Clinicians applying dose-equivalence models to identical scenarios agreed only 25.8%, exposing major variability in treatment gaps, hypofractionation and reirradiation.
ATG7 inhibition plus radiation doubled median survival versus untreated mice and produced long-term tumor-free survival in 40%.
A systematic review argues that α/β is disease- and context-specific rather than a fixed biological constant across radiotherapy settings.
Hybrid ultra-high and conventional dose-rate irradiation retained FLASH sparing in mice, but protection diminished as the ultra-high-rate dose contribution decreased.
Berberine enhanced radiation response in HNSCC models by increasing DNA damage and apoptosis while suppressing DNA repair and stemness pathways.
Metformin plus radiotherapy prolonged survival in two syngeneic glioblastoma models while shifting macrophage and T-cell populations toward antitumor phenotypes.
Paquinimod blockade of S100A8/A9 improved survival, intestinal regeneration and barrier recovery after abdominal irradiation in preclinical models.
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.