ArticleCell reports2014
NF-κB functions in tumor initiation by suppressing the surveillance of both innate and adaptive immune cells.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis 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
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review.Signal transduction and targeted therapy · 2023Pooled it
- Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB-Mediated Inflammatory Response in Triple-Negative Breast Cancer.Cancer research · 2026Article
- RelB/ILF2-GM-CSF loop sustains tumor-MDSC communication in prostate cancer immunosuppression.Cell death & disease · 2026Article
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Mass spectrometry-based proteomics to study gastric carcinogenesis: pathophysiological molecular characterization.Scientific reports · 2026Article
- Ambivalent Copper: Mechanistically Distinct Immune Effects Driving Innovation in Cancer Nanomedicine.Pharmaceutics · 2026Review
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- Harnessing nanomedicine to target NF-κB signalling in cancer: at the intersection of inflammatory signalling, metabolic reprogramming, and therapeutic innovation.Cell communication and signaling : CCS · 2026Review
- Targeting DNA Polymerase Epsilon Leads to Tumor Clearance and Activation of an NF-κB-mediated inflammatory response in Triple Negative Breast Cancer.bioRxiv : the preprint server for biology · 2025Article
- MyoD is essential in rhabdomyosarcoma by promoting survival through differentiation and CYLD.iScience · 2025Article
- Activation of the Drosophila innate immune system accelerates growth in cooperation with oncogenic Ras.PLoS biology · 2025Article
- Development of a novel prognostic signature based on cytotoxic T lymphocyte-evasion genes for hepatocellular carcinoma patient management.Discover oncology · 2025Article
- NF-κB role on tumor proliferation, migration, invasion and immune escape.Cancer gene therapy · 2024Review
- Biological basis of extensive pleiotropy between blood traits and cancer risk.Genome medicine · 2024Article
- Molecular Determinants of Calcitriol Signaling and Sensitivity in Glioma Stem-like Cells.Cancers · 2023Article
- Oncogenic Ras and ΔNp63α cooperate to recruit immunosuppressive polymorphonuclear myeloid-derived suppressor cells in a mouse model of squamous cancer pathogenesis.Frontiers in immunology · 2023Article
- NF-κB mediated regulation of tumor cell proliferation in hypoxic microenvironment.Frontiers in pharmacology · 2023Review
- Inhibition of triple negative breast cancer-associated inflammation and progression by N- acylethanolamine acid amide hydrolase (NAAA).Scientific reports · 2022Article
- In vivo genome-wide CRISPR screening identifies ZNF24 as a negative NF-κB modulator in lung cancer.Cell & bioscience · 2022Article
- Indirect Mechanisms of Transcription Factor-Mediated Gene Regulation during Cell Fate Changes.Advanced genetics (Hoboken, N.J.) · 2022Article
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 1 institution in 1 country.
Funding
Abstract
NF-κB is considered a major contributor to tumor development, but how this factor functions in the initial stages of oncogenesis is not clear. In a model of Ras-induced transformation, we probed NF-κB function as preneoplastic cells formed tumors in mice. As previously shown, the p65 subunit of NF-κB acts as a tumor suppressor in normal cells by sustaining senescence following DNA damage. Our current data reveal that, following immortalization, p65 switches to an oncogene by counteracting the surveillance properties of immune cells. NF-κB exerts this effect by protecting transformed cells against macrophage-derived proapoptotic factors, tumor necrosis factor, and nitric oxide. Additionally, NF-κB acts through transforming growth factor beta (TGF-β) to mitigate T cell cytotoxicity and other factors to expand myeloid-derived suppressor cells. Together, these data suggest that NF-κB functions in the early stages of transformation by suppressing immune surveillance of both innate and adaptive immune cells, information that may be useful for targeted immunotherapies.
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.