ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Liver tumor promotion by 2,3,7,8-tetrachlorodibenzo-p-dioxin is dependent on the aryl hydrocarbon receptor and TNF/IL-1 receptors.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 43 citations in OpenAlex.
- TCDD dysregulation of lncRNA expression, liver zonation and intercellular communication across the liver lobule.Toxicology and applied pharmacology · 2023Article
- TCDD dysregulation of lncRNA expression, liver zonation and intercellular communication across the liver lobule.bioRxiv : the preprint server for biology · 2023Article
- The Improvement of the Adaptation Process of Tocopherol and Acetylsalicylic Acid in Offspring of Mothers Exposed to TCDD.Animals : an open access journal from MDPI · 2021Article
- Rodent genetic models of Ah receptor signaling.Drug metabolism reviews · 2021Review
- Generation of an Allelic Series at the Ahr Locus Using an Edited Recombinant Approach.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Prediction Model of Aryl Hydrocarbon Receptor Activation by a Novel QSAR Approach, DeepSnap-Deep Learning.Molecules (Basel, Switzerland) · 2020Article
- A Protective Role of Aryl Hydrocarbon Receptor Repressor in Inflammation and Tumor Growth.Cancers · 2019Article
- Constitutive Activation of the Human Aryl Hydrocarbon Receptor in Mice Promotes Hepatocarcinogenesis Independent of Its Coactivator Gadd45b.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Risk for animal and human health related to the presence of dioxins and dioxin-like PCBs in feed and food.EFSA journal. European Food Safety Authority · 2018Article
- The association between chemical-induced porphyria and hepatic cancer.Toxicology research · 2018Review
- Analysis of expression profile data identifies key genes and pathways in hepatocellular carcinoma.Oncology letters · 2018Article
- Review
- The Aryl Hydrocarbon Receptor and Tumor Immunity.Frontiers in immunology · 2018Review
- Role of the aryl hydrocarbon receptor in carcinogenesis and potential as an anti-cancer drug target.Archives of toxicology · 2017Review
- Dioxin-induced increase in leukotriene B4 biosynthesis through the aryl hydrocarbon receptor and its relevance to hepatotoxicity owing to neutrophil infiltration.The Journal of biological chemistry · 2017Article
- The aryl hydrocarbon receptor repressor - More than a simple feedback inhibitor of AhR signaling: Clues for its role in inflammation and cancer.Current opinion in toxicology · 2017Article
- Transgenic Overexpression of Aryl Hydrocarbon Receptor Repressor (AhRR) and AhR-Mediated Induction of CYP1A1, Cytokines, and Acute Toxicity.Environmental health perspectives · 2016Article
- Aryl hydrocarbon receptor-dependent apoptotic cell death induced by the flavonoid chrysin in human colorectal cancer cells.Cancer letters · 2016Article
- Environmental Ligands of the Aryl Hydrocarbon Receptor and Their Effects in Models of Adult Liver Progenitor Cells.Stem cells international · 2016Review
- Ah Receptor Pathway Intricacies; Signaling Through Diverse Protein Partners and DNA-Motifs.Toxicology research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
We set out to better understand the signal transduction pathways that mediate liver tumor promotion by 2,3,7,8-tetrachlorodibenzo-p-dioxn ("dioxin"). To this end, we first employed congenic mice homozygous for either the Ahr(b1) or Ahr(d) alleles (encoding an aryl hydrocarbon receptor (AHR) with high or low binding affinity for dioxin, respectively) and demonstrated that hepatocellular tumor promotion in response to dioxin segregated with the Ahr locus. Once we had genetic evidence for the importance of AHR signaling, we then asked if tumor promotion by dioxin was influenced by "interleukin-1 (IL-1)-like" inflammatory cytokines. The importance of this question arose from our earlier observation that aspects of the acute hepatocellular toxicity of dioxin are dependent upon IL1-like cytokine signaling. To address this issue, we employed a triple knock-out (TKO) mouse model with null alleles at the loci encoding the three relevant receptors for tumor necrosis factors α and β and IL-1α and IL-1β (i.e., null alleles at the Tnfrsf1a, Tnfrsf1b, and Il-1r1 loci). The observation that TKO mice were resistant to the tumor promoting effects of dioxin in liver suggests that inflammatory cytokines play an important step in dioxin mediated liver tumor promotion in the mouse. Collectively, these data support the idea that the mechanism of dioxin acute hepatotoxicity and its activity as a promoter in a mouse two stage liver cancer model may be similar, i.e., tumor promotion by dioxin, like acute hepatotoxicity, are mediated by the linked action of two receptor systems, the AHR and the receptors for the "IL-1-like" cytokines.
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.