Evidence map›Paper›PMID 19996281›Full record

ArticleCancer research2010

The aryl hydrocarbon receptor functions as a tumor suppressor of liver carcinogenesis.

Yunxia Fan, Gregory P Boivin, Erik S Knudsen, Daniel W Nebert, Ying Xia, Alvaro Puga

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
6.6field-weighted citation impact, top 3% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

106 citing papers in PubMed, 177 citations in OpenAlex.

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46 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Yunxia FanDepartment of Environmental Health, University of Cincinnati Medical Center, College of Medicine, Cincinnati, Ohio 45267-0056, USA.
Gregory P Boivin
Erik S Knudsen
Daniel W Nebert
Ying Xia
Alvaro Puga
Thomas Jefferson University · USUniversity of Cincinnati Medical Center · USSidney Kimmel Cancer Center · USWright State University · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI PINNEY, SUSAN MENGEL · 1992 to 2022
$35.4M
MOLECULAR MECHANISMS OF COMPLEX MIXTURE TOXICITYR01ES010807 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 2001 to 2021
$8.0M
MOLECULAR MECHANISMS OF DIOXIN ACTIONR01ES006273 · NIEHS · UNIVERSITY OF CINCINNATI · PI PUGA, ALVARO · 1993 to 2015
$4.6M
NIEHS NIH HHS P30 ES006096NIEHS NIH HHS P30 ES06096NIEHS NIH HHS R01 ES006273NIEHS NIH HHS R01 ES010807NIEHS NIH HHS R01 ES06273NIEHS NIH HHS R01 ES10807
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the biological and toxic effects of its xenobiotic ligands. Previous cell culture studies have shown that, in addition to controlling the xenobiotic detoxification response, AHR activation leads to G0-G1 arrest, diminished capacity for DNA replication, and inhibition of cell proliferation. In fact, recent work from our own and from other laboratories suggests that AHR may function as a tumor suppressor gene that becomes silenced during the process of tumor formation. To test this hypothesis and determine whether the mouse Ahr gene acts as a tumor suppressor gene in vivo, we have examined the role of Ahr ablation in liver tumorigenesis induced by the genotoxic chemical diethylnitrosamine (DEN), a hepatic carcinogen that is not an AHR ligand. In mice given a single i.p. injection of DEN, AHR antagonized liver tumor formation and growth by regulating cell proliferation, inflammatory cytokine expression, and DNA damage, parameters which were significantly elevated in the livers of control and, more so, of DEN-exposed Ahr-/- mice. Ahr-/- hepatocytes also showed significantly higher numbers of 4N cells, increased expression of proliferative markers, and repression of tumor suppressor genes. These data support the concept that in its basal state in the absence of a xenobiotic ligand, the Ahr gene functions as a tumor suppressor gene, and that its silencing may be associated with cancer progression.

Indexed as

AnimalsCarcinogensDiethylnitrosamineFemaleGenes, Tumor SuppressorLiver NeoplasmsMaleMiceMice, KnockoutReceptors, Aryl HydrocarbonReverse Transcriptase Polymerase Chain ReactionSex FactorsCarcinogensDiethylnitrosamineReceptors, Aryl Hydrocarbon

Identifiers

PMID19996281
PMCPMC2939500
OpenAlexW2107459338

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.