ReviewOncogene2008
Role of Toll-like receptors in gastrointestinal malignancies.
Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 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
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.
- Inflammation and Stem Cell Stochasticity of HPV-induced Cervical Cancer: Epigenetics based Biomarkers through Microbiome and Metabolome for Personalized Medicine: A Systematic Review.Current medicinal chemistry · 2025Pooled it
- PICK1 modulates the proliferation and migration of gastric cancer cells by regulating TLR4.Journal of Zhejiang University. Science. B · 2025Article
- Transformation-associated recombination and heterologous expression of noncanonical depsipeptide nonribosomal peptide synthetase derived from marineMarine life science & technology · 2025Article
- TLR4/MyD88 expression patterns and novel genetic variants: association with aggressive clinicopathological features in colorectal cancer.Frontiers in oncology · 2025Article
- Toll-like receptors 1, 2, 4, 5, and 6 in gastric cancer.Virchows Archiv : an international journal of pathology · 2024Article
- Xinghamide A, a New Cyclic Nonapeptide Found inMarine drugs · 2023Article
- The TLR/MyD88 signalling cascade in inflammation and gastric cancer: the immune regulatory network of Helicobacter pylori.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Recent Advances on Small-Molecule Antagonists Targeting TLR7.Molecules (Basel, Switzerland) · 2023Review
- In Silico Tool for Identification, Designing, and Searching of IL13-Inducing Peptides in Antigens.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Umbelliferone ameliorates ulcerative colitis induced by acetic acid via modulation of TLR4/NF-κB-p65/iNOS and SIRT1/PPARγ signaling pathways in rats.Environmental science and pollution research international · 2022Article
- Unique TLR9 Activation by Helicobacter pylori Depends on the cag T4SS, But Not on VirD2 Relaxases or VirD4 Coupling Proteins.Current microbiology · 2022Article
- The Relation Between Host TLR9 -1486T/C, rs187084 Gene Polymorphisms andPolish journal of microbiology · 2022Article
- Comprehensive Bioinformatics Analysis of Toll-Like Receptors (TLRs) in Pan-Cancer.BioMed research international · 2022Article
- Design and optimisation of a small-molecule TLR2/4 antagonist for anti-tumour therapy.RSC medicinal chemistry · 2021Article
- Innate immunity - the hallmark ofWorld journal of clinical cases · 2021Article
- Toll-Like Receptors (TLRs): Structure, Functions, Signaling, and Role of Their Polymorphisms in Colorectal Cancer Susceptibility.BioMed research international · 2021Review
- Role of microbial dysbiosis in carcinogenesis & cancer therapies.The Indian journal of medical research · 2020Review
- Role of gut microbiota-immunity axis in patients undergoing surgery for colorectal cancer: Focus on short and long-term outcomes.World journal of gastroenterology · 2020Review
- Cellular evasion strategies of Helicobacter pylori in regulating its intracellular fate.Seminars in cell & developmental biology · 2020Review
- Review
38 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Mounting evidence supports the tenet that innate immune responses to luminal microbes participate in the development of gastrointestinal malignancies. The gastrointestinal tract is relatively unique in that it has evolved in the presence of diverse enteric microflora. Intestinal flora is required to develop a normal adaptive immune response in the periphery. With the characterization of the innate immune system, we have begun to understand the adaptations the intestine has made to the microbiota. The interaction between the microbiota and the intestinal mucosa through Toll-like receptors (TLRs) is required to maintain intestinal homeostasis. In particular, intestinal epithelial cells and lamina propria mononuclear cells such as antigen-presenting cells and T cells must respond to breaches in the mucosal barrier by activating TLR-dependent pathways that result in increased epithelial proliferation, wound healing and recruitment of acute inflammatory cells. In the setting of chronic inflammation such as Helicobacter pylori (H. pylori) infection in the stomach or idiopathic inflammatory bowel disease, the process of repair may eventually result in carcinogenesis. The following review highlights human and animal data that support a role for innate immune responses and TLRs specifically in promoting gastrointestinal malignancies. Candidate pathways linking TLRs to gastrointestinal malignancies include activation of nuclear factor-kappaB and cyclooxygenase-2. Studying the link between innate immune signaling and gastrointestinal malignancies offers the possibility to identify novel ways to both prevent and treat gastrointestinal cancer.
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.