Role of DNA repair in removal of fludarabine treatment from DNA

Abstract

MRE11 nuclease plays an important role in responding to earilire to DNA damage, and, in turn, in repairing double-strand breaks. Another protein, DNA polymerase epsilon nuclease, is involved in duplication synthesis. Thus, mutations in these two proteins may lead to mutation accumulation and the development of cancer cells. These two nucleases have been reported to have a role in removing nucleoside analogues (gemcitabine and cytarabine) from DNA replication, allowing replication progression and nucleoside-analogue treatment resistance. Fludarabine is a nucleoside analogue (purine analogue) and acts as a chain terminator that can be used in the treatment of leukaemia and lymphoma. We illustrate that MRE11 exonuclease activity might remove fludarabine from DNA genomic, which could contribute to fludarabine resistance and DNA replication progression