Journal
DNA REPAIR
Volume 71, Issue -, Pages 118-126Publisher
ELSEVIER
DOI: 10.1016/j.dnarep.2018.08.015
Keywords
Cancer; Base excision repair; Chemical biology; Cancer therapy; DNA repair; Synthetic lethality
Categories
Funding
- SweLife
- Knut and Alice Wallenberg Foundation
- Swedish Foundation for Strategic Research
- Swedish Research Council
- Swedish Cancer Society
- Swedish Children's Cancer Foundation
- Swedish Pain Relief Foundation
- Torsten and Ragnar Soderberg Foundation
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Base excision repair (BER) repairs mutagenic or genotoxic DNA base lesions, thought to be important for both the etiology and treatment of cancer. Cancer phenotypic stress induces oxidative lesions, and deamination products are responsible for one of the most prevalent mutational signatures in cancer. Chemotherapeutic agents induce genotoxic DNA base damage that are substrates for BER, while synthetic lethal approaches targeting BER-related factors are making their way into the clinic. Thus, there are three strategies by which BER is envisioned to be relevant in cancer chemotherapy: (i) to maintain cellular growth in the presence of endogenous DNA damage in stressed cancer cells, (ii) to maintain viability after exogenous DNA damage is introduced by therapeutic intervention, or (iii) to confer synthetic lethality in cancer cells that have lost one or more additional DNA repair pathways. Here, we discuss the potential treatment strategies, and briefly summarize the progress that has been made in developing inhibitors to core BER-proteins and related factors.
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