Evidence map›Paper›PMID 35268641›Full record

ReviewMolecules (Basel, Switzerland)2022

DNA Damage Clustering after Ionizing Radiation and Consequences in the Processing of Chromatin Breaks.

Veronika Mladenova, Emil Mladenov, Martin Stuschke, George Iliakis

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.0field-weighted citation impact, top 2% of its field
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

53 citing papers in PubMed, 76 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Veronika MladenovaClinic and Polyclinic for Radiation Therapy, Medical School, University of Duisburg-Essen, 45122 Essen, Germany.
Emil MladenovClinic and Polyclinic for Radiation Therapy, Medical School, University of Duisburg-Essen, 45122 Essen, Germany.
Martin StuschkeClinic and Polyclinic for Radiation Therapy, Medical School, University of Duisburg-Essen, 45122 Essen, Germany.
George IliakisClinic and Polyclinic for Radiation Therapy, Medical School, University of Duisburg-Essen, 45122 Essen, Germany.
University of Duisburg-Essen · DE

Funding

Bundesministerium für Wirtschaft und Technologie BMWi: ESA-AO-IBER-2017, 50WB1836Federal Ministry of Education and Research 02NUK043B, COLLARFederal Ministry of Education and Research 03NUK005C
6 · The paper itself

Abstract

Charged-particle radiotherapy (CPRT) utilizing low and high linear energy transfer (low-/high-LET) ionizing radiation (IR) is a promising cancer treatment modality having unique physical energy deposition properties. CPRT enables focused delivery of a desired dose to the tumor, thus achieving a better tumor control and reduced normal tissue toxicity. It increases the overall radiation tolerance and the chances of survival for the patient. Further improvements in CPRT are expected from a better understanding of the mechanisms governing the biological effects of IR and their dependence on LET. There is increasing evidence that high-LET IR induces more complex and even clustered DNA double-strand breaks (DSBs) that are extremely consequential to cellular homeostasis, and which represent a considerable threat to genomic integrity. However, from the perspective of cancer management, the same DSB characteristics underpin the expected therapeutic benefit and are central to the rationale guiding current efforts for increased implementation of heavy ions (HI) in radiotherapy. Here, we review the specific cellular DNA damage responses (DDR) elicited by high-LET IR and compare them to those of low-LET IR. We emphasize differences in the forms of DSBs induced and their impact on DDR. Moreover, we analyze how the distinct initial forms of DSBs modulate the interplay between DSB repair pathways through the activation of DNA end resection. We postulate that at complex DSBs and DSB clusters, increased DNA end resection orchestrates an increased engagement of resection-dependent repair pathways. Furthermore, we summarize evidence that after exposure to high-LET IR, error-prone processes outcompete high fidelity homologous recombination (HR) through mechanisms that remain to be elucidated. Finally, we review the high-LET dependence of specific DDR-related post-translational modifications and the induction of apoptosis in cancer cells. We believe that in-depth characterization of the biological effects that are specific to high-LET IR will help to establish predictive and prognostic signatures for use in future individualized therapeutic strategies, and will enhance the prospects for the development of effective countermeasures for improved radiation protection during space travel.

Indexed as

ChromatinDNA Breaks, Double-StrandedCluster AnalysisDNA DamageDNA RepairHumansRadiation, IonizingChromatinATMATRcharged-particle radiotherapycomplex double-strand breaksDNA damage responsedouble-strand break clustersdouble-strand breaksheavy ionshigh-LET ionizing radiationionizing radiationprotons

Identifiers

PMID35268641
PMCPMC8911773
OpenAlexW4214526686

What OpenQuestion holds

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LicenceCC BY
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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.