ArticleInternational journal of radiation biology2015
Ku-dependent non-homologous end-joining as the major pathway contributes to sublethal damage repair in mammalian cells.
Article in International journal of radiation biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Elevated α/β ratio after hypofractionated radiotherapy correlated with DNA damage repairment in an experimental model of prostate cancer.Journal of radiation research · 2024Article
- Dose Rate Effects from the 1950s through to the Era of FLASH.Radiation research · 2024Review
- Biological effects in normal human fibroblasts following chronic and acute irradiation with both low- and high-LET radiation.Frontiers in public health · 2024Article
- Article
- TP53 modulates radiotherapy fraction size sensitivity in normal and malignant cells.Scientific reports · 2021Article
- Diminished or inversed dose-rate effect on clonogenic ability in Ku-deficient rodent cells.Journal of radiation research · 2021Article
- Biology of high single doses of IORT: RBE, 5 R's, and other biological aspects.Radiation oncology (London, England) · 2017Review
- DNA repair pathway choice at various conditions immediately post irradiation.International journal of radiation biology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
purposeSublethal damage repair (SLDR) is a type of repair that occurs in split-dose irradiated cells, which was discovered more than 50 years ago. However, due to conflicting reported data, it remains unclear which DNA double-strand break (DSB) repair pathway, non-homologous end-joining (NHEJ) repair, homologous recombination repair (HRR) or both, contributes to SLDR, particularly in human cells. We were interested in clarifying this question. METHODS AND MATERIALS: Mammalian cell lines, including human, mouse and Chinese hamster ovary (CHO) cell lines, wild type, deficient in NHEJ or HRR were irradiated with either single dose or two split doses at 2- or 4-h intervals. The clonogenic assay was used to evaluate these cell radiosensitivities.
resultsAll wild-type or HRR-deficient cells (including human, mouse and CHO cells) showed a higher survival rate after exposure to split-dose versus single-dose radiation; however, all classical NHEJ-deficient cells (including human, mouse and hamster cells) did not show any apparent sensitivity changes between single-dose and split-dose irradiation.
conclusionClassical NHEJ mainly contributes to SLDR in mammalian cells (including human cells). These results have the potential to improve radiotherapy.
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Registered trials
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.