Evidence map›Paper›PMID 41854291›Full record

ArticleMolecular oncology2026

Cell-cycle-specific lesion evolution rather than inhibition of double-strand-break repair underpins cisplatin radiosensitization.

Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular oncology, 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

11 authors.

Ye QiuDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.
Xixi LinDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.ORCID https://orcid.org/0000-0002-3161-0253
Emil MladenovDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.
Veronika MladenovaDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.
Jürgen ThomaleInstitute of Cell Biology, University Hospital Essen, Germany.
Ali SakDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.
Yao WangDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.
Yunxuan DengDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.
Eleni GkikaRadiation Biology Laboratory, Department of Radiotherapy and Radiation Oncology, University Hospital Bonn, Germany.
Martin StuschkeDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.
George IliakisDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Germany.ORCID https://orcid.org/0000-0002-1152-5342

Funding

Bundesministerium für Forschung Technologie und Raumfahrt (BMFTR) 02NUK037BBundesministerium für Forschung Technologie und Raumfahrt (BMFTR) 02NUK043BBundesministerium für Forschung Technologie und Raumfahrt (BMFTR) 02NUK054BBundesministerium für Wirtschaft und Technologie (BMWi) BMWi-50WB1836Deutsche Forschungsgemeinschaft DFG-IL51.10Deutsche Forschungsgemeinschaft GRK1739Deutsche Forschungsgemeinschaft IL51.11Deutscher Akademischer Austausch Dienst #57515880
6 · The paper itself

Abstract

DNA double-strand breaks (DSBs) generated from collisions of DNA replication forks with cisplatin-induced interstrand crosslinks underpin cisplatin cytotoxicity. Yet, the impact of cell-cycle-dependent cisplatin-DNA adduct (CDA) formation on cell cycle progression and interactions with DNA replication remain incompletely characterized. Also, although cisplatin enhances tumor response to ionizing radiation (IR), the underpinning radiosensitizing mechanisms remain unresolved. Here, we close this void and analyze CDAs (GpG crosslinks) and DSB (γH2AX foci) induction and repair in a strictly cell-cycle-dependent manner. We report for the first time that CDAs form in a dose- and time-dependent manner in all cell cycle phases, whereas DSBs emerge only in S-phase. Repair of IR-induced DSBs remains largely unaffected by CDAs in G

Indexed as

Cell CycleCisplatinDNA Breaks, Double-StrandedDNA RepairRadiation-Sensitizing AgentsRadiation ToleranceCell Line, TumorDNA AdductsDNA ReplicationHistonesHumansCisplatincisplatin-DNA adductDNA AdductsHistonesRadiation-Sensitizing Agentscell cyclecisplatincisplatin‐DNA adductsDNA double‐strand breaksDNA repairradiosensitization

Identifiers

PMID41854291
PMCPMC13352966

What OpenQuestion holds

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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.