Tumor DNA (as target of beta emission from yttrium-90)

The phrase "Tumor cell DNA damage via beta emission from yttrium-90" describes a **therapeutic process** rather than a discrete molecular target or receptor. Yttrium-90 (Y-90) is a radioactive isotope that emits beta particles; when Y-90-labeled microspheres are delivered (e.g., via selective internal radiation therapy or brachytherapy), these particles become embedded in the local microvasculature of tumors, most commonly in the liver. As Y-90 decays, the emitted beta radiation penetrates a few millimeters into adjacent tissue, directly causing DNA double-stranded breaks within nearby tumor cells, leading to cell death. Therefore, DNA is not a specific molecular target in the classical sense (like a receptor or enzyme), but rather, DNA damage is the **ultimate mediator of the radiotoxic effect**. No unique receptor, transporter, or protein is targeted—rather, the beta emission physically disrupts the DNA of all irradiated cells, with therapeutic selectivity achieved by localizing the radioactive microspheres to the tumor. **Note:** This entry is marked as incorrect as a "target" because "tumor cell DNA damage via beta emission from yttrium-90" is a pathological process, not a molecule or receptor that is a canonical pharmacologic or therapeutic target. The true target class is broader ("DNA" as a macromolecule or cellular process subject to radiation)—the functionally relevant detail is the radiotoxic double-strand break induction, not a structurally targetable receptor or protein.

Other names

DNA double-stranded breaks from yttrium-90DNA damage by Y-90DNA beta irradiationRadiotoxic effect of yttrium-90

Localized beta particle emission leads to DNA double-stranded breaks and apoptosis in tumor cells