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The phrase "Tumor tissue via beta-radiation emission" does not refer to a specific molecular target, receptor, or protein. Instead, it describes a therapeutic strategy in which tumor tissues are targeted by the delivery of beta particle-emitting radionuclides. In this approach, radioactive isotopes (such as iodine‑131 or yttrium‑90) are attached to carrier molecules—often antibodies or peptides—that specifically bind tumor-associated antigens or receptors. Once localized at the tumor site, these agents emit beta particles, which penetrate several millimeters into surrounding tissue and induce DNA damage in cancer cells, leading primarily to apoptosis and cell cycle arrest with minimal impact on adjacent healthy cells. This method is widely used in nuclear medicine for treating various cancers—including thyroid cancer (with iodine‑131), lymphomas (with yttrium‑90), bone metastases (with strontium‑89 or samarium‑153), and neuroendocrine tumors using peptide receptor radionuclide therapy (PRRT). The effectiveness depends on precise targeting; otherwise, there is risk of collateral damage to normal tissues. Because "tumor tissue via beta-radiation emission" refers broadly to a treatment modality rather than a discrete molecular entity or canonical target structure, it should not be classified as a standard therapeutic target such as an enzyme or receptor. Therefore: There is something incorrect about this entry—it does not represent an individual molecule/receptor but rather describes the process by which tumors are treated using targeted delivery of beta-emitting radioisotopes. If you need structured information about specific targets involved in this therapy—such as somatostatin receptor 2 for PRRT—please specify that particular molecule.
Delivery of beta-emitting radionuclides to tumor tissue, causing DNA damage and cell death through ionizing radiation
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