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Homologous recombination DNA repair is a high-fidelity cellular process that uses a homologous DNA template to mend harmful double-strand breaks in DNA, playing a crucial role in maintaining genome stability[1][2][5][6][7]. Multiple proteins—including RAD51, BRCA1, BRCA2, and others—participate in the process, which is essential for proper cell division, prevention of mutations, and suppression of tumorigenesis. Deficiency in homologous recombination repair leads to genomic instability and predisposes to various cancers (notably breast and ovarian cancer) and genetic disorders such as Fanconi anemia. While not a single molecular target, components of this pathway, especially when defective, are therapeutically targeted by agents like PARP inhibitors, exploiting the concept of synthetic lethality in tumor cells deficient in homologous recombination.
Inhibition of DNA repair (synthetic lethality via PARP inhibition) Modulation of DNA double-strand break repair pathway choice
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