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- W4384627178 abstract "RNA splicing factor SF3B1 is recurrently mutated in various cancers, particularly in hematological ma-lignancies. We previously reported that co-expression of Sf3b1 mutation and Atm deletion in B cells, but not either lesion alone, leads to the onset of chronic lymphocytic leukemia (CLL) with CLL cells harbor-ing chromosome amplification. However, the exact role of Sf3b1 mutation and Atm deletion in chromo-somal instability (CIN) remains unclear. Here, we demonstrate that SF3B1 mutation promotes centro-meric R-loop (cen-R-loop) accumulation, leading to increased chromosome oscillation, impaired chromo-some segregation, altered spindle architecture and aneuploidy, which can be alleviated by removal of cen-R-loop and exaggerated by deletion of ATM. Aberrant splicing of key genes involved in R-loop processing underlies augmentation of cen-R-loop as overexpression of the normal isoform, but not the altered form, mitigates mitotic stress in SF3B1 mutant cells. Our study underscores the critical role of novel splice variants in linking RNA splicing dysregulation and CIN, and highlights cen-R-loop augmen-tation as a key mechanism for leukemogenesis." @default.
- W4384627178 created "2023-07-19" @default.
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- W4384627178 date "2023-09-01" @default.
- W4384627178 modified "2023-09-25" @default.
- W4384627178 title "SF3B1 mutation and ATM deletion codrive leukemogenesis via centromeric R-loop dysregulation" @default.
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- W4384627178 doi "https://doi.org/10.1172/jci163325" @default.
- W4384627178 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37463047" @default.
- W4384627178 hasPublicationYear "2023" @default.
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