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Auger electron emission is a physical phenomenon where an atom, after undergoing an inner-shell vacancy (typically via electron capture or internal conversion), releases a cascade of low-energy electrons known as Auger electrons [2, 4]. These electrons possess extremely short ranges (2–500 nm) and high linear energy transfer (LET), making them highly effective at inducing lethal, clustered double-strand breaks in DNA when the emitting radionuclide is localized within or near the cell nucleus [5, 11]. In clinical oncology, this process is harnessed through targeted radiopharmaceuticals—composed of an Auger-emitting isotope (e.g., Iodine-125, Indium-111, or Terbium-161) conjugated to a targeting vector like a monoclonal antibody or small molecule [1, 14]. While highly precise and capable of sparing healthy neighboring tissue due to their limited range, the therapeutic efficacy of Auger-emitting agents depends heavily on successful intracellular internalization and nuclear translocation [6, 13]. Current research focuses on overcoming these delivery challenges and utilizing specific biomarkers, such as PARP-1 or cancer-specific cell surface receptors, to improve treatment outcomes for micrometastases and disseminated disease [8, 10].
Auger electron emission occurs when an inner-shell electron vacancy is filled by an outer-shell electron, triggering a cascade that ejects multiple low-energy electrons with a very short range (2–500 nm) and high linear energy transfer (LET) [2, 5, 11]. When localized in the nucleus, these electrons cause dense ionization that results in lethal, clustered DNA double-strand breaks [4, 6, 12].
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