Evidence map›Paper›PMID 37506922›Full record

ArticleBiochemical pharmacology2023

Suppression of Ah Receptor (AhR) increases the aggressiveness of TNBC cells and 11-Cl-BBQ-activated AhR inhibits their growth.

Daniel J Elson, Bach D Nguyen, Nicholas A Korjeff, Sierra F Wilferd, Veronica Puig-Sanvicens, Hyo Sang Jang, Sebastian Bernales, Sarvajit Chakravarty, Sebastián Belmar, Gonzalo Ureta and 3 more

Abstract read
In one paragraph

Article in Biochemical pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 8 citations in OpenAlex.

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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

13 authors at 4 institutions in 2 countries.

Daniel J ElsonCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, United States.
Bach D NguyenCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, United States.
Nicholas A KorjeffCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, United States.
Sierra F WilferdSchool of Biological and Health Systems Engineering, Arizona State University, Tempe, AZ 85287, United States.
Veronica Puig-SanvicensCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, United States.
Hyo Sang JangCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, United States.
Sebastian BernalesPraxis Biotech, San Francisco, CA 94158, United States; Fundación Ciencia & Vida, Centro Científico y Tecnológico Ciencia & Vida, Avda. Del valle Norte 725, Santiago, Chile.
Sarvajit ChakravartyPraxis Biotech, San Francisco, CA 94158, United States.
Sebastián BelmarPraxis Biotech, San Francisco, CA 94158, United States; Merken Biotech, Avda. Del valle Norte 725, Santiago, Chile.
Gonzalo UretaPraxis Biotech, San Francisco, CA 94158, United States; Merken Biotech, Avda. Del valle Norte 725, Santiago, Chile.
Darren FinlaySanford Burnham Prebys Medical Discovery Institute, NCI Designated Cancer Center, La Jolla, CA 92037, United States.
Christopher L PlaisierSchool of Biological and Health Systems Engineering, Arizona State University, Tempe, AZ 85287, United States.
Siva K KolluriCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, United States; Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, United States. Electronic address: siva.kolluri@oregonstate.edu.
Oregon State University · USArizona State University · USDiscovery Institute · USFundación Ciencia and Vida · CL

Funding

MODE OF ACTION OF ENVIRONMENTAL TOXICANTST32ES007060 · NIEHS · OREGON STATE UNIVERSITY · PI Jamie DeWitt, Siva Kumar Kolluri · 1985 to 2026
$11.6M
Aryl Hydrocarbon Receptor Modulators for the Treatment of Hepatocellular CarcinomR21ES019000 · NIEHS · OREGON STATE UNIVERSITY · PI KOLLURI, SIVA KUMAR · 2011 to 2012
$402k
NIEHS NIH HHS R21 ES019000NIEHS NIH HHS T32 ES007060
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) represents around 15% of the 2.26 million breast cancers diagnosed worldwide annually and has the worst outcome. Despite recent therapeutic advances, there remains a lack of targeted therapies for this breast cancer subtype. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor with biological roles in regulating development, xenobiotic metabolism, cell cycle progression and cell death. AhR activation by select ligands can promote tumor suppression in multiple cancer types. AhR can negatively regulate the activity of different oncogenic signaling pathways and can directly upregulate tumor suppressor genes such as p27

Indexed as

Triple Negative Breast NeoplasmsCell Line, TumorCell ProliferationHumansLigandsReceptors, Aryl HydrocarbonLigandsReceptors, Aryl Hydrocarbon11-Cl-BBQAhRGrowth inhibitionTNBCTumor suppressor

Identifiers

PMID37506922
PMCPMC13197171
OpenAlexW4385261120

What OpenQuestion holds

Textmetadata
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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.