DNA damage in tumor cells induced by ionizing radiation

Ionizing radiation induces various types of DNA damage in tumor cells, including base modifications, apurinic/apyrimidinic sites, single-strand breaks (SSBs), double-strand breaks (DSBs), and complex clustered lesions. DSBs are considered the most lethal form and are primarily repaired via homologous recombination or non-homologous end joining pathways. The biological consequences include cell cycle arrest, apoptosis or cell death if repair fails; however, misrepair can lead to mutations and carcinogenesis. Clustered DNA lesions—especially those caused by high linear energy transfer radiation—are more difficult for cellular machinery to repair and contribute significantly to the cytotoxic effect exploited during radiotherapy. While this process underpins the effectiveness of radiotherapy against tumors, it also poses risks such as off-target toxicity and induction of secondary malignancies due to similar effects on normal tissues.[1][2][3][5] This entry does not represent a canonical molecular target like an enzyme or receptor but rather describes a cellular process resulting from exposure to ionizing radiation. Therefore: is_target: false; is_incorrect: true. The term refers broadly to "damage" rather than any specific molecule that could be selectively targeted by drugs or biologics. For structured databases focused on molecular targets suitable for pharmacological intervention, this would be considered an incorrect entry type. DNA itself is not directly targeted by drugs; however, radiosensitizers and radioprotectors may modulate the effects of ionizing radiation. No direct biomarkers for "DNA damage" as a target; however, markers such as γ-H2AX foci are used to monitor double-strand breaks after irradiation[2].

Other names

Radiation-induced DNA damageIonizing radiation-induced DNA lesionsIR-induced DNA damage

Not applicable—this is not a druggable target but rather the result of physical/chemical insult to cellular macromolecules.