Several cannabinoids reduced therapy-induced glioblastoma apoptosis and enhanced clonogenic survival in vitro, raising concern about concurrent use during treatment.
Both dose rates increased mitochondrial respiration after irradiation, with no clear FLASH-specific mitochondrial phenotype under normoxic conditions.
Ultra-high dose-rate protons produced fewer DNA breaks at low scavenger concentration, but the effect diminished or reversed under other experimental conditions.
CHAF1A supported homologous recombination and non-homologous end joining, while its depletion increased radiosensitivity in xenograft models.
Chemoradiotherapy suppressed LAMC2–macrophage signalling, while immunoradiotherapy enriched CCL5-positive CD8 T cells in preclinical esophageal squamous-cell carcinoma models.
Inter-patient radiosensitivity explained 85–97% of modeled TCP steepness, while uncertainty in delivered dose exceeded uncertainty in local-control estimates.
Electron FLASH changed DNA-damage, transcriptomic, cytokine, and microtubule responses but did not alter clonogenic survival under normoxic conditions.
USP15 stabilized FIS1, suppressed oxidative phosphorylation, and increased radiosensitivity; metformin restored radiation response in USP15-low bladder cancer models.
Systemic tetrathiomolybdate reduced collagen deposition and preserved saliva secretion after irradiation of mouse submandibular glands.
EQD2 should remain the reporting standard, but delivery time, dose gradients, biological assumptions and dose accumulation materially affect its interpretation.
FLASH preserved corneal thickness and collagen organization better than conventional irradiation at 10 and 15 Gy, but protection weakened at 20 Gy.
Chemotherapy and radiotherapy resistance may converge on shared DNA-repair, redox, metabolic, stemness and microenvironmental adaptations.
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.