ReviewPharmaceuticals (Basel, Switzerland)2025
Inflammation-Driven Genomic Instability: A Pathway to Cancer Development and Therapy Resistance.
Review in Pharmaceuticals (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed.
- Failure of morphogenesis in chronic inflammation-associated early tumourigenesis: Extracellular matrix biomechanics as an integrative layer.Biochemistry and biophysics reports · 2026Review
- Periodontitis as a Modulator of Malignant Transformation in Oral Potentially Malignant Disorders: A Narrative Review of Biological Mechanisms and Clinical Implications.Current oncology reports · 2026Review
- The Molecular Heterogeneity of NRAS Variants in Thyroid Nodules.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2026Article
- Review
- Association of the global inflammatory-nutritional index (GINI) with time to next treatment and overall survival in patients with metastatic colorectal cancer receiving third-line therapy: a real-world retrospective study.Journal of gastrointestinal oncology · 2026Article
- An Exploratory In Silico Analysis ofCancers · 2026Article
- YBX1 Expression Marks Proliferative Tumour States with Context-Dependent Genomic Instability: A Pan-Cancer Analysis.International journal of molecular sciences · 2026Article
- Unravelling Mechanisms of Oxinflammation Induced by Heavy Metals.Metabolites · 2026Review
- Targeting Inflammation and Immune Regulation in Chronic Inflammation Associated Cancers.Cancer science · 2026Review
- From Chronic Inflammation to Cancer: The Role of Trained Immunity in IBD-Associated Colorectal Carcinogenesis.Medical sciences (Basel, Switzerland) · 2026Review
- Salivary Oxidative Stress and Antioxidant Markers in Oral Leukoplakia: A Systematic Review and Meta-Analysis.Antioxidants (Basel, Switzerland) · 2026Review
- Review
- Understanding Cancer Health Disparities.Cancers · 2026Review
- Review
- Genome doubling as a dynamic driver of ovarian cancer evolution: insights from single-cell sequencing.Journal of ovarian research · 2025Review
- Effect of Social Determinants of Health and Geography on Uveal Melanoma.Clinical ophthalmology (Auckland, N.Z.) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Chronic inflammation, while originally a protective physiological response, is increasingly recognized as a key contributor to carcinogenesis. Prolonged inflammatory signaling leads to the sustained production of reactive oxygen and nitrogen species (ROS/RNS), resulting in direct and indirect DNA damage, including base modifications, strand breaks, and DNA cross-linking. Simultaneously, pro-inflammatory mediators such as NF-κB, IL-6, and TNF-α can interfere with DNA repair mechanisms, altering the efficiency of key pathways such as base excision and mismatch repair. Immune cells infiltrating chronically inflamed tissues, including macrophages and neutrophils, further exacerbate genomic instability through ROS/RNS release and cytokine production, creating a tumor-promoting microenvironment. Additionally, chronic inflammation has been implicated in the development of resistance to chemotherapy and radiotherapy by modulating DNA damage response pathways. Understanding the interplay between inflammation, genomic instability, and therapy resistance provides a framework for novel treatment strategies. Targeting chronic inflammation with non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or biological agents such as monoclonal antibodies offers promising avenues for cancer prevention and treatment. Targeting inflammation with NSAIDs, corticosteroids, and monoclonal antibodies shows promise in cancer prevention and therapy, particularly in lung and pancreatic cancer. These agents act by blocking key inflammatory pathways like COX-2, NF-κB, and cytokine signaling. However, potential adverse effects require further clinical evaluation.
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What Socratic 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 Socratic graph.