Evidence map›Paper›PMID 41827755›Full record

ArticleCancers2026

ATR Blockade Potentiates the Effects of Genotoxic Agents In Vitro and Promotes Antitumor Immunity in a Mouse Model of Non-Small Cell Lung Cancer.

Dimitra Mavroeidi, Christina Papanikolaou, Elisavet Deligianni, Panagiotis Malamos, Panagiota Stamou, Konstantinos N Syrigos, Vassilis L Souliotis

Abstract read
In one paragraph

Article in Cancers, 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. Article
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.

Dimitra MavroeidiInstitute of Chemical Biology, National Hellenic Research Foundation, 116 35 Athens, Greece.
Christina PapanikolaouInstitute of Chemical Biology, National Hellenic Research Foundation, 116 35 Athens, Greece.
Elisavet DeligianniInstitute of Chemical Biology, National Hellenic Research Foundation, 116 35 Athens, Greece.
Panagiotis MalamosInstitute of Chemical Biology, National Hellenic Research Foundation, 116 35 Athens, Greece.ORCID 0000-0002-5771-5352
Panagiota StamouInstitute of Chemical Biology, National Hellenic Research Foundation, 116 35 Athens, Greece.
Konstantinos N SyrigosThird Department of Medicine, Sotiria General Hospital for Chest Diseases, National and Kapodistrian University of Athens, 115 27 Athens, Greece.
Vassilis L SouliotisInstitute of Chemical Biology, National Hellenic Research Foundation, 116 35 Athens, Greece.ORCID 0000-0002-2945-1329

Funding

This work was supported by the Hellenic Society of Medical Oncology (HeSMO) 9597/19-6-2024 research grants
6 · The paper itself

Abstract

BACKGROUND/

objectivesNon-small cell lung cancer (NSCLC) is the most frequent type of lung cancer, and its main treatments include chemotherapy with genotoxic drugs and immunotherapy. Central to the cellular response to genotoxic stress is the DNA damage response (DDR) network, regulated by key kinases such as ataxia-telangiectasia mutated and Rad3-related (ATR). Herein, we tested the hypothesis that inhibition of ATR enhances the cytotoxicity of genotoxic agents and the antitumor immune response.

methodsDDR-related parameters and redox status, expressed as GSH/GSSG ratio, and apurinic/apyrimidinic lesions, were evaluated in human (A549, H1299) and murine (LLC) NSCLC cell lines after co-exposure to ATR inhibitor (AZD6738) and ultraviolet C (UVC) irradiation or cisplatin. Using a syngeneic LLC model, treatments of AZD6738 alone or in combination with cisplatin and/or anti-programmed cell death 1 antibody (anti-PD1) were examined.

resultsIn all cell lines, combined treatment with AZD6738 and cisplatin or UVC irradiation markedly decreased cell viability, DNA repair efficiency, and GSH/GSSG ratios; increased drug-induced DNA damage; and augmented apurinic/apyrimidinic lesions. In vivo, following treatment with AZD6738 and cisplatin, flow cytometry analysis performed in tumor cells revealed an increased infiltration of CD3

conclusionsThese results demonstrate that ATR blockade concurrently enhances the efficacy of genotoxic agents and immune checkpoint inhibitors, thus paving the way for combination therapies in NSCLC.

Indexed as

anti-PD1ataxia telangiectasia and Rad3-related kinase (ATR)ceralasertib (AZD6738)cisplatinDNA damage response (DDR)immune checkpoint inhibitorinterstrand cross-link repair (ICL/R)non-small cell lung cancer (NSCLC)nucleotide excision repair (NER)redox status

Identifiers

PMID41827755
PMCPMC12984715

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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.