Evidence map›Paper›PMID 36361653›Full record

ArticleInternational journal of molecular sciences2022

Cell Type-Specific Patterns in the Accumulation of DNA Damage Following Multifractional Radiation Exposure.

Pamela Akuwudike, Adrianna Tartas, Milagrosa López-Riego, Iuliana Toma-Dasu, Andrzej Wojcik, Lovisa Lundholm

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. 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
0.3field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  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

6 authors at 2 institutions in 2 countries.

Pamela AkuwudikeCentre for Radiation Protection Research, Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 10691 Stockholm, Sweden.ORCID 0000-0001-7616-4237
Adrianna TartasBiomedical Physics Division, Faculty of Physics, Institute of Experimental Physics, University of Warsaw, 02-093 Warsaw, Poland.ORCID 0000-0003-1247-7482
Milagrosa López-RiegoCentre for Radiation Protection Research, Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 10691 Stockholm, Sweden.
Iuliana Toma-DasuDepartment of Oncology-Pathology, Karolinska Institutet, 17176 Stockholm, Sweden.
Andrzej WojcikCentre for Radiation Protection Research, Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 10691 Stockholm, Sweden.ORCID 0000-0002-3951-774X
Lovisa LundholmCentre for Radiation Protection Research, Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 10691 Stockholm, Sweden.ORCID 0000-0003-2023-7454
Stockholm University · SEUniversity of Warsaw · PL

Funding

The Swedish Childhood Cancer Foundation PR2020-0169The Swedish Radiation Safety Authority SSM2020-2054, SSM2019-9651
6 · The paper itself

Abstract

Predicting the risk of second malignant neoplasms is complicated by uncertainties regarding the shape of the dose-response relationship at high doses. Limited understanding of the competitive relationship between cell killing and the accumulation of DNA lesions at high doses, as well as the effects of other modulatory factors unique to radiation exposure during radiotherapy, such as dose heterogeneity across normal tissue and dose fractionation, contribute to these uncertainties. The aim of this study was to analyze the impact of fractionated irradiations on two cell systems, focusing on the endpoints relevant for cancer induction. To simulate the heterogeneous dose distribution across normal tissue during radiotherapy, exponentially growing VH10 fibroblasts and AHH-1 lymphoblasts were irradiated with 9 and 12 fractions (VH10) and 10 fractions (AHH-1) at 0.25, 0.5, 1, or 2 Gy per fraction. The effects on cell growth, cell survival, radiosensitivity and the accumulation of residual DNA damage lesions were analyzed as functions of dose per fraction and the total absorbed dose. Residual γH2AX foci and other DNA damage markers (micronuclei, nuclear buds, and giant nuclei) were accumulated at high doses in both cell types, but in a cell type-dependent manner. The competitive relationship between cell killing and the accumulation of carcinogenic DNA damage following multifractional radiation exposure is cell type-specific.

Indexed as

DNA DamageRadiation ExposureDose Fractionation, RadiationDose-Response Relationship, RadiationRadiation ToleranceDNA damagegiant nucleimicronucleimultifractionated radiation exposurenuclear budsradiotherapyresidual DNA damagesecond malignant neoplasms (SMN)

Identifiers

PMID36361653
PMCPMC9655477
OpenAlexW4307552159

What OpenQuestion holds

Textmetadata
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.