DNA Damage Induced by Alkylating Agents and Repair Pathways

Abstract

The cytotoxic effects of alkylating agents are strongly attenuated by cellular DNA repair processes, necessitating a clear understanding of the repair mechanisms. Simple methylating agents form adducts at N ‐ and O ‐atoms. N ‐methylations are removed by base excision repair, AlkB homologues, or nucleotide excision repair (NER). O 6 ‐methylguanine (MeG), which can eventually become cytotoxic and mutagenic, is repaired by O 6 ‐methylguanine‐DNA methyltransferase, and O 6 MeG:T mispairs are recognized by the mismatch repair system (MMR). MMR cannot repair the O 6 MeG/T mispairs, which eventually lead to double‐strand breaks. Bifunctional alkylating agents form interstrand cross‐links (ICLs) which are more complex and highly cytotoxic. ICLs are repaired by complex of NER factors (e.g., endnuclease xeroderma pigmentosum complementation group F‐excision repair cross‐complementing 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.

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Cited by papers we hold 4

• Cancer chemotherapy and beyond: Current status, drug candidates, associated risks and progress in targeted therapeutics · 2023
  Corrected
• DNA repair mechanisms in cancer development and therapy · 2015
  No notice
• Effects of hyperthermia on DNA repair pathways: one treatment to inhibit them all · 2015
  No notice
• Genotoxic Anti-Cancer Agents and Their Relationship to DNA Damage, Mitosis, and Checkpoint Adaptation in Proliferating Cancer Cells · 2014
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