摘要
Dear Editor, DNA interstrand crosslinks （ICLs） are toxic to cells because they covalently link the two strands in the duplex. ICLs can be induced by crosslinking agents and by cell endogenous metabolites, and physically prevent transcription and replication in both directions （MacKay et al., 2010）. This type of DNA damage must be properly repaired to maintain genomic and cellular integrity, and this repair is primarily accomplished by the Fanconi anemia pathway （FA pathway） （Moldovan and D＇Andrea, 2009）.
Dear Editor, DNA interstrand crosslinks （ICLs） are toxic to cells because they covalently link the two strands in the duplex. ICLs can be induced by crosslinking agents and by cell endogenous metabolites, and physically prevent transcription and replication in both directions （MacKay et al., 2010）. This type of DNA damage must be properly repaired to maintain genomic and cellular integrity, and this repair is primarily accomplished by the Fanconi anemia pathway （FA pathway） （Moldovan and D＇Andrea, 2009）.
