Evidence map›Paper›PMID 30379881›Full record

ArticlePloS one2018

Simultaneous induction of dispersed and clustered DNA lesions compromises DNA damage response in human peripheral blood lymphocytes.

Lei Cheng, Beata Brzozowska, Alice Sollazzo, Lovisa Lundholm, Halina Lisowska, Siamak Haghdoost, Andrzej Wojcik

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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  16. Hadrontherapy Interactions in Molecular and Cellular Biology.International journal of molecular sciences · 2019
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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 at 2 institutions in 2 countries.

Lei ChengCentre for Radiation Protection Research, Department of Molecular Biosciences, the Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Beata BrzozowskaCentre for Radiation Protection Research, Department of Molecular Biosciences, the Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Alice SollazzoCentre for Radiation Protection Research, Department of Molecular Biosciences, the Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Lovisa LundholmCentre for Radiation Protection Research, Department of Molecular Biosciences, the Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Halina LisowskaInstitute of Biology, Jan Kochanowski University, Kielce, Poland.
Siamak HaghdoostCentre for Radiation Protection Research, Department of Molecular Biosciences, the Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Andrzej WojcikCentre for Radiation Protection Research, Department of Molecular Biosciences, the Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.ORCID 0000-0002-3951-774X
Stockholm University · SEJan Kochanowski University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to its ability to induce DNA damage in a space and time controlled manner, ionising radiation is a unique tool for studying the mechanisms of DNA repair. The biological effectiveness of ionising radiation is related to the ionisation density which is defined by the linear energy transfer (LET). Alpha particles are characterised by high LET, while X-rays by low LET values. An interesting question is how cells react when exposed to a mixed beam of high and low LET radiation. In an earlier study carried out with human peripheral blood lymphocytes (PBL) we could demonstrate that alpha radiation X-rays interact in producing more chromosomal aberrations than expected based on additivity. The aim of the present investigation was to look at the mechanism of the interaction, especially with respect to the question if it is due to an augmented level of initial damage or impaired DNA repair. PBL were exposed to various doses of alpha particles, X-rays and mixed beams. DNA damage and the kinetics of damage repair was quantified by the alkaline comet assay. The levels of phosphorylated, key DNA damage response (DDR) proteins ATM, p53 and DNA-PK were measured by Western blotting and mRNA levels of 6 damage-responsive genes were measured by qPCR. Alpha particles and X-rays interact in inducing DNA damage above the level predicted by assuming additivity and that the repair of damage occurs with a delay. The activation levels of DDR proteins and mRNA levels of the studied genes were highest in cells exposed to mixed beams. The results substantiate the idea that exposure to mixed beams presents a challenge for the cellular DDR system.

Indexed as

DNA DamageAdultAlpha ParticlesAtaxia Telangiectasia Mutated ProteinsChromosome AberrationsDNA-Activated Protein KinaseDNA RepairDNA Repair EnzymesDose-Response Relationship, RadiationGene Expression RegulationHumansLinear Energy TransferLymphocytesMaleMiddle AgedNuclear ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanDNA-Activated Protein KinaseDNA Repair EnzymesNuclear ProteinsPRKDC protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30379881
PMCPMC6209146
OpenAlexW2899489182

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.