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The interaction of radiation with biological tissues may cause some damage. To quantify it, studying cells in vitro is one methodology for analyzing dose deposition in biological tissues because once exposed to radiation, different methods can quantify the biological damage. However, biological tissue culture exposure forms mostly employ high-energy beams (MeV). Thus, this study aims to characterize the radiation field from X-ray equipment using thermoluminescent dosimeters (TLD), to establish an in vitro irradiation protocol of breast cancer and glioblastoma cells for low energies. First, the central axis alignment test was performed to ensure the equipment followed the Normativa IN 90. Then the variation of radiation intensity was analyzed for a 5 x 5 cm² field at distances between 30 and 90 cm from the focal point to the detector. Subsequently, TLD immersed in breast cancer and glioblastoma cellular media were irradiated in a 106 kV and 71 mAs beam to evaluate the dose in cellular media. Simulations were performed with the PENELOPE code to compare with experimental results. The result of the central axis alignment showed that the equipment complies with the current Normativa. The dose distributions for the evaluated distances were more homogeneous for the 40 cm distance, with a standard deviation of 1.7% and 0.9% of the distributions obtained with the TLD and simulation, respectively. Thus, the irradiation field for low energy beams was characterized for a 5 x 5 cm² field for 106 kV and 71 mAs beams at a DFS of 40 cm.

The interaction of radiation with biological tissues may cause some damage. To quantify it, studying cells in vitro is one methodology for analyzing dose deposition in biological tissues because once exposed to radiation, different methods can quantify the biological damage. However, biological tissue culture exposure forms mostly employ high-energy beams (MeV). Thus, this study aims to characterize the radiation field from X-ray equipment using thermoluminescent dosimeters (TLD), to establish an in vitro irradiation protocol of breast cancer and glioblastoma cells for low energies. First, the central axis alignment test was performed to ensure the equipment followed the Normativa IN 90. Then the variation of radiation intensity was analyzed for a 5 x 5 cm² field at distances between 30 and 90 cm from the focal point to the detector. Subsequently, TLD immersed in breast cancer and glioblastoma cellular media were irradiated in a 106 kV and 71 mAs beam to evaluate the dose in cellular media. Simulations were performed with the PENELOPE code to compare with experimental results. The result of the central axis alignment showed that the equipment complies with the current Normativa. The dose distributions for the evaluated distances were more homogeneous for the 40 cm distance, with a standard deviation of 1.7% and 0.9% of the distributions obtained with the TLD and simulation, respectively. Thus, the irradiation field for low energy beams was characterized for a 5 x 5 cm² field for 106 kV and 71 mAs beams at a DFS of 40 cm.

Topoisomerase 2 (TOP2) inhibitors are drugs widely used in the treatment of different types of cancer. Processing of their induced-lesions create double-strand breaks (DSBs) in the DNA, which is the main toxic mechanism of topoisomerase inhibitors to kill cancer cells. It was established that the Nucleotide Excision Repair pathway respond to TOP2-induced lesions, mainly through the Cockayne Syndrome B (CSB) protein. In this paper, we further define the mechanism and type of lesions induced by TOP2 inhibitors when CSB is abrogated. In the absence of TOP2, but not during pharmacological inhibition, an increase in R-Loops was detected. We also observed that CSB knockdown provokes the accumulation of DSBs induced by TOP2 inhibitors. Consistent with a functional interplay, interaction between CSB and TOP2 occurred after TOP2 inhibition. This was corroborated with in vitro DNA cleavage assays where CSB stimulated the activity of TOP2. Altogether, our results show that TOP2 is stimulated by the CSB protein and prevents the accumulation of R-loops/DSBs linked to genomic instability.