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December 8, 2025BloodOpen Access

Cooperative activation of NF-κB by inv(3)/t(3;3) and NRAS mutations drives myeloid leukemogenesis

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Authors

HKHiroyoshi KunimotoAMAyaka MiuraMSMayoko Shirafuta

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Overview

Transgenic mice show accelerated myeloid leukemia development with NRAS mutations, suggesting NF-κB as a therapeutic target.

Key Points

  • This research examines how inv(3)/t(3;3) and NRAS mutations lead to myeloid leukemia.
  • Used 3q21q26 and NrasG12D transgenic mice models to study leukemogenesis.
  • Conducted flow cytometric analysis to evaluate myeloid cell populations.
  • Performed RNA-seq to investigate molecular characteristics of leukemic stem cells.
  • 3q21q26/NrasG12D mice developed severe myeloid leukemia and had worse overall survival than controls.
  • Significant expansion of immature myeloid cells and leukemic stem cell fractions were observed.
  • Inhibition of NF-κB significantly improved blood cell counts and decreased leukemic burden.

Cite This Study

Kunimoto et al. (2025) studied this question.

synapsesocial.com/papers/69362f444fa91c937236d57ehttps://doi.org/10.1182/blood-2025-3226
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Also Consider

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  1. 1Modeling KRAS mutations in KMT2A::MLLT3 acute myeloid leukemia promotes leukemic progression and transcriptional rewiring2026
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  5. 5KRAS G12D Blocks Erythroid Differentiation and Promotes Inflammatory Pathways at the Single Cell Level in Myeloid Malignancies 22515712026