title: DNA interstrand crosslink repair and cancer.
abstract: Interstrand crosslinks (ICLs) are highly toxic DNA lesions that prevent transcription and replication by inhibiting DNA strand separation. Agents that induce ICLs were one of the earliest, and are still the most widely used, forms of chemotherapeutic drug. Only recently, however, have we begun to understand how cells repair these lesions. Important insights have come from studies of individuals with Fanconi anaemia (FA), a rare genetic disorder that leads to ICL sensitivity. Understanding how the FA pathway links nucleases, helicases and other DNA-processing enzymes should lead to more targeted uses of ICL-inducing agents in cancer treatment and could provide novel insights into drug resistance.
authors.affiliation: London Research Institute, Cancer Research UK, Clare Hall Laboratories, South Mimms EN63LD, UK.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Deans
authors.forename: Stephen C
authors.initials: SC
authors.lastname: West
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D003432:Cross-Linking Reagents / Q000494:pharmacology*; D004249:DNA Damage; D004260:DNA Repair; D019008:Drug Resistance, Neoplasm; D005199:Fanconi Anemia / Q000235:genetics; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy* / Q000209:etiology / Q000235:genetics; D011995:Recombination, Genetic
chemical_list: D000970:Antineoplastic Agents; D003432:Cross-Linking Reagents