Block the chemical switch that lets cells hide from treatment
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.
- Acquired resistance to every therapy · Nearly every targeted therapy stops working within months to a few years as the tumour adapts.
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Shares EZH2, Epigenetic drugs (HDAC, DNMT, EZH2, IDH, menin, BET).
- IdeaCut off the emergency programme cancer cells use to survive treatment
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
- IdeaTurn off the error-prone repair that manufactures resistance mutations
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
- IdeaMake post-progression sampling a condition of accelerated approval
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
- IdeaKill the sleeping survivor cells with iron-dependent cell death
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
- IdeaEvery resistance mechanism found in a patient must be rebuilt in the laboratory
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
- IdeaSMART designs to test treatment strategies, not just single drugs
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.
- IdeaStarve the survivors: target the energy pathway drug-tolerant cells switch to
Shares Drug resistance (primary and acquired), Acquired resistance to every therapy.