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Several antitumour drugs react with DNA to form interstrand cross-links, causing chromosomal alterations like DNA strand breakage and hyper-recombination on the DNA helix, necessitating repair of damage on both strands of the DNA. Two basic processes by which interstrand cross-link lesions are repaired, an error-free process and an error-prone process, rely on proteins in the nucleotide incision repair, homologous recombination and translesion DNA synthesis pathways.

The article discusses the mechanism for the formation and repair of highly toxic DNA interstrand cross-links. At the genetic level, protein members of several repair pathways play a role in the repair of damaged DNA. The repair of DNA interstrand cross-links in eukaryotes involves factors from the nucleotide excision repair and homologous recombination pathways.