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“Ionizing radiation to tumor tissue” refers to the application of ionizing radiation as a therapeutic modality to damage DNA in cancer cells and tumor-associated vasculature; it is not a discrete molecule or receptor but a treatment approach with biological effects including DNA double-strand breaks, activation of cell-cycle checkpoints and apoptosis, induction of senescence, endothelial activation with increased adhesion molecule expression, and context-dependent interactions with antiangiogenic and other agents in the tumor microenvironment[1][2][3][4].
Ionizing radiation induces DNA double-strand breaks leading to cell death, mitotic catastrophe, or senescence. It activates p53/ATM pathways causing G1/S arrest and apoptosis in susceptible cells. Furthermore, it triggers endothelial oxidative injury and NF-κB–mediated expression of ICAM-1, E-selectin, and P-selectin, promoting inflammation and thrombosis within tumor vasculature. It also interacts with antiangiogenic/vasculature-targeting agents to enhance cytotoxicity to endothelial cells and reduce tumor blood vessels.
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