• Ra-223 binding to bone-like structures is extreme without any uptake in cancer cells. • Clustered DNA double-strand break (DSB) were induced in prostate tumor cells. • These DSB activated non-homologous end-joining (NHEJ) repair. • This triggered apoptosis and inhibited cell growth independent of cell type. • Ra-223 bound to bone-like structures increases the tumor cell-killing.

In children, ketamine sedation is often used during radiological procedures. Combined exposure of ketamine and radiation at doses that alone did not affect learning and memory induced permanent cognitive impairment in mice. The aim of this study was to elucidate the mechanism behind this adverse outcome. Neonatal male NMRI mice were administered ketamine (7.5 mg kg⁻¹) and irradiated (whole-body, 100 mGy or 200 mGy, ¹³⁷Cs) one hour after ketamine exposure on postnatal day 10. The control mice were injected with saline and sham-irradiated. The hippocampi were analyzed using label-free proteomics, immunoblotting, and Golgi staining of CA1 neurons six months after treatment. Mice co-exposed to ketamine and low-dose radiation showed alterations in hippocampal proteins related to neuronal shaping and synaptic plasticity. The expression of brain-derived neurotrophic factor, activity-regulated cytoskeleton-associated protein, and postsynaptic density protein 95 were significantly altered only after the combined treatment (100 mGy or 200 mGy combined with ketamine, respectively). Increased numbers of basal dendrites and branching were observed only after the co-exposure, thereby constituting a possible reason for the displayed alterations in behavior. These data suggest that the risk of radiation-induced neurotoxic effects in the pediatric population may be underestimated if based only on the radiation dose.

Research on different types of ionizing radiation’s effects has been ongoing for years, revealing its efficacy in damaging cancer cells. Solid tumors comprise diverse cell types, each being able to respond differently to radiation. This study evaluated the radiobiological response of established (MDA-MB-231 (Triple negative breast cancer, TNBC), MCF-7 (Luminal A)) and patient-derived malignant cell lines, cancer-associated fibroblasts, and skin fibroblasts following proton IRR. All cell line types were irradiated with the proton dose of 2, 4, and 6 Gy. The radiobiological response was assessed using clonogenic assay, γH2AX, and p53 staining. It was noticeable that breast cancer lines of different molecular subtypes displayed no significant variations in their response to proton IRR. In terms of cancer-associated fibroblasts extracted from the tumor tissue, the line derived from a TNBC subtype tumor demonstrated higher resistance to ionizing radiation compared to lines isolated from luminal A tumors. Fibroblasts extracted from patients’ skin responded identically to all doses of proton radiation. This study emphasizes that tumor response is not exclusively determined by the elimination of breast cancer cells, but also takes into account tumor microenvironmental variables and skin reactions.

The Tenth International Symposium on Neutron Dosimetry (NEUDOS 10) took place in Uppsala, Sweden, 12–16, June 2006. The conference had the theme ‘Progress in dosimetry of neutrons and light nuclei’, reflecting the widening of the scope of the conference to include not only neutron dosimetry, but also all hadronic particles. This is also a recognition of the fact that the dose due to neutrons is delivered not by the neutron itself, but via secondary particles created in neutron-induced nuclear reactions, i.e. protons, deuterons, alpha particles and various other ions released in tissue. Thereby, the dosimetry of neutrons has a large scientific overlap with dosimetry in proton and heavy ion therapy.

This study presents a multi-center comparison of in vitro cell survival measurements and RBE calculations following proton irradiations conducted under harmonized experimental conditions across six European institutions participating in the INSPIRE framework. V79-4 cells were irradiated using spread-out Bragg peak (SOBP) proton fields of two configurations delivering 6 and 8 Gy with widths of 6 and 4 cm, respectively. Each center adhered to a standardized protocol, utilizing the same phantom design to minimize uncertainties related to sample positioning. X-ray reference irradiations were also performed to assess cell radiosensitivity across the participating centers. Despite the consistent protocol, significant inter-institutional variability was observed in the survival measurements. For both treatment plans, the largest variation was detected in the most distal points of the SOBP (coefficients of variation of 43 % and 60 % for the 6 Gy and 8 Gy plans, respectively). Kruskal-Wallis statistical test confirmed the significant differences between the centers for each of the measured position in the proton field for both SOBP configurations. Discrepancies were observed in calculated RBE data as well, albeit preserving the expected trend for the values to slightly increase towards the distal edge of the SOBP (up to 1.5 and 1.3 for the 6 Gy and 8 Gy plans, respectively). The results of the study highlight the minimal biological variation one could expect performing proton RBE measurements in well-aligned experimental conditions and challenges in conducting large-scale, multi-center radiobiological experiments and inter-comparisons between literature data sets.

The effectiveness of radiation therapy can be enhanced by understanding the fragmentation mechanisms of iodine-doped DNA oligonucleotide under tender X-rays, as explored experimentally and computationally in our study. By primarily targeting iodine atoms above their L-edge ionization energies, we observed a significant increase in the production of fragments critical to DNA backbone breakage, particularly within mass ranges associated with phosphate and sugar groups. The mass spectroscopy experiments demonstrated that iodine-doped DNA oligonucleotides undergo intense fragmentation at long distances from the initial photoactivation site. Born–Oppenheimer based molecular dynamics simulations confirmed the generation of numerous small fragments, including reactive oxygen species, which are pivotal in enhancing the radiation damage. These findings highlight the effectiveness of iodine doping in amplifying DNA damage in radiotherapy via iodine photoactivation, thereby improving the potential for targeted cancer treatment.