DNA damage process

The "DNA damage process" refers broadly to the collection of events by which cells recognize and respond to various forms of injury inflicted upon their genetic material. This includes detection mechanisms that sense damaged bases or strand breaks; signaling cascades that halt cell division; recruitment and activation of specialized proteins responsible for excision, reversal, or bypassing lesions; and ultimate decisions between successful restoration versus programmed cell death if errors are irreparable. The main types include direct reversal mechanisms, base excision repair, nucleotide excision repair, mismatch correction systems, non-homologous end joining (NHEJ), homologous recombination (HR), among others[1][2][3]. While individual proteins within these pathways are valid therapeutic targets—especially in oncology—the overall "process" is not considered a discrete molecular entity suitable for targeted drug development.

Other names

DNA damage responseDNA repair processGenomic integrity maintenanceCellular response to DNA damage

Drugs targeting this area generally: - Inhibit specific enzymes required for DNA repair, leading to accumulation of lethal lesions. - Induce excessive DNA damage beyond the capacity for cellular repair, triggering apoptosis.