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Under treatment stress, cancer cells switch on sloppy DNA copying that generates the mutations they need to survive. Blocking that machinery could stop resistance being invented.
Stress-induced mutagenesis through translesion synthesis polymerases (REV1, POLZ) accelerates the emergence of resistance in bacteria and in cancer cells. REV1 inhibitors have been described and shown to reduce chemotherapy-induced mutagenesis and delay resistance in models. Given as an adjunct rather than a cytotoxic, the aim is to lower the mutation supply rate rather than to kill cells.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.