ArticleThe Journal of experimental medicine2008
RAGE signaling sustains inflammation and promotes tumor development.
Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 3 of them syntheses that pooled it.
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
213 citing papers in PubMed, 3 syntheses or guidelines pooled it, 375 citations in OpenAlex.
- Effect of tumor microenvironment on pathogenesis of the head and neck squamous cell carcinoma: a systematic review.Molecular cancer · 2019Pooled it
- Pooled it
- Robust shifts in S100a9 expression with aging: a novel mechanism for chronic inflammation.Scientific reports · 2013Pooled it
- Trial
- Evidence that serum levels of the soluble receptor for advanced glycation end products are inversely associated with pancreatic cancer risk: a prospective study.Cancer research · 2011Trial
- Structure-guided discovery of a dual JAK2/RAGE modulator reveals a computationally driven strategy for targeting convergent oncogenic signaling in renal cell carcinoma.Journal of computer-aided molecular design · 2026Article
- Crosstalk Between nNOS/NO and COX-2 Enhances Interferon-Gamma-Stimulated Melanoma Progression.Cancers · 2025Article
- Mechanism of action of HMGB1 in urologic malignancies.Frontiers in oncology · 2025Review
- The alarmin tandem: unraveling the complex effect of S100A8/A9 - from atherosclerosis to cardiac arrhythmias.Frontiers in immunology · 2025Review
- Integrative analysis of crotonylation-associated genes reveals prognostic and therapeutic targets in gliomas.Frontiers in oncology · 2025Article
- Article
- The RAGE Pathway in Skin Pathology Development: A Comprehensive Review of Its Role and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Article
- In-Depth Analysis ofBiology · 2024Article
- Role of innate host defense proteins in oral cancerogenesis.Periodontology 2000 · 2024Review
- Investigating Snake-Venom-Induced Dermonecrosis and Inflammation Using an Ex Vivo Human Skin Model.Toxins · 2024Article
- Immune Cell Migration to Cancer.Cells · 2024Review
- Progress of research on the relationship between efferocytosis and tumor.Frontiers in oncology · 2024Review
- Intestinal Biomarkers and Their Importance in Canine Enteropathies.Veterinary medicine international · 2024Review
- RAGE engagement by SARS-CoV-2 enables monocyte infection and underlies COVID-19 severity.Cell reports. Medicine · 2023Article
153 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A broad range of experimental and clinical evidence has highlighted the central role of chronic inflammation in promoting tumor development. However, the molecular mechanisms converting a transient inflammatory tissue reaction into a tumor-promoting microenvironment remain largely elusive. We show that mice deficient for the receptor for advanced glycation end-products (RAGE) are resistant to DMBA/TPA-induced skin carcinogenesis and exhibit a severe defect in sustaining inflammation during the promotion phase. Accordingly, RAGE is required for TPA-induced up-regulation of proinflammatory mediators, maintenance of immune cell infiltration, and epidermal hyperplasia. RAGE-dependent up-regulation of its potential ligands S100a8 and S100a9 supports the existence of an S100/RAGE-driven feed-forward loop in chronic inflammation and tumor promotion. Finally, bone marrow chimera experiments revealed that RAGE expression on immune cells, but not keratinocytes or endothelial cells, is essential for TPA-induced dermal infiltration and epidermal hyperplasia. We show that RAGE signaling drives the strength and maintenance of an inflammatory reaction during tumor promotion and provide direct genetic evidence for a novel role for RAGE in linking chronic inflammation and cancer.
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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.