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Curr Med Chem. 2018 Feb 13. doi: 10.2174/0929867325666180214113154. [Epub ahead of print]

DNA Double Strand Breaks Repair Inhibitors: Relevance as Potential New Anticancer Therapeutics.

Author information

1
Department of Immunopathology, Faculty of Biomedical Sciences and Postgraduate Training, Medical University of Lodz, Lodz 90-752. Poland.
2
Department of Molecular Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz 90-236. Poland.
3
Department of Pharmaceutical Sciences, Nesbitt School of Pharmacy, Wilkes University, Wilkes-Barre, PA 18766. United States.

Abstract

DNA Double-strand breaks are considered one of the most lethal form 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:

DNA double strand breaks; Double-strand breaks repair; anti-cancer therapy; homologous recombination; inhibitors.; non-homologous end joining

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