DNA damage in tumor cell by ionizing proton radiation

The entry "Tumor cell DNA damage by ionizing radiation from protons" does **not** refer to a specific molecule, receptor, enzyme, or protein. Instead, it describes the **physical and biological process** whereby **proton beam therapy** induces various forms of **DNA damage**—including single-strand breaks (SSBs), double-strand breaks (DSBs), base modifications, and clustered lesions—in the nuclei of tumor cells[2][4]. This process is central to the therapeutic effect of proton therapy in cancer treatment. Proton beams deliver energy with high precision at the Bragg peak within tissue, causing concentrated and often complex clusters of DNA lesions that are more difficult for cells to repair compared to those caused by conventional photon-based radiotherapy[3]. The most lethal form of this damage is typically DSBs—especially when they occur in clusters—which can overwhelm cellular repair mechanisms and lead to apoptosis or mitotic catastrophe. The biomarker γ-H2AX is commonly used experimentally and clinically as an indicator of DSBs following irradiation[1][5]. Because this entry refers broadly to a type of cellular injury rather than a discrete molecular entity or canonical druggable target, it should be flagged as an incorrect or non-standard therapeutic target according to typical pharmacological conventions. It lacks specificity required for structured databases focused on proteins/genes/receptors. If you require information about specific molecular targets involved in sensing or repairing such proton-induced DNA damage—such as ATM kinase, PARP1, or components of non-homologous end joining—you may wish to specify those molecules individually.

Other names

Proton-induced DNA damageDNA double-strand breaks by protonsRadiation-induced clustered DNA damage (proton)Proton therapy target (DNA)