Epithelial ovarian cancer is a serious public health problem worldwide with the highest mortality
rate of all gynecologic cancers. The current standard-of-care for the treatment of ovarian cancer is
based on chemotherapy based on adjuvant cisplatin/carboplatin and taxane regimens that represent the
first-line agents for patients with advanced disease. The DNA repair activity of cancer cells determines
the efficacy of anticancer drugs. These features make DNA repair mechanisms a promising target for
novel cancer treatments. In this context a better understanding of the DNA damage response caused by
antitumor agents has provided the basis for the use of DNA repair inhibitors to improve the therapeutic
use of DNA-damaging drugs. In this review, we will discuss the functions of DNA repair proteins and
the advances in targeting DNA repair pathways with special emphasis in the inhibition of HRR and BER
in ovarian cancer. We focused in the actual efforts in the development and clinical use of poly (ADPribose)
polymerase (PARP) inhibitors for the intervention of BRCA1/BRCA2-deficient ovarian tumors.
The clinical development of PARP inhibitors in ovarian cancer patients with germline BRCA1/2 mutations
and sporadic high-grade serous ovarian cancer is ongoing. Some phase II and phase III trials have
been completed with promising results for ovarian cancer patients.
Keywords: Ovarian cancer, DNA repair, homologous recombination repair, base excision repair, poly (ADP-ribose) polymerase
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