DNA damage induced by beta radiation from Lutetium-177

The target described is not a specific molecule but a therapeutic effect: DNA damage caused by beta radiation emission from Lutetium-177 after its selective internalization into tumor cells via targeted radiopharmaceuticals. Lutetium-177 emits beta particles (high-energy electrons) with a short tissue penetration range, which, when internalized in cancer cells, induces DNA strand breaks—primarily indirectly by generating free radicals and directly by ionizing DNA. These DNA lesions, if not effectively repaired, initiate apoptosis or other forms of cell death, providing the antitumor effect in cancers expressing the relevant molecular targets (such as somatostatin receptors or PSMA). DNA damage induction via this process is central to the therapeutic activity of ^177Lu-based radioligand therapies.

Other names

DNA damage from Lutetium-177 beta emissionLu-177-induced DNA lesionsBeta radiation-mediated DNA strand breaksRadiopharmaceutical-induced DNA damage (Lutetium-177)

Beta emission from Lutetium-177 delivers localized ionizing radiation following ligand-targeted internalization. This leads to single- and double-strand DNA breaks via direct ionization and indirect formation of reactive oxygen species, ultimately initiating apoptosis or mitotic catastrophe and resulting in tumor cell death if damage is not repaired.