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Simple methylating agents form adducts at <jats:italic>N<\/jats:italic>\u2010 and <jats:italic>O<\/jats:italic>\u2010atoms. <jats:italic>N<\/jats:italic>\u2010methylations are removed by base excision repair, AlkB homologues, or nucleotide excision repair (NER). <jats:italic>O<\/jats:italic><jats:sup>6<\/jats:sup>\u2010methylguanine (MeG), which can eventually become cytotoxic and mutagenic, is repaired by <jats:italic>O<\/jats:italic><jats:sup>6<\/jats:sup>\u2010methylguanine\u2010DNA methyltransferase, and <jats:italic>O<\/jats:italic><jats:sup>6<\/jats:sup>MeG:T mispairs are recognized by the mismatch repair system (MMR). MMR cannot repair the <jats:italic>O<\/jats:italic><jats:sup>6<\/jats:sup>MeG\/T mispairs, which eventually lead to double\u2010strand breaks. Bifunctional alkylating agents form interstrand cross\u2010links (ICLs) which are more complex and highly cytotoxic. ICLs are repaired by complex of NER factors (e.g., endnuclease  xeroderma pigmentosum complementation group F\u2010excision repair cross\u2010complementing rodent repair deficiency complementation group 1), Fanconi anemia repair, and homologous recombination. A detailed understanding of how cells cope with DNA damage caused by alkylating agents is therefore potentially useful in clinical medicine.<\/jats:p>","DOI":"10.4061\/2010\/543531","type":"journal-article","created":{"date-parts":[[2010,11,21]],"date-time":"2010-11-21T17:34:25Z","timestamp":1290360865000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":258,"title":["DNA Damage Induced by Alkylating Agents and Repair 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