Evidence map›Paper›PMID 20106901›Full record

ReviewCarcinogenesis2010

The aryl hydrocarbon receptor (AhR) in the regulation of cell-cell contact and tumor growth.

Cornelia Dietrich, Bernd Kaina

Open access · greenAbstract readReview
In one paragraph

Review in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
14.2field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 237 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. AhR signaling in skin-resident CD207Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Factors underlying the association betweenGut microbiome (Cambridge, England) · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Redox Proteomic Profile of Tirapazamine-Resistant Murine Hepatoma Cells.International journal of molecular sciences · 2023
    Article
  20. Article

36 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

2 authors at 1 institution in 1 country.

Cornelia DietrichInstitute of Toxicology, Medical Center of the Johannes Gutenberg-University, Mainz, Germany. cdietric@uni-mainz.de
Bernd Kaina
Johannes Gutenberg University Mainz · DE

Funding

Synthetic Organic Chemistry CoreP30ES006676 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 1995 to 2017
$21.7M
Aryl Hydrocarbon Receptor-Mediated Epigenetic ProcessesR01ES026874 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 2016 to 2020
$2.2M
A Novel Paradigm for Aryl Hydrocarbon Receptor SignalingR21ES024607 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 2015 to 2016
$426k
NIEHS NIH HHS P30 ES006676NIEHS NIH HHS R01 ES026874NIEHS NIH HHS R21 ES024607
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, which is activated by a large group of environmental pollutants including polycyclic aromatic hydrocarbons, dioxins and planar polychlorinated biphenyls. Ligand binding leads to dimerization of the AhR with aryl hydrocarbon receptor nuclear translocator and transcriptional activation of several xenobiotic phase I and phase II metabolizing enzymes, such as cytochrome P4501A1 and glutathione-S-transferase, respectively. Since phase I enzymes convert inert carcinogens to active genotoxins, the AhR plays a key role in tumor initiation. Besides this classical route, the AhR mediates tumor promotion and recent evidence suggests that the AhR also plays a role in tumor progression. To date, no mechanistic link could be established between the canonical pathway involving xenobiotic metabolism and AhR-dependent tumor promotion and progression. A hallmark of tumor promotion is unbalanced proliferation, whereas tumor progression is characterized by dedifferentiation, increased motility and metastasis of tumor cells. Tumor progression and presumably also tumor promotion are triggered by loss of cell-cell contact. Cell-cell contact is known to be a critical regulator of proliferation, differentiation and cell motility in vitro and in vivo. Increasing evidence suggests that activation of the AhR may lead to deregulation of cell-cell contact, thereby inducing unbalanced proliferation, dedifferentiation and enhanced motility. In line with this is the finding of increased AhR expression and malignancy in some animal and human cancers. Here, we summarize our current knowledge on non-canonical AhR-driven pathways being involved in deregulation of cell-cell contact and discuss the data with respect to tumor initiation, promotion and progression.

Indexed as

Cell AdhesionCell CommunicationCell CycleCell DivisionCell MembraneEpithelial CellsHomeostasisHumansMembrane ProteinsNeoplasmsReceptors, Aryl HydrocarbonSignal TransductionMembrane ProteinsReceptors, Aryl Hydrocarbon

Identifiers

PMID20106901
PMCPMC6276890
OpenAlexW2097989455

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.