DNA crosslink induced by cisplatin

DNA crosslinking by cisplatin refers to the formation of covalent bonds between platinum(II) from the chemotherapy drug cisplatin and DNA bases, primarily at the N7 position of guanine residues[2][4][6]. Cisplatin induces mainly intrastrand crosslinks (about 90% of lesions), but also forms interstrand crosslinks and DNA–protein crosslinks[2][3][4][6]. These crosslinks distort the DNA helix, block DNA replication and transcription, and activate multiple cellular DNA repair pathways including nucleotide excision repair (NER), homologous recombination, and the Fanconi anemia/BRCA pathway[2][6][7]. The inability to repair these lesions results in cell death, making this process central to cisplatin’s antitumor activity[2][6][7]. Is there something wrong with this target? Yes. “DNA crosslinking by cisplatin” is not a molecular entity (such as a receptor, enzyme, or transporter) but rather a description of a drug-induced chemical lesion or modification to DNA. It is an effect rather than a defined, single biomolecule or canonical target, although this process is fundamental to the therapeutic (and toxic) effects of cisplatin and related drugs[2][3][6]. Additional points: - There is no standard abbreviation for “DNA crosslinking by cisplatin.” - This is not a true drug target in the conventional sense (it is neither a protein nor a nucleic acid target) but a key type of drug action and molecular damage. For these reasons, this entry should be marked as incorrect for a canonical therapeutic target.

Other names

cisplatin–DNA crosslinkcisplatin–DNA adductDNA–cisplatin adductcisplatin-induced DNA crosslinkplatinum–DNA crosslink

Generation of DNA intrastrand and interstrand crosslinks by platinum adducts, blocking DNA polymerase and transcription Induction of DNA damage responses leading to apoptosis