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SF3B1-mutant cells succumb to replication stress under PARP inhibition

Across multiple cancer types, hotspot mutations in SF3B1 confer selective sensitivity to multiple clinically available PARP inhibitors. This sensitivity is due to reduced levels of CINP specifically in SF3B1-mutant cells, which leads to a loss of the canonical replication stress response after challenge with PARP inhibitors.

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Fig. 1: SF3B1MUT cells have a defective replication stress response.


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This is a summary of: Bland, P. et al. SF3B1 hotspot mutations confer sensitivity to PARP inhibition by eliciting a defective replication stress response. Nat. Genet. (2023).

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SF3B1-mutant cells succumb to replication stress under PARP inhibition. Nat Genet 55, 1265–1266 (2023).

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