FSP1 and histone deacetylases suppress cancer persister cell ferroptosis.

Cancer persister cells populate minimal residual disease and contribute to acquired drug resistance. We previously discovered that persister cells are sensitized to ferroptosis. However, our understanding of this emergent persister cell vulnerability remains limited, impeding ferroptosis drug development efforts.

DFFB suppresses interferon to enable cancer persister cell regrowth.

Oncogene targeted cancer therapies can provide deep responses but frequently suffer from acquired resistance. Therapeutic approaches to treat tumours which have acquired drug resistance are complicated by continual tumour evolution and multiple co-occurring resistance mechanisms. Rather than treating resistance after it emerges, it may possible to prevent it by inhibiting the adaptive processes which initiate resistance but these are poorly understood.

Antigenic cancer persister cells survive direct T cell attack.

Drug-tolerant persister cancer cells were first reported fifteen years ago as a quiescent, reversible cell state which tolerates unattenuated cytotoxic drug stress. It remains unknown whether a similar phenomenon contributes to immune evasion. Here we report a persister state which survives weeks of direct cytotoxic T lymphocyte (CTL) attack.