Researchers at Tokyo Metropolitan University have newly identified a mechanism by which cells tolerate the effects of alovudine, a chain-terminating nucleoside analog (CTNA) used in antiviral and cancer treatments. The study, published in Nucleic Acids Research , reveals how the DNA repair protein flap endonuclease-1 (Fen1) counteracts alovudine toxicity by suppressing the harmful activity of another protein, 53BP1.

The researchers suggest that understanding CTNA resistance mechanisms may support the development of new therapeutic strategies and guide the use of existing drugs like alovudine in targeted cancer therapy.

CTNAs have been used as cancer and antiviral therapies since the 1980s due to their ability to disrupt DNA replication. One CTNA, lamivudine, is an approved drug for t

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