SF3B1 hotspot mutations confer sensitivity to PARP inhibition by eliciting a defective replication stress response.

doi:10.1038/s41588-023-01460-5

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Article

SF3B1 hotspot mutations confer sensitivity to PARP inhibition by eliciting a defective replication stress response.

Nature genetics - 1 Aug 2023

Bland Philip, Saville Harry, Wai Patty T, Curnow Lucinda, Muirhead Gareth, Nieminuszczy Jadwiga, Ravindran Nivedita, John Marie Beatrix, Hedayat Somaieh, Barker Holly E, Wright James, Yu Lu, Mavrommati Ioanna, Read Abigail, Peck Barrie, Allen Mark, Gazinska Patrycja, Pemberton Helen N, Gulati Aditi, Nash Sarah, Noor Farzana, Guppy Naomi, Roxanis Ioannis, Pratt Guy, Oldreive Ceri, Stankovic Tatjana, Barlow Samantha, Kalirai Helen, Coupland Sarah E, Broderick Ronan, Alsafadi Samar, Houy Alexandre, Stern Marc-Henri, Pettit Stephen, Choudhary Jyoti S, Haider Syed, Niedzwiedz Wojciech, Lord Christopher J, Natrajan Rachael

Abstract excerpt

SF3B1 hotspot mutations are associated with a poor prognosis in several tumor types and lead to global disruption of canonical splicing. Through synthetic lethal drug screens, we identify that SF3B1 mutant (SF3B1MUT) cells are selectively sensitive to poly (ADP-ribose) polymerase inhibitors (PARPi), independent of hotspot mutation and tumor site. SF3B1MUT cells display a defective response to PARPi-induced...

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Identifiers

PMID: 37524790
DOI: 10.1038/s41588-023-01460-5
PMCID: PMC10412459

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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