: a meta-analysis of literature studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- An official ATS clinical practice guideline: interpretation of exhaled nitric oxide levels (FENO) for clinical applications.American journal of respiratory and critical care medicine · 2011Guideline
- Nitric oxide synthase variants and disease-free survival among treated and untreated breast cancer patients in a Southwest Oncology Group clinical trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Trial
- Mutant and Wild-Type RAS Cross-talk and Stoichiometric Deficiencies Are Determinants of Sensitivity to Targeted Therapies in KRASG12R Pancreatic Ductal Adenocarcinoma.Cancer research · 2026Article
- S-nitrosylation of IRF7 induced by NOS1 expression in melanoma suppresses anti-tumor immunity.Cell death & disease · 2026Article
- Loss of inducible nitric oxide synthase promotes Kras/Pten-driven lung tumorigenesis.Frontiers in cell and developmental biology · 2026Article
- Gasotransmitters bridging tumor biology and immunity: from pathophysiological insights to therapeutic potential.Frontiers in immunology · 2026Review
- Article
- Recent Anti-KRASCancers · 2025Review
- Oncogenic mutant KRAS inhibition through oxidation at cysteine 118.Molecular oncology · 2025Article
- High Intelectin-1 Expression Associated with Aggressive Tumor Behavior and Worse Survival in Rectal Cancer.OncoTargets and therapy · 2025Article
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- Imaging Techniques and Biochemical Biomarkers: New Insights into Diagnosis of Pancreatic Cancer.Cell biochemistry and biophysics · 2024Review
- Liposomal encapsulated curcumin attenuates lung cancer proliferation, migration, and induces apoptosis.Heliyon · 2024Article
- Nitric Oxide Signaling and Sensing in Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Ionizable lipid nanoparticles for RAS protease delivery to inhibit cancer cell proliferation.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- Evaluate the Serum of Irisin, Omentin-1, and Oxidative Status in Males with Prostatic Cancer.Reports of biochemistry & molecular biology · 2024Article
- Primary and Secondary Coordination Sphere Effects on the Structure and Function ofJournal of the American Chemical Society · 2023Article
- Critical requirement of SOS1 for tumor development and microenvironment modulation in KRASNature communications · 2023Article
- DAB2IP Is a Bifunctional Tumor Suppressor That Regulates Wild-Type RAS and Inflammatory Cascades in KRAS Mutant Colon Cancer.Cancer research · 2023Article
112 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Tumour cells become addicted to the expression of initiating oncogenes like Ras, such that loss of oncogene expression in established tumours leads to tumour regression. HRas, NRas or KRas are mutated to remain in the active GTP-bound oncogenic state in many cancers. Although Ras activates several proteins to initiate human tumour growth, only PI3K, through activation of protein kinase B (PKB; also known as AKT), must remain activated by oncogenic Ras to maintain this growth. Here we show that blocking phosphorylation of the AKT substrate, endothelial nitric oxide synthase (eNOS or NOS3), inhibits tumour initiation and maintenance. Moreover, eNOS enhances the nitrosylation and activation of endogenous wild-type Ras proteins, which are required throughout tumorigenesis. We suggest that activation of the PI3K-AKT-eNOS-(wild-type) Ras pathway by oncogenic Ras in cancer cells is required to initiate and maintain tumour growth.
Indexed as
Identifiers
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.