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December 8, 2025BloodOpen Access

Novel therapeutics for SF3B1 mutant cancers which exploit the missplicing of DCAF16

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Authors

MSMichał SekreckiRLRohan LattupallyKLKenny Le

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Overview

Novel therapeutic approach reduces tumor burden in chronic lymphocytic leukemia by targeting DCAF16 missplicing.

Key Points

  • This research identifies DCAF16 as a therapeutic target in cancers with SF3B1 mutations, particularly focusing on the mechanism of missplicing.
  • Systematic analysis of mRNA untranslated regions (UTRs) in SF3B1 mutant versus wildtype cancers.
  • Utilization of RNA sequencing, 3' end sequencing, and Nanopore long read sequencing to explore missplicing events.
  • Comparative profiling of DCAF16 protein levels across various cell lines and cancer specimens.
  • DCAF16 identified as a target due to its association with SF3B1 missplicing.
  • Increased DCAF16 protein levels were found in SF3B1 mutant cells compared to wildtype controls.
  • DCAF16-based degraders demonstrated preferential efficacy in SF3B1 mutant cell lines and primary chronic lymphocytic leukemia specimens.

Cite This Study

Sekrecki et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dcc1https://doi.org/10.1182/blood-2025-1474
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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  2. 213.05 A novel approach for neoantigen discovery from splicing factor mutated cancers2024 · 1 citations
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  5. 5<i>SF3B1</i>-mutant mis-splicing of<i>UBA1</i>confers a targetable therapeutic vulnerability through UBA1 inhibition2024