ArticleRadiation and environmental biophysics2016
DNA damage induced by boron neutron capture therapy is partially repaired by DNA ligase IV.
Article in Radiation and environmental biophysics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- 'Cell knife' for cancer: the clinician's perspective.Frontiers in immunology · 2025Review
- Review
- Profile of miRNAs in small extracellular vesicles released from glioblastoma cells treated by boron neutron capture therapy.Journal of neuro-oncology · 2024Article
- DNA damage and repair dependencies of ionising radiation modalities.Bioscience reports · 2023Review
- Review
- Boron-peptide conjugates with angiopep-2 for boron neutron capture therapy.Frontiers in medicine · 2023Article
- Article
- Boron Neutron Capture Therapy Eliminates Radioresistant Liver Cancer Cells by Targeting DNA Damage and Repair Responses.Journal of hepatocellular carcinoma · 2022Article
- Molecular Mechanisms of Specific Cellular DNA Damage Response and Repair Induced by the Mixed Radiation Field During Boron Neutron Capture Therapy.Frontiers in oncology · 2021Review
- Glioma Stem-Like Cells Can Be Targeted in Boron Neutron Capture Therapy with Boronophenylalanine.Cancers · 2020Article
- Boron neutron capture therapy: Current status and future perspectives.Cancer communications (London, England) · 2020Review
- DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer.Signal transduction and targeted therapy · 2020Review
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Boron neutron capture therapy (BNCT) is a particle radiation therapy that involves the use of a thermal or epithermal neutron beam in combination with a boron ((10)B)-containing compound that specifically accumulates in tumor. (10)B captures neutrons and the resultant fission reaction produces an alpha ((4)He) particle and a recoiled lithium nucleus ((7)Li). These particles have the characteristics of high linear energy transfer (LET) radiation and therefore have marked biological effects. High-LET radiation is a potent inducer of DNA damage, specifically of DNA double-strand breaks (DSBs). The aim of the present study was to clarify the role of DNA ligase IV, a key player in the non-homologous end-joining repair pathway, in the repair of BNCT-induced DSBs. We analyzed the cellular sensitivity of the mouse embryonic fibroblast cell lines Lig4-/- p53-/- and Lig4+/+ p53-/- to irradiation using a thermal neutron beam in the presence or absence of (10)B-para-boronophenylalanine (BPA). The Lig4-/- p53-/- cell line had a higher sensitivity than the Lig4+/+ p53-/-cell line to irradiation with the beam alone or the beam in combination with BPA. In BNCT (with BPA), both cell lines exhibited a reduction of the 50 % survival dose (D 50) by a factor of 1.4 compared with gamma-ray and neutron mixed beam (without BPA). Although it was found that (10)B uptake was higher in the Lig4+/+ p53-/- than in the Lig4-/- p53-/- cell line, the latter showed higher sensitivity than the former, even when compared at an equivalent (10)B concentration. These results indicate that BNCT-induced DNA damage is partially repaired using DNA ligase IV.
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