Evidence map›Paper›PMID 40211813›Full record

ArticleCancer research and treatment2026

Elimusertib, a Novel ATR Inhibitor, Induces Anti-tumor Effects through Replication Catastrophe in Breast Cancers.

Mudong Kim, Ahrum Min, Sohyeon Kim, Seongyeong Kim, Yu-Jin Kim, Sujin Ham, Miso Lee, Eunice Yoojin Lee, Jinyong Kim, Dae-Won Lee and 2 more

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In one paragraph

Article in Cancer research and treatment, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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.

Mudong KimCancer Research Institute, Seoul National University, Seoul, Korea.
Ahrum MinCancer Research Institute, Seoul National University, Seoul, Korea.
Sohyeon KimCancer Research Institute, Seoul National University, Seoul, Korea.
Seongyeong KimCancer Research Institute, Seoul National University, Seoul, Korea.
Yu-Jin KimCancer Research Institute, Seoul National University, Seoul, Korea.
Sujin HamCancer Research Institute, Seoul National University, Seoul, Korea.
Miso LeeCancer Research Institute, Seoul National University, Seoul, Korea.
Eunice Yoojin LeeDepartment of Internal Medicine, University of California San Francisco, San Francisco, CA, USA.
Jinyong KimCancer Research Institute, Seoul National University, Seoul, Korea.
Dae-Won LeeCancer Research Institute, Seoul National University, Seoul, Korea.
Kyung-Hun LeeCancer Research Institute, Seoul National University, Seoul, Korea.
Seock-Ah ImCancer Research Institute, Seoul National University, Seoul, Korea.

Funding

Ministry of Science and ICTNational Research Foundation of Korea 2020R1A2C301088311Seoul National University
6 · The paper itself

Abstract

purposeSustained cell proliferation and cell cycle acceleration in cancer cells inherently increase DNA damage, which interferes with homeostatic replication and transcription. Ataxia telangiectasia and Rad3-related (ATR) is crucial for initiation of the DNA damage response, and ATR inhibitors, such as elimusertib, induce increased replication stress and DNA damage. We investigated the anti-tumor effects of elimusertib and its mechanism of action in relation to replication stress. MATERIALS AND

methodsAnti-tumor effects were evaluated by MTT assay and colony formation assay in breast cancer cell lines in vitro, in breast cancer cell xenografts in vivo, and in patient-derived xenograft models. Cell cycle was assessed by flow cytometry and BrdU assay was used to measure replicating cells and S-phase progression. Alkaline and neutral comet assay was used to measure single and double-stranded DNA damages, respectively.

resultsElimusertib delayed S-phase progression in MDA-MB-453 and MDA-MB-231 cells and induced caspase-7-dependent apoptosis. Furthermore, the increase in sub-G1 population in the fluorescence-activated cell sorting analysis and Annexin V assay also confirmed apoptotic cell death. In the BrdU assay, single-stranded DNA (ssDNA) increased in sensitive cells and aberrant ssDNA induced DNA damage in S-phase and eventually caused replication catastrophe. Finally, these anti-tumor effects were proven in in vivo xenograft and patient-derived xenograft models.

conclusionElimusertib had anti-tumor effects and induced replication catastrophe in breast cancer cells with a high replication rate. Moreover, cells under high DNA replication stress were sensitive to elimusertib. Further studies and treatment strategies with elimusertib are warranted for cancers with a high replication rate.

Indexed as

Antineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsBreast NeoplasmsDNA ReplicationAnimalsApoptosisCell Line, TumorCell ProliferationDNA DamageFemaleHumansMiceXenograft Model Antitumor AssaysAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsATR protein, humanATR inhibitorCell cycle progressionDNA damageReplication catastropheReplication stress

Identifiers

PMID40211813
PMCPMC12800941

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Registered trials

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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.