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Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
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Updated: Jun 27, 2026

Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice
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Impaired NHEJ function in multiple myeloma.

Clara Yang1, Christopher Betti, Sheetal Singh

  • 1Department of Radiation Oncology, University of California, Davis, CA 95817, USA.

Mutation Research
|November 26, 2008
PubMed
Summary
This summary is machine-generated.

Multiple myeloma cell lines exhibit faulty DNA repair mechanisms, specifically non-homologous end joining (NHEJ). Inhibiting DNA-PK paradoxically increased survival in radiation-sensitive myeloma cells, suggesting complex DNA repair pathway interactions.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Multiple myeloma (MM) is characterized by genomic instability due to chromosomal aberrations.
  • DNA repair pathways are crucial for maintaining genomic integrity.
  • Understanding DNA repair defects in MM is vital for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of DNA repair, particularly non-homologous end joining (NHEJ), in the genomic instability of multiple myeloma (MM).
  • To assess the response of MM cell lines to ionizing radiation and DNA-PK inhibition.
  • To elucidate the mechanisms underlying DNA repair deregulation in MM.

Main Methods:

  • Clonogenic survival assays were performed on three MM cell lines (U266, RPMI 8226, OPM2) after ionizing radiation exposure.
  • The effect of the DNA-PK inhibitor NU7026 on radiation survival was evaluated.
  • In vitro DNA repair assays, including blunt-ended DNA ligation and a bacterial-based functional assay, were used to measure NHEJ capacity.
  • Western blotting and immunofluorescence were employed to examine gamma-H2AX foci as a marker of DNA double-strand breaks.

Main Results:

  • Radiation sensitivity varied among MM cell lines, with U266 and RPMI 8226 being sensitive and OPM2 resistant.
  • DNA-PK inhibition (NU7026) suppressed survival in OPM2 but paradoxically increased survival in U266 and RPMI 8226.
  • RPMI 8226 showed impaired blunt-ended DNA ligation and reduced rejoining fidelity in functional NHEJ assays.
  • All three MM cell lines displayed evidence of corrupt NHEJ repair.
  • Gamma-H2AX response to ionizing radiation was modulated by pre-existing DNA repair status.

Conclusions:

  • Multiple myeloma cell lines exhibit defective non-homologous end joining (NHEJ) repair.
  • Inhibition of DNA-PK in radiation-sensitive MM cells may redirect DNA breaks to alternative repair pathways, increasing survival.
  • Deregulation of DNA repair contributes to the genomic instability observed in multiple myeloma.