Evidence map›Paper›PMID 41154337›Full record

ArticleCancers2025

Artemis (DCLRE1C) Acts as a Target to Enhance Radiotherapy Response in Triple-Negative Breast Cancer.

Vasudeva Bhat, Kelsie L Thu, Anayra de Fatima Goncalves Santiago, Anna C Bonvissuto, Farhad Ghasemi, David Goodale, Michael V Roes, Daniel T Passos, Frederick A Dick, David W Cescon and 2 more

Abstract read
In one paragraph

Article in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Vasudeva BhatDepartment of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 3K7, Canada.ORCID 0000-0003-2228-6217
Kelsie L ThuKeenan Research Centre for Biomedical Science, St Michael's Hospital Unity Health Toronto, Toronto, ON M5B 1T8, Canada.ORCID 0000-0001-9262-7238
Anayra de Fatima Goncalves SantiagoDepartment of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 3K7, Canada.
Anna C BonvissutoDepartment of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 3K7, Canada.
Farhad GhasemiDivision of General Surgery, Department of Surgery, Schulich School of Medicine and Dentistry, Western University, St Joseph's Health Care and London Health Sciences Centre, London, ON N6A 4V2, Canada.
David GoodaleVerspeeten Family Cancer Centre, London Health Sciences Centre and London Health Sciences Centre Research Inc., London, ON N6A 5W9, Canada.
Michael V RoesDepartment of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 5C1, Canada.
Daniel T PassosDepartment of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 5C1, Canada.ORCID 0000-0002-3530-2821
Frederick A DickVerspeeten Family Cancer Centre, London Health Sciences Centre and London Health Sciences Centre Research Inc., London, ON N6A 5W9, Canada.
David W CesconDepartment of Medical Oncology and Hematology, University of Toronto, Princess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 2C1, Canada.ORCID 0000-0002-1080-0998
Alison L AllanDepartment of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 3K7, Canada.
Armen ParsyanDepartment of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 3K7, Canada.ORCID 0000-0003-0084-8733

Funding

Breast Cancer Canada NACanadian Institute of Health Research NALondon Regional Cancer Program Catalyst Grant for Translational Cancer Research, Western University, London ON NASmall Town Cancer Fighter PhD scholarship. NAthe AMOSO 2023-34 Academic Health Sciences Centre Alternative Funding Plan Clinical Innovation Fund Award (#INN24-017), ON, Canada NAThe Department of Surgery Internal Research Fund for Clinical Academics, Western University, London, ON. A.P., is supported by the Clinician Scientist Award, Depart-ment of Surgery, Western University, London, ON, Canada NAthe Surgical Oncology Catalyst Grant for Research, Division of Surgical Oncology, De-partment of Oncology, Schulich School of Medicine and Dentistry, western University, London ON NAUnity Health Toronto and the Canada Research Chairs program 233198
6 · The paper itself

Abstract

BACKGROUND/

objectivesThe lack of canonical biomarkers and strategies to target radioresistance contribute to poor patient outcomes in triple-negative breast cancer (TNBC). Identifying and targeting novel radioresistance genes will benefit in enhancing radiotherapy response and treatment outcomes in TNBC patients.

methodsA genome-wide CRISPR screen was performed to identify radioresistance genes in the TNBC cell line. An in vitro clonogenic assay was used to assess the antiproliferative effects of Artemis knockout or pharmacologic inhibition of Artemis, either alone or in combination with RT. Tumor doubling time and animal survival were assessed using an in vivo xenograft model. RNA-seq analysis was performed to identify genes and pathways deregulated under Artemis knockout conditions, both alone and in combination with RT. Cellular senescence was evaluated using a β-galactosidase assay.

resultsOur CRISPR screen identified Artemis as a top hit in RT-treated TNBC cells, whose depletion led to radiosensitization in TNBC. Artemis knockout significantly reduced cell proliferation and enhanced the antiproliferative effects of RT in vitro. Compared to mice-bearing control MDA-MB-231 xenografts, Artemis knockout exhibited prolonged survival that was further enhanced with RT. Bulk RNA-sequencing indicated that the antiproliferative and radiosensitization effects of Artemis depletion were mediated by the activation of cellular senescence which was confirmed with a β-galactosidase assay.

conclusionsTaken together, our results highlight the critical role of Artemis in TNBC cell proliferation and response to radiation. Our findings identify Artemis as a potential biomarker indicative of sensitivity to radiation and a putative target that could be inhibited to enhance the efficacy of RT in TNBC.

Indexed as

breast cancercellular senescenceCRISPR screenDCLRE1C (Artemis)radiosensitizing target

Identifiers

PMID41154337
PMCPMC12564160

What Socratic 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 Socratic graph.