ArticleThe Journal of experimental medicine2010
MyD88-mediated signaling prevents development of adenocarcinomas of the colon: role of interleukin 18.
Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 246 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
246 citing papers in PubMed, 423 citations in OpenAlex.
- Interleukin-18 armours antitumour immune effectors.Nature reviews. Immunology · 2026Review
- Urolithin A activates aryl hydrocarbon receptor-NLRP6-mediated pathways in intestinal epithelial cells to modulate mucosal immunity and strengthen gut barrier integrity.Nature communications · 2026Article
- Review
- Pyroptosis: Turning Up the Heat on Cancer.Annual review of immunology · 2026Review
- Gut microbiota-innate immune crosstalk in the initiation and progression of CRC: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Microbiota and mycobiota in chronic inflammatory demyelinating polyneuropathy: clinical and pathophysiological correlations.Frontiers in molecular neuroscience · 2026Article
- Inulin aggravates colitis through gut microbiota modulation and MyD88/IL-18 signaling.Gut microbes · 2025Article
- Gastrointestinal microbiota and inflammasomes interplay in health and disease: a gut feeling.Gut · 2025Review
- IL-1R2 promotes tumorigenesis and modulates the tumor immune microenvironment in colorectal cancer.Cancer immunology, immunotherapy : CII · 2025Article
- Unveiling the Intricate Causal Nexus Between 91 Circulating Inflammatory Proteins and Perianal Abscess Through a Comprehensive Bidirectional Two-Sample Mendelian Randomization Analysis.Health science reports · 2025Article
- Gut Microbiota and Colorectal Cancer: A Balance Between Risk and Protection.International journal of molecular sciences · 2025Review
- Genetic and metabolic inflammation signatures in chronic inflammatory demyelinating polyneuropathy: the role ofFrontiers in molecular neuroscience · 2025Article
- Clinical Detection and Management of Colorectal Cancer Concerning the Gut Microbiome.Scientifica · 2025Review
- Dendritic cell-derived MYD88 potentiates as a biomarker for immune regulation in hepatocellular carcinoma and may predict a better immunological result.Frontiers in cell and developmental biology · 2025Article
- Inflammasomes in Intestinal Disease: Mechanisms of Activation and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- NLRC4, inflammation and colorectal cancer (Review).International journal of oncology · 2024Review
- MyD88 and Its Inhibitors in Cancer: Prospects and Challenges.Biomolecules · 2024Review
- The broad impact of cell death genes on the human disease phenome.Cell death & disease · 2024Article
- Epithelial regulation of microbiota-immune cell dynamics.Mucosal immunology · 2024Review
- Decreased expression of the NLRP6 inflammasome is associated with increased intestinal permeability and inflammation in obesity with type 2 diabetes.Cellular and molecular life sciences : CMLS · 2024Article
186 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
12 authors at 4 institutions in 1 country.
Funding
Abstract
Signaling through the adaptor protein myeloid differentiation factor 88 (MyD88) promotes carcinogenesis in several cancer models. In contrast, MyD88 signaling has a protective role in the development of azoxymethane (AOM)/dextran sodium sulfate (DSS) colitis-associated cancer (CAC). The inability of Myd88(-/-) mice to heal ulcers generated upon injury creates an altered inflammatory environment that induces early alterations in expression of genes encoding proinflammatory factors, as well as pathways regulating cell proliferation, apoptosis, and DNA repair, resulting in a dramatic increase in adenoma formation and progression to infiltrating adenocarcinomas with frequent clonal mutations in the beta-catenin gene. Others have reported that toll-like receptor (Tlr) 4-deficient mice have a similar susceptibility to colitis to Myd88-deficient mice but, unlike the latter, are resistant to CAC. We have observed that mice deficient for Tlr2 or Il1r do not show a differential susceptibility to colitis or CAC. However, upon AOM/DSS treatment Il18(-/-) and Il18r1(-/-) mice were more susceptible to colitis and polyp formation than wild-type mice, suggesting that the phenotype of Myd88(-/-) mice is, in part, a result of their inability to signal through the IL-18 receptor. This study revealed a previously unknown level of complexity surrounding MyD88 activities downstream of different receptors that impact tissue homeostasis and carcinogenesis.
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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.