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December 8, 2025Blood

Mis-splicing of Mdm4 activates TRP53 and impairs HSPC growth in a mouse model of myelodysplastic syndromes

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Authors

JSJin ShaoJFJennifer A. Foltz

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Overview

Observational analysis showed splicing factor mutations impair growth in hematopoietic stem and progenitor cells, indicating potential therapeutic vulnerabilities in acute myeloid leukemia.

Key Points

  • Impaired growth of hematopoietic stem and progenitor cells is linked to TRP53 activation.
  • RNAseq showed upregulation of TP53 target genes in splicing factor mutant models.
  • Competitive bone marrow transplants indicated deletion of Trp53 rescues growth in U2af1S34F HSPCs.
  • Understanding TRP53 activation may lead to targeted therapies for acute myeloid leukemia.

Cite This Study

Shao et al. (2025) studied this question.

synapsesocial.com/papers/69362f5d4fa91c937236dc6bhttps://doi.org/10.1182/blood-2025-230
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Also Consider

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

  1. 1Examining the role of U2AF1 and TET2 mutations in a myeloid malignancy mouse model2025
  2. 2Transcriptional and splicing dysregulation by U2AF1 mutations contribute to inflammatory and migratory alterations in MDS2025
  3. 3An actionable DNA repair defect in myeloid malignancies with U2AF1 S34 mutations2025
  4. 4DDX41-R525H mutation promotes dysplastic hematopoiesis via aberrant splicing of key regulators of HSC biology2025 · 1 citations
  5. 5U2AF1S34F mutant HSPCs have a fitness advantage in aged and inflamed bone marrow2025 · 1 citations