Evidence map›Paper›PMID 34916568›Full record

ArticleScientific reports2021

Activation of efficient DNA repair mechanisms after photon and proton irradiation of human chondrosarcoma cells.

Birgit Lohberger, Dietmar Glänzer, Nicole Eck, Sylvia Kerschbaum-Gruber, Elisabeth Mara, Simon Deycmar, Tobias Madl, Karl Kashofer, Petra Georg, Andreas Leithner and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 16 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

11 authors at 4 institutions in 2 countries.

Birgit LohbergerDepartment of Orthopedics and Trauma, Medical University of Graz, Auenbruggerplatz 5-7, 8036, Graz, Austria. birgit.lohberger@medunigraz.at.
Dietmar GlänzerDepartment of Orthopedics and Trauma, Medical University of Graz, Auenbruggerplatz 5-7, 8036, Graz, Austria.
Nicole EckDepartment of Orthopedics and Trauma, Medical University of Graz, Auenbruggerplatz 5-7, 8036, Graz, Austria.
Sylvia Kerschbaum-GruberDepartment of Radiation Oncology, Medical University of Vienna, 1090, Vienna, Austria.
Elisabeth MaraMedAustron Ion Therapy Center, 2700, Wiener Neustadt, Austria.
Simon DeycmarLaboratory for Applied Radiobiology, University Zurich, 8006, Zurich, Switzerland.
Tobias MadlGottfried Schatz Research Center for Cell Signaling, Metabolism and Aging Molecular Biology and Biochemistry, Medical University of Graz, 8010, Graz, Austria.
Karl KashoferInstitute of Pathology, Medical University of Graz, 8010, Graz, Austria.
Petra GeorgMedAustron Ion Therapy Center, 2700, Wiener Neustadt, Austria.
Andreas LeithnerDepartment of Orthopedics and Trauma, Medical University of Graz, Auenbruggerplatz 5-7, 8036, Graz, Austria.
Dietmar GeorgDepartment of Radiation Oncology, Medical University of Vienna, 1090, Vienna, Austria.
Medical University of Graz · ATMedAustron · ATMedical University of Vienna · ATUniversity of Zurich · CH

Funding

Austrian Science Fund FWF P 32103
6 · The paper itself

Abstract

Although particle therapy with protons has proven to be beneficial in the treatment of chondrosarcoma compared to photon-based (X-ray) radiation therapy, the cellular and molecular mechanisms have not yet been sufficiently investigated. Cell viability and colony forming ability were analyzed after X-ray and proton irradiation (IR). Cell cycle was analyzed using flow cytometry and corresponding regulator genes and key players of the DNA repair mechanisms were measured using next generation sequencing, protein expression and immunofluorescence staining. Changes in metabolic phenotypes were determined with nuclear magnetic resonance spectroscopy. Both X-ray and proton IR resulted in reduced cell survival and a G2/M phase arrest of the cell cycle. Especially 1 h after IR, a significant dose-dependent increase of phosphorylated γH2AX foci was observed. This was accompanied with a reprogramming in cellular metabolism. Interestingly, within 24 h the majority of clearly visible DNA damages were repaired and the metabolic phenotype restored. Involved DNA repair mechanisms are, besides the homology directed repair (HDR) and the non-homologous end-joining (NHEJ), especially the mismatch mediated repair (MMR) pathway with the key players EXO1, MSH3, and PCNA. Chondrosarcoma cells regenerates the majority of DNA damages within 24 h. These molecular mechanisms represent an important basis for an improved therapy.

Indexed as

Proton TherapyCell CycleCell SurvivalChondrosarcomaDNA Breaks, Double-StrandedDNA RepairDose-Response Relationship, RadiationHumansPhotonsRadiotherapy DosageTime FactorsTumor Cells, Cultured

Identifiers

PMID34916568
PMCPMC8677811
OpenAlexW4200485319

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.