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- W1982244574 abstract "Cancer genome instability arises from diverse defects in DNA-repair machinery, which make cancer cells more susceptible to DNA targeting agents. The interrelation between DNA repair deficiency and the increased effect of DNA targeting agents highlights the double-strand break (DSB) repair, which comprises the homologous recombination (HR) and non-homologous end joining (NHEJ) pathways. The DNA targeting agents are classified into two major groups: non-covalent DNA binding agents and covalent DNA-reactive agents. Although these agents have well-known limitations, such as resistance and secondary carcinogenesis risk, they are extremely important in today's real-life cancer therapy in combination with targeted therapy and immunotherapy. Indeed, DNA targeting drugs are promising therapeutics with a precise application through the background of cancer-specific DNA repair failure. In the current review, the mechanisms of action of diversified DNA-targeting agents, as well as the modulation of DNA repair pathways to increase the DNA-damaging drugs efficacy are presented. Finally, DNA-targeting-based therapies are discussed considering risks, resistance and its uses in the medicine precision era." @default.
- W1982244574 created "2016-06-24" @default.
- W1982244574 creator A5054694355 @default.
- W1982244574 creator A5056421558 @default.
- W1982244574 date "1987-01-01" @default.
- W1982244574 modified "2023-10-10" @default.
- W1982244574 title "Quantitative estimation of cisplatin-induced DNA interstrand cross-links and their repair in mammalian cells: Relationship to toxicity" @default.
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- W1982244574 doi "https://doi.org/10.1016/0163-7258(87)90012-x" @default.
- W1982244574 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/3317452" @default.
- W1982244574 hasPublicationYear "1987" @default.
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