ArticleGenes & cancer2011
Inflammation and p53: A Tale of Two Stresses.
Article in Genes & cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 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
116 citing papers in PubMed, 195 citations in OpenAlex.
- Review
- Review
- Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Insights into FACT in Cancers with Targeted Therapeutic Implications.Molecular and cellular biology · 2026Review
- Network-based integrative analysis of multi-level regulatory mechanisms associated with glyphosate exposure.Frontiers in bioinformatics · 2026Article
- Basophils activate splenic B cells and dendritic cells via IL-13 signaling in acute traumatic brain injury.Journal of neuroinflammation · 2025Article
- Expression characteristics of miR-502-5p/p53/NF-κB signaling pathway in patients with different degrees of knee osteoarthritis: a cross-sectional observational study with methodological limitations.Journal of orthopaedic surgery and research · 2025Observational
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- The molecular mechanism of NF-κB dysregulation across different subtypes of renal cell carcinoma.Journal of advanced research · 2025Review
- Targeting p53-p21 signaling to enhance mesenchymal stem cell regenerative potential.Regenerative therapy · 2025Review
- Exploring the Genetic Orchestra of Cancer: The Interplay Between Oncogenes and Tumor-Suppressor Genes.Cancers · 2025Review
- Molecular evidence of the inhibitory potential of melatonin against sodium arsenite toxicity.Heliyon · 2025Article
- Ribosomal proteins: the missing piece in the inflammation puzzle?Molecular and cellular biochemistry · 2025Review
- P53 and the Ultraviolet Radiation-Induced Skin Response: Finding the Light in the Darkness of Triggered Carcinogenesis.Cancers · 2024Review
- Epithelial RANKL Limits Experimental Periodontitis via Langerhans Cells.Journal of dental research · 2024Article
- The Dual Role of Amyloid Beta-Peptide in Oxidative Stress and Inflammation: Unveiling Their Connections in Alzheimer's Disease Etiopathology.Antioxidants (Basel, Switzerland) · 2024Review
- Transcriptomic Analysis of Hub Genes Reveals Associated Inflammatory Pathways in Estrogen-Dependent Gynecological Diseases.Biology · 2024Article
- Human Umbilical Cord Mesenchymal-Stem-Cell-Derived Extracellular Vesicles Reduce Skin Inflammation In Vitro.International journal of molecular sciences · 2023Article
- Emerging role and therapeutic implications of p53 in intervertebral disc degeneration.Cell death discovery · 2023Review
- Higher gestational weight gain delays wound healing and reduces expression of long non-coding RNA KLRK1-AS1 in neonatal endothelial progenitor cells.The Journal of physiology · 2023Article
56 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Numerous observations indicate a strong link between chronic inflammation and cancer. This link is supported by substantial experimental evidence indicating mutual negative regulation of NF-κB, the major regulator of inflammation, and p53, the major tumor suppressor. This antagonistic relationship reflects the opposite principles of the physiological responses driven by these transcription factors, which act as sensors and mediators of intrinsic and extrinsic cell stresses, respectively. Constitutive activation of NF-κB, the underlying cause of chronic inflammation, is a common acquired characteristic of tumors. A variety of experimental methods have been used to demonstrate that constitutive activation of NF-κB reduces the tumor suppressor activity of p53, thereby creating permissive conditions for dominant oncogene-mediated transformation. Loss of p53 activity is also a characteristic of the majority of tumors and results in unleashed inflammatory responses due to loss of p53-mediated NF-κB suppression. On the other hand, in natural or pharmacological situations of enforced p53 activation, NF-κB activity, inflammation, and immune responses are reduced, resulting in different pathologies. It is likely that the chronic inflammation that is commonly acquired in various tissues of older mammals leads to general suppression of p53 function, which would explain the increased risk of cancer observed in aging animals and humans. Although the molecular mechanisms underlying reciprocal negative regulation of p53 and NF-κB remain to be deciphered, this phenomenon has important implications for pharmacological prevention of cancer and aging and for new approaches to control inflammation.
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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.