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Tumor cell irradiation refers to the use of ionizing radiation to kill or prevent the proliferation of cancer cells by inducing DNA strand breaks, generating reactive oxygen species, and activating multiple cell death pathways including apoptosis, necrosis, and mitotic catastrophe[5][3][2]. Beyond direct cellular cytotoxicity, irradiation also modulates the tumor microenvironment and the immune response by promoting antigen release, upregulating damage-associated molecular patterns (DAMPs), and altering cytokine signaling[1][2][4]. These changes can prime both adaptive and innate immune responses, leading to systemic anti-tumor effects. Tumor cells can adapt to irradiation through enhanced DNA repair mechanisms and signaling pathway reprogramming, resulting in radioresistance, which poses a challenge for effective therapy[3][4]. Tumor cell irradiation is a cornerstone of modern oncological practice, most commonly utilized in combination with other therapies such as immune checkpoint inhibitors and molecular pathway inhibitors, but is not itself a molecular target, receptor, or protein[1][3][5].
Direct ionization of DNA leading to cell death; Generation of reactive oxygen species (ROS) causing cellular and mitochondrial damage; Induction of immunogenic cell death via release of damage-associated molecular patterns (DAMPs) and tumor-associated antigens (TAAs), promoting adaptive and innate immune responses; Activation of cell signaling cascades (e.g., EGFR, PI3K/Akt/mTOR, JAK/STAT3), impacting cell survival, proliferation, and radioresistance
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