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Cells that survive treatment do so by changing which genes they use, not their DNA. Drugs that block that change may stop survivors from forming at all.
The persister state depends on chromatin regulators including KDM5A, LSD1 and BRD4, and pharmacological inhibition of these reduced persister formation in the original studies of drug-tolerant cells. The proposal is to use these inhibitors not as continuous therapy but as short pulses during the induction phase, when the persister state is being established, minimising the toxicity that has limited epigenetic drugs.
Shares EZH2, Epigenetic drugs (HDAC, DNMT, EZH2, IDH, menin, BET).
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 EZH2, Epigenetic drugs (HDAC, DNMT, EZH2, IDH, menin, BET).
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