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Radiation sensitivity, also known as radiosensitivity, refers to the susceptibility of cells, tissues, or organisms to the damaging effects of ionizing radiation. It is not a specific molecule or receptor but rather a biological property determined by multiple factors including DNA damage repair capacity, apoptosis regulation, cellular senescence mechanisms, and epigenetic modifications. Radiosensitivity varies among different cell types; rapidly dividing cells such as lymphocytes and blood-forming cells are generally more sensitive than slowly dividing cells like muscle and nerve tissue. In oncology, understanding the molecular mechanisms underlying radiation sensitivity has led to targeted therapies—such as PARP inhibitors—that exploit defects in DNA repair pathways in cancer cells. Biomarkers based on genetic profiling are increasingly used for patient selection and monitoring efficacy during radiotherapy[1][2]. Note: "Radiation sensitivity" does not refer to a single protein/gene/receptor/enzyme/transporter; it describes a phenotype influenced by many molecular targets. Therefore it should not be treated as an individual therapeutic target according to standard conventions[1][2].
Modulation of DNA repair pathways to enhance or reduce cellular sensitivity to radiation; Induction of apoptosis and cell cycle arrest via p53-mediated pathways
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