DNA Double-strand breaks are considered one of the most lethal forms of DNA
damage. Many effective anticancer therapeutic approaches used chemical and physical methods
to generate DNA double-strand breaks in the cancer cells. They include: IR and drugs
which mimetic its action, topoisomerase poisons, some alkylating agents or drugs which affected
DNA replication process. On the other hand, cancer cells are mostly characterized by
highly effective systems of DNA damage repair. There are two main DNA repair pathways
used to fix double-strand breaks: NHEJ and HRR. Their activity leads to a decreased effect of
chemotherapy. Targeting directly or indirectly the DNA double-strand breaks response by inhibitors
seems to be an exciting option for anticancer therapy and is a part of novel trends that
arise after the clinical success of PARP inhibitors. These trends will provide great opportunities
for the development of DNA repair inhibitors as new potential anticancer drugs. The main
objective of this article is to address these new promising advances.
Keywords: Double-strand breaks repair, DNA double strand breaks, homologous recombination, non-homologous end joining, anti-cancer therapy, inhibitors.
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