DNA damage via ionizing radiation leading to cell death

Ionizing radiation induces DNA lesions, most lethally double-strand breaks, directly or through reactive oxygen species. These breaks activate the DNA damage response, arrest the cell cycle, and, if damage is excessive or irreparable, commit the cell to death by apoptosis, mitotic catastrophe, autophagy, or other modalities. This process underpins radiotherapy, exploiting the relative radiosensitivity of cancer cells, but can also affect normal tissues and provoke adverse effects. γ-H2AX foci are widely used to monitor DNA damage in response to radiation. The process is not a canonical molecular target but describes a therapeutic strategy and its cellular underpinnings.[1][3][4][5][6][7] Key clarification: This entry should not be treated as a druggable target molecule (such as a receptor or enzyme). If structured data is required, focus on individual molecular constituents (e.g., DNA, ATM, PARP1, DNA-PK) instead.

Other names

Radiation-induced DNA damageIonizing radiation-induced cell deathRadiogenic DNA damage

Induction of DNA double-strand breaks leading to cell cycle arrest and various forms of cell death (e.g., apoptosis, mitotic catastrophe, autophagy)[1][5][6]; Modulation of DNA damage response and repair pathways[4][7]