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December 8, 2025BloodOpen Access

Examining the role of U2AF1 and TET2 mutations in a myeloid malignancy mouse model

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Authors

MCMatthew ChengSPSambuddha PaulHMHannah M. Maul-Newby

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Overview

Observational analysis revealed altered blood counts and myelopoiesis in U2AF1 and TET2 mutant mice, indicating a potential MDS phenotype.

Key Points

  • Increased myelopoiesis disruption was observed in U2AF1 and TET2 mutant mice over 14 weeks, showing phenotypic changes associated with MDS.
  • Complete blood count readings displayed consistent retention of mutant U2AF1 cells throughout the analysis period, supporting ongoing malignancy development.
  • Analysis utilized Tamoxifen-activated HSC-SCL Cre-ER mice to study pathogenic mechanisms and evaluate blood characteristics.
  • Results demonstrate potential for long-term examination of myeloid malignancies in U2AF1/TET2 mutant mouse models for therapeutic insights.

Cite This Study

Cheng et al. (2025) studied this question.

synapsesocial.com/papers/69362f4e4fa91c937236d827https://doi.org/10.1182/blood-2025-3837
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Also Consider

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

  1. 1Transcriptional and splicing dysregulation by U2AF1 mutations contribute to inflammatory and migratory alterations in MDS2025
  2. 2Mis-splicing of Mdm4 activates TRP53 and impairs HSPC growth in a mouse model of myelodysplastic syndromes2025
  3. 3Impact of different Sf3b1 mutations on hematopoietic function and erythropoiesis2025
  4. 4SF3B1 mutations K700E, K666N, and R625H: Gene expression and aberrant splicing consequences2025
  5. 5Sf3b1+/K700E hematopoietic stem cells create their own expansion niche2025