Evidence map›Paper›PMID 40422251›Full record

ReviewCells2025

Cancer Vulnerabilities Through Targeting the ATR/Chk1 and ATM/Chk2 Axes in the Context of DNA Damage.

Anell Fernandez, Maider Artola, Sergio Leon, Nerea Otegui, Aroa Jimeno, Diego Serrano, Alfonso Calvo

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Evolutionary study of oncogenes and tumor suppressor genes in breast carcinoma.Journal of Taibah University Medical Sciences · 2026
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  16. Research Progress of RAD51AP1 in Malignant Tumors of the Female Reproductive System.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

7 authors.

Anell FernandezProgram in Solid Tumors, CIMA, Cancer Center Clinica Universidad de Navarra (CCUN), University of Navarra, Avenida de Pio XII, 55, 31008 Pamplona, Spain.ORCID 0009-0003-7210-2321
Maider ArtolaDepartment of Pathology, Anatomy and Physiology, School of Medicine, University of Navarra, 31008 Pamplona, Spain.
Sergio LeonProgram in Solid Tumors, CIMA, Cancer Center Clinica Universidad de Navarra (CCUN), University of Navarra, Avenida de Pio XII, 55, 31008 Pamplona, Spain.
Nerea OteguiProgram in Solid Tumors, CIMA, Cancer Center Clinica Universidad de Navarra (CCUN), University of Navarra, Avenida de Pio XII, 55, 31008 Pamplona, Spain.ORCID 0009-0009-7470-0847
Aroa JimenoDepartment of Pathology, Anatomy and Physiology, School of Medicine, University of Navarra, 31008 Pamplona, Spain.
Diego SerranoProgram in Solid Tumors, CIMA, Cancer Center Clinica Universidad de Navarra (CCUN), University of Navarra, Avenida de Pio XII, 55, 31008 Pamplona, Spain.ORCID 0000-0002-3729-9195
Alfonso CalvoProgram in Solid Tumors, CIMA, Cancer Center Clinica Universidad de Navarra (CCUN), University of Navarra, Avenida de Pio XII, 55, 31008 Pamplona, Spain.ORCID 0000-0003-4074-4242

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eliciting DNA damage in tumor cells continues to be one of the most successful strategies against cancer. This is the case for classical chemotherapy drugs and radiotherapy. In the modern era of personalized medicine, this strategy tries to identify specific vulnerabilities found in each patient's tumor, to inflict DNA damage in certain cell contexts that end up in massive cancer cell death. Cells rely on multiple DNA repair pathways to fix DNA damage, but cancer cells frequently exhibit defects in these pathways, many times being tolerant to the damage. Key vulnerabilities, such as

Indexed as

Ataxia Telangiectasia Mutated ProteinsCheckpoint Kinase 1Checkpoint Kinase 2DNA DamageNeoplasmsAnimalsDNA RepairHumansSignal TransductionAtaxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanCheckpoint Kinase 1Checkpoint Kinase 2CHEK1 protein, humanCHEK2 protein, humanATMATRChk1Chk2DNA damageimmunotherapysynthetic lethality

Identifiers

PMID40422251
PMCPMC12110066

What OpenQuestion holds

Textmetadata
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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.