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The phrase "DNA damage via beta radiation from Yttrium‑90" does not refer to a canonical molecular target such as a receptor, enzyme, or transporter. Instead, it describes a **cellular effect**—specifically, the induction of **DNA double-strand breaks**—caused by exposure to high-energy beta particles emitted during the radioactive decay of yttrium‑90. Yttrium‑90 (^90Y) is a pure beta-emitting radioisotope with a half-life of about 64 hours and is widely used in cancer therapy through modalities such as radioimmunotherapy and selective internal radiation therapy (SIRT)[4][6][8]. When ^90Y-labeled compounds are delivered specifically to tumors—either as microspheres lodged within tumor vasculature or attached to monoclonal antibodies targeting cancer cell antigens—the emitted beta particles cause dense ionization tracks that result in direct and indirect **double-strand breaks in cellular DNA**, ultimately leading to cell death if repair mechanisms fail[2][7]. This mechanism underlies the therapeutic efficacy but also presents risks; off-target irradiation can cause collateral damage and toxicity in normal tissues near treated sites. The biological response includes activation of apoptosis pathways when unrepaired DSBs accumulate beyond cellular repair capacity; resistance may occur if tumor cells have proficient DSB-repair mechanisms such as nonhomologous end joining (NHEJ)[1]. Because this entry describes an effect rather than a discrete molecular entity, it should not be considered a canonical therapeutic "target" per se. It lacks standard nomenclature conventions associated with proteins or receptors. > "Once bound [to its target], the emitted beta radiation from yttrium‐90 induces double‐strand breaks in the DNA of cancer cells, leading to cell death."[2] > "Radioresistant leukemia cells... were deficient in activation of caspase‐8, caspase‐9... after treatment with [Y‐90]... suggesting that caspase activation and cleavage... depends on NHEJ DNA–DSB–repair."[1]
Induction of lethal DNA double-strand breaks in target cells via emission of high-energy beta particles, leading to apoptosis or necrosis if the damage is irreparable[2][7].
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