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A Unified Model: Chromatin-Bound Multicomponent Condensates.

Benjamin K Lau1,2, Elena L Haarer3, Jeong Hyun Ahn4

  • 1Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, North Carolina.

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|January 2, 2026
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Biomolecular condensates, like those formed by NPM1c mutations in acute myeloid leukemia (AML), are crucial for cancer development. Targeting these "onco-condensates" may offer new cancer treatments.

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Area of Science:

  • Cell biology
  • Molecular oncology
  • Biophysics

Background:

  • Biomolecular condensates are essential for cellular function and implicated in cancer pathogenesis.
  • Mutations like NPM1c drive acute myeloid leukemias (AMLs) through condensate formation.

Purpose of the Study:

  • To investigate the role of NPM1c in forming nuclear condensates (C-bodies) in AML.
  • To explore the function and therapeutic potential of targeting these NPM1c-driven condensates.

Main Methods:

  • Cellular studies of NPM1c condensation and co-partitioning of transcriptional coactivators.
  • Systematic deletion analysis of NPM1c regions.
  • Biophysical comparison of different onco-condensates.

Main Results:

  • NPM1c is necessary and sufficient for forming C-bodies, which sequester key coactivators like NUP98, KMT2A/MLL1, Menin, and XPO1/CRM1.
  • Inhibiting components within C-bodies alters their function; NPM1c region deletions impact condensate formation.
  • C-bodies and other cancer-related condensates (e.g., from NUP98 or KMT2A/MLL1 fusions) are biophysically similar, suggesting a shared pathogenic mechanism.

Conclusions:

  • NPM1c-driven C-bodies are critical for AML.
  • Cancer-associated condensates represent a shared pathogenic mechanism across various genetic drivers.
  • Targeting these chromatin-bound onco-condensates could lead to broad-spectrum cancer therapies.