Evidence map›Paper›PMID 37408267›Full record

ArticleCells2023

Regulation of IDO2 by the Aryl Hydrocarbon Receptor (AhR) in Breast Cancer.

Sarah Y Kado, Keith Bein, Alejandro R Castaneda, Arshia A Pouraryan, Nicole Garrity, Yasuhiro Ishihara, Andrea Rossi, Thomas Haarmann-Stemmann, Colleen A Sweeney, Christoph F A Vogel

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Harnessing IDO inhibitors to optimize cancer immunotherapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
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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

10 authors at 3 institutions in 3 countries.

Sarah Y KadoCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA.
Keith BeinCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA.
Alejandro R CastanedaCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA.
Arshia A PouraryanCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA.
Nicole GarrityCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA.ORCID 0009-0000-5209-8546
Yasuhiro IshiharaGraduate School of Integrated Arts and Sciences, Hiroshima University, Hiroshima 739-8521, Japan.
Andrea RossiLeibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.ORCID 0000-0001-5863-6448
Thomas Haarmann-StemmannLeibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Colleen A SweeneyDepartment of Biochemistry & Molecular Medicine, School of Medicine, University of California, Davis, CA 95817, USA.
Christoph F A VogelCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA.
University of California, Davis · USLeibniz Institute of Environmental Medicine · DEHiroshima University · JP

Funding

UC Davis Environmental Health Sciences Core CenterP30ES023513 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Irva Hertz-Picciotto · 2015 to 2026
$26.0M
Air pollution, atherosclerosis, and the role of the aryl hydrocarbon receptorR01ES029126 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2019 to 2023
$1.8M
The impact of Aryl hydrocarbon receptor signaling on Toll like receptor-mediated inflammationR01ES032827 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHRISTOPH F A VOGEL · 2022 to 2026
$1.7M
NIEHS NIH HHS P30 ES023513NIEHS NIH HHS R01 ES029126NIEHS NIH HHS R01 ES032827
6 · The paper itself

Abstract

Indoleamine 2,3-dioxygenase 2 (IDO2) is a tryptophan-catabolizing enzyme and a homolog of IDO1 with a distinct expression pattern compared with IDO1. In dendritic cells (DCs), IDO activity and the resulting changes in tryptophan level regulate T-cell differentiation and promote immune tolerance. Recent studies indicate that IDO2 exerts an additional, non-enzymatic function and pro-inflammatory activity, which may play an important role in diseases such as autoimmunity and cancer. Here, we investigated the impact of aryl hydrocarbon receptor (AhR) activation by endogenous compounds and environmental pollutants on the expression of IDO2. Treatment with AhR ligands induced IDO2 in MCF-7 wildtype cells but not in CRISPR-cas9 AhR-knockout MCF-7 cells. Promoter analysis with IDO2 reporter constructs revealed that the AhR-dependent induction of IDO2 involves a short-tandem repeat containing four core sequences of a xenobiotic response element (XRE) upstream of the start site of the human

Indexed as

Breast NeoplasmsIndoleamine-Pyrrole 2,3,-DioxygenaseReceptors, Aryl HydrocarbonBasic Helix-Loop-Helix ProteinsCell DifferentiationFemaleHumansImmune ToleranceTryptophanTumor MicroenvironmentAHR protein, humanBasic Helix-Loop-Helix ProteinsIDO2 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseReceptors, Aryl HydrocarbonTryptophanAhRbreast cancerIDOIDO2immunityPMTCDDtumor microenvironment

Identifiers

PMID37408267
PMCPMC10216785
OpenAlexW4377195770

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.