Cyclobutane pyrimidine dimer DNA lesion (CPD)

Cyclobutane pyrimidine dimer DNA lesions are a type of DNA damage caused primarily by ultraviolet (UV) radiation, where adjacent pyrimidine bases (thymine or cytosine) become covalently linked, forming a cyclobutane ring.[1][3][5][6] This lesion leads to disruption of normal base pairing, distorts the DNA helix, and blocks essential processes such as replication and transcription. The most common biological consequences include acute sunburn, immune suppression, chronic mutation induction, and skin cancer.[8] Repair mechanisms in cells include nucleotide excision repair and, in certain organisms, photoreactivation by photolyase enzymes, which humans lack.[4][5] The persistence of these lesions, especially in skin exposed to sunlight, is a major mutagenic factor contributing to skin carcinogenesis such as melanoma and non-melanoma skin cancers. Cyclobutane pyrimidine dimer is not a classical druggable target, but rather a lesion or damage site subject to repair by cellular mechanisms; direct targeting is limited to experimental enzyme therapies or bioengineering of DNA repair pathways.[1][5][6]

Other names

Cyclobutane pyrimidine dimerCPDDNA cyclobutane pyrimidine dimerUV-induced dimer

Photoreactivation (by photolyase enzymes: repair via absorption of blue light and enzymatic cleavage of the dimerized bases[4][5])\nNucleotide excision repair (removal and replacement of damaged DNA segment[1][2][3])\nInduction of DNA damage response pathways (ATM, p53-mediated cell cycle arrest and DNA repair[2][3])