At equal physical dose, carbon ions produced transcriptional changes distinct from X-rays, including stronger suppression of mitotic and chromatin-regulatory programmes.
FLASH spared mitochondrial integrity in non-tumorigenic pancreatic models while producing tumour effects comparable with conventional-dose-rate irradiation.
Circadian dysregulation could impair DNA repair and haematopoietic control after radiation exposure, but direct evidence linking it to acute myeloid leukaemia is lacking.
A translational review proposes shared reporting and quality-assurance principles for model-dependent biological dose in proton, carbon-ion and boron neutron capture therapy.
This systematic review found that optimal radiotherapy-immunotherapy sequencing depends on the immune mechanism being targeted.
Immuno-Eclipse radiotherapy improved bulky tumor control in mice through natural killer and cytotoxic T-cell immunity.
Scanned and scattered clinical proton beams produced similar Ewing sarcoma cell survival despite higher oxidative stress signals after scanned delivery.
Regional lymph node irradiation was linked to attenuated local cytokine shifts and nodal damage and cell-death signatures after sinonasal stereotactic radiotherapy.
Oxygen-ion irradiation showed higher biological effectiveness and more persistent DNA damage than carbon ions or photons in pancreatic cancer cells.
Convergent 60 keV photons matched orthovoltage radiation and showed comparable or greater biological effectiveness than 6 MV photons, depending on cell type.
Hydrogen peroxide production decreased as proton dose rate increased, with Geant4-DNA simulations reproducing the oxygen-dependent experimental trend.
In mice, ultrahigh dose-rate X-rays caused less early testicular damage than conventional irradiation, with protection linked to ferroptosis suppression.
Radioresistant tumors showed impaired ferroptosis and regulatory T-cell accumulation, while sorafenib enhanced the response to irradiation in mice.
FLASH radiotherapy preserved hepatic structure and metabolic homeostasis while maintaining tumor control in a preclinical breast cancer model.