Evidence map›Paper›PMID 37470014›Full record

ArticleACS pharmacology & translational science2023

Induction of Aryl Hydrocarbon Receptor-Mediated Cancer Cell-Selective Apoptosis in Triple-Negative Breast Cancer Cells by a High-Affinity Benzimidazoisoquinoline.

Daniel J Elson, Bach D Nguyen, Sebastian Bernales, Sarvajit Chakravarty, Hyo Sang Jang, Nicholas A Korjeff, Yi Zhang, Sierra F Wilferd, David J Castro, Christopher L Plaisier and 3 more

Open access · greenAbstract read
In one paragraph

Article in ACS pharmacology & translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-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

12 citing papers in PubMed, 11 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 5 institutions in 2 countries.

Daniel J ElsonCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon, 97331, United States.
Bach D NguyenCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon, 97331, United States.
Sebastian BernalesPraxis Biotech, San Francisco, California, 94158, United States.
Sarvajit ChakravartyPraxis Biotech, San Francisco, California, 94158, United States.ORCID https://orcid.org/0009-0001-5438-1801
Hyo Sang JangCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon, 97331, United States.ORCID https://orcid.org/0000-0003-0460-9924
Nicholas A KorjeffCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon, 97331, United States.
Yi ZhangCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon, 97331, United States.
Sierra F WilferdSchool of Biological and Health Systems Engineering, Arizona State University, Tempe, Arizona 85287, United States.
David J CastroSanford Burnham Prebys Medical Discovery Institute, NCI Designated Cancer Center, La Jolla, California, 92037, United States.
Christopher L PlaisierSchool of Biological and Health Systems Engineering, Arizona State University, Tempe, Arizona 85287, United States.
Darren FinlaySanford Burnham Prebys Medical Discovery Institute, NCI Designated Cancer Center, La Jolla, California, 92037, United States.
Robert G OshimaSanford Burnham Prebys Medical Discovery Institute, NCI Designated Cancer Center, La Jolla, California, 92037, United States.
Siva K KolluriCancer Research Laboratory, Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon, 97331, United States.ORCID https://orcid.org/0000-0003-1031-9827
Oregon State University · USArizona State University · USSanford Burnham Prebys Medical Discovery Institute · USFundación Ciencia and Vida · CLOregon Health & Science University · US

Funding

MODE OF ACTION OF ENVIRONMENTAL TOXICANTST32ES007060 · NIEHS · OREGON STATE UNIVERSITY · PI Jamie DeWitt, Siva Kumar Kolluri · 1985 to 2026
$11.6M
Zebrafish Biomedical Research Facility CoreP30ES030287 · NIEHS · OREGON STATE UNIVERSITY · PI Jamie DeWitt · 2020 to 2026
$9.8M
NIEHS NIH HHS P30 ES030287NIEHS NIH HHS T32 ES007060
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) remains a disease with a paucity of targeted treatment opportunities. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is involved in a wide range of physiological processes, including the sensing of xenobiotics, immune function, development, and differentiation. Different small-molecule AhR ligands drive strikingly varied cellular and organismal responses. In certain cancers, AhR activation by select small molecules induces cell cycle arrest or apoptosis via activation of tumor-suppressive transcriptional programs. AhR is expressed in triple-negative breast cancers, presenting a tractable therapeutic opportunity. Here, we identify a novel ligand of the aryl hydrocarbon receptor that potently and selectively induces cell death in triple-negative breast cancer cells and TNBC stem cells via the AhR. Importantly, we found that this compound, Analog 523, exhibits minimal cytotoxicity against multiple normal human primary cells. Analog 523 represents a high-affinity AhR ligand with potential for future clinical translation as an anticancer agent.

Identifiers

PMID37470014
PMCPMC10353065
OpenAlexW4379618967

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.