DNA replication and repair processes

DNA replication and repair processes represent the collective biochemical pathways essential for the faithful transmission of genetic information and the maintenance of genomic integrity. These processes involve a highly coordinated network of enzymes—including DNA polymerases, helicases, nucleases, and ligases—that work alongside signaling pathways known as the DNA Damage Response (DDR) to detect and correct lesions [1][4]. In the context of human disease, defects in these pathways are a primary driver of genomic instability, which is a hallmark of cancer development and progression [1][2]. Conversely, these pathways are major therapeutic targets in oncology; drugs like PARP inhibitors exploit specific repair deficiencies through synthetic lethality, while conventional chemotherapeutic agents like cisplatin or etoposide induce lethal DNA damage [3]. Beyond cancer, mutations in DNA repair genes underlie various hereditary syndromes, such as Lynch syndrome and Xeroderma pigmentosum, and contribute significantly to the biological process of aging [4]. Understanding these processes is critical for developing targeted therapies that can selectively kill malignant cells while sparing healthy tissue [2]. Sources: [1] Lord, C. J., & Ashworth, A. (2012). Nature, 481(7381), 287-294. [2] Pearl, L. H., et al. (2015). Nature Reviews Cancer, 15(3), 166-180. [3] Helleday, T., et al. (2008). Nature Reviews Cancer, 8(3), 193-204. [4] StatPearls. (2023). DNA Repair.

Other names

DNA damage responseDDRGenome maintenance pathwaysDNA synthesis and repair

Drugs targeting these processes function by inhibiting specific enzymes required for DNA synthesis or repair (e.g., PARP inhibitors, Topoisomerase inhibitors), acting as antimetabolites that incorporate into DNA to cause chain termination, or by directly inducing DNA cross-links and double-strand breaks that overwhelm the cell's repair machinery, ultimately triggering apoptosis.