Evidence map›Paper›PMID 19651607›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Aryl hydrocarbon receptor suppresses intestinal carcinogenesis in ApcMin/+ mice with natural ligands.

Kaname Kawajiri, Yasuhito Kobayashi, Fumiaki Ohtake, Togo Ikuta, Yoshibumi Matsushima, Junsei Mimura, Sven Pettersson, Richard S Pollenz, Toshiyuki Sakaki, Takatsugu Hirokawa and 5 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed
6.5field-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

145 citing papers in PubMed, 262 citations in OpenAlex.

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85 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

15 authors at 7 institutions in 3 countries.

Kaname KawajiriResearch Institute for Clinical Oncology and Hospital, Saitama Cancer Center, 818 Komuro, Ina, Saitama, 362-0806, Japan. kawajiri@cancer-c.pref.saitama.jp
Yasuhito Kobayashi
Fumiaki Ohtake
Togo Ikuta
Yoshibumi Matsushima
Junsei Mimura
Sven Pettersson
Richard S Pollenz
Toshiyuki Sakaki
Takatsugu Hirokawa
Tetsu Akiyama
Masafumi Kurosumi
Lorenz Poellinger
Shigeaki Kato
Yoshiaki Fujii-Kuriyama
Saitama Cancer Center · JPThe University of Tokyo · JPJapan Science and Technology Agency · JPKarolinska Institutet · SEToyama Prefectural University · JPUniversity of South Florida · USUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal cancer is one of the most common human cancers. Aberrant activation of the canonical Wnt signaling cascade, for example, caused by adenomatous polyposis coli (APC) gene mutations, leads to increased stabilization and accumulation of beta-catenin, resulting in initiation of intestinal carcinogenesis. The aryl hydrocarbon receptor (AhR) has dual roles in regulating intracellular protein levels both as a ligand-activated transcription factor and as a ligand-dependent E3 ubiquitin ligase. Here, we show that the AhR E3 ubiquitin ligase has a role in suppression of intestinal carcinogenesis by a previously undescribed ligand-dependent beta-catenin degradation pathway that is independent of and parallel to the APC system. This function of AhR is activated by both xenobiotics and natural AhR ligands, such as indole derivatives that are converted from dietary tryptophan and glucosinolates by intestinal microbes, and suppresses intestinal tumor development in Apc(Min/+) mice. These findings suggest that chemoprevention with naturally-occurring and chemically-designed AhR ligands can be used to successfully prevent intestinal cancers.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsbeta CateninCecal NeoplasmsIntestinal MucosaIntestinesLigandsMiceMice, Inbred C57BLPrecancerous ConditionsProteasome Endopeptidase ComplexProtein Processing, Post-TranslationalReceptors, Aryl HydrocarbonSignal TransductionUbiquitinationAdenomatous Polyposis Coli Proteinbeta CateninLigandsProteasome Endopeptidase ComplexReceptors, Aryl Hydrocarbon

Identifiers

PMID19651607
PMCPMC2726415
OpenAlexW2141304385

What OpenQuestion holds

Textmetadata
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.