ReviewWorld journal of gastroenterology2010
Alcohol, nutrition and liver cancer: role of Toll-like receptor signaling.
Review in World journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Acute alcoholic hepatitis, end stage alcoholic liver disease and liver transplantation: an Italian position statement.World journal of gastroenterology · 2014Guideline
- Mechanisms by which the intestinal microbiota affects gastrointestinal tumours and therapeutic effects.Molecular biomedicine · 2023Review
- Chronic Inflammatory and Immune Microenvironment Promote Hepatocellular Carcinoma Evolution.Journal of inflammation research · 2023Review
- Tollip promotes hepatocellular carcinoma progression via PI3K/AKT pathway.Open medicine (Warsaw, Poland) · 2022Article
- Activation of the Toll‑like receptor 2 signaling pathway inhibits the proliferation of HCC cells in vitro.Oncology reports · 2019Article
- Role of cytokines and chemokines in alcohol-induced tumor promotion.OncoTargets and therapy · 2017Review
- Melatonin attenuates the TLR4-mediated inflammatory response through MyD88- and TRIF-dependent signaling pathways in an in vivo model of ovarian cancer.BMC cancer · 2015Article
- Alcohol and hepatocellular carcinoma: a review and a point of view.World journal of gastroenterology · 2014Review
- Should a Toll-like receptor 4 (TLR-4) agonist or antagonist be designed to treat cancer? TLR-4: its expression and effects in the ten most common cancers.OncoTargets and therapy · 2013Review
- Balloon liver cells forming Mallory-Denk-bodies are progenitor cells.Experimental and molecular pathology · 2013Article
- Chronic ingestion of ethanol induces hepatocellular carcinoma in mice without additional hepatic insult.Digestive diseases and sciences · 2013Article
- Alcoholic hepatitis.Journal of medicine and life · 2013Article
- Guardian and selective killer: the versatile functions of TLR3 in hepatocellular carcinoma.Journal of the National Cancer Institute · 2012Article
- Alcoholic liver disease - Hepatocellular carcinoma transformation.Journal of gastrointestinal oncology · 2012Article
- Immunobiology of hepatocellular carcinoma.Langenbeck's archives of surgery · 2012Review
- The association between Toll-like receptor 2 single-nucleotide polymorphisms and hepatocellular carcinoma susceptibility.BMC cancer · 2012Article
- The role of innate immunity in the pathogenesis of preneoplasia in drug-induced chronic hepatitis based on a mouse model.Experimental and molecular pathology · 2011Review
- Increased expression of toll-like receptors (TLR) 2, 4 and 5 in gastric dysplasia.Pathology oncology research : POR · 2011Article
- The immunoproteasome in steatohepatitis: its role in Mallory-Denk body formation.Experimental and molecular pathology · 2011Article
- New potential instrument to fight hepatocellular cancer by restoring p53.Hepatitis monthly · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
This article reviews the evidence that ties the development of hepatocellular carcinoma (HCC) to the natural immune pro-inflammatory response to chronic liver disease, with a focus on the role of Toll-like receptor (TLR) signaling as the mechanism of liver stem cell/progenitor transformation to HCC. Two exemplary models of this phenomenon are reviewed in detail. One model applies chronic ethanol/lipopolysaccharide feeding to the activated TLR4 signaling pathway. The other applies chronic feeding of a carcinogenic drug, in which TLR2 and 4 signaling pathways are activated. In the drug-induced model, two major methyl donors, S-adenosylmethionine and betaine, prevent the upregulation of the TLR signaling pathways and abrogate the stem cell/progenitor proliferation response when fed with the carcinogenic drug. This observation supports a nutritional approach to liver cancer prevention and treatment. The observation that upregulation of the TLR signaling pathways leads to liver tumor formation gives evidence to the popular concept that the chronic pro-inflammatory response is an important mechanism of liver oncogenesis. It provides a nutritional approach, which could prevent HCC from developing in many chronic liver diseases.
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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.