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Updated: Feb 21, 2026

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
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Melphalan modifies the bone microenvironment by enhancing osteoclast formation.

Ryan C Chai1, Michelle M McDonald1, Rachael L Terry1

  • 1Bone Biology Division, Garvan Institute of Medical Research, Darlinghurst, Australia.

Oncotarget
|October 6, 2017
PubMed
Summary
This summary is machine-generated.

Melphalan chemotherapy for multiple myeloma (MM) increases osteoclast formation, leading to bone loss. This process, dependent on cell stress response, may reactivate dormant cancer cells.

Keywords:
bone lossbone microenvironmentcell stresschemotherapyosteoclast

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Area of Science:

  • Oncology
  • Bone Biology
  • Cancer Therapeutics

Background:

  • Melphalan is a chemotherapy agent for multiple myeloma (MM).
  • Osteoclasts remodel bone, potentially reactivating dormant MM cells in the endosteal niche.
  • The effect of melphalan on osteoclast formation and the endosteal niche is not well understood.

Purpose of the Study:

  • To investigate whether melphalan treatment increases osteoclast formation.
  • To determine the mechanism by which melphalan influences osteoclastogenesis.
  • To assess the impact of melphalan-induced osteoclast activity on the bone microenvironment and dormant MM cells.

Main Methods:

  • Melphalan treatment in mice and assessment of bone parameters and osteoclast numbers.
  • In vitro studies using bone marrow cells (BMCs) and RAW264.7 cells to evaluate osteoclast formation.
  • Inhibition of cell stress response (CSR) using KNK437.
  • Analysis of gene expression for key osteoclast regulators (MITF, NFATc1) and fusion factors (Dc-stamp, Oc-stamp).

Main Results:

  • Melphalan treatment reduced bone volume and endosteal bone surface, correlating with increased osteoclast numbers in mice.
  • BMCs from melphalan-treated mice exhibited enhanced osteoclast formation, indicating increased osteoclast progenitors.
  • Melphalan stimulated osteoclastogenesis in vitro, an effect reversed by the CSR inhibitor KNK437.
  • Melphalan upregulated MITF and MITF-dependent fusion genes (Dc-stamp, Oc-stamp), but not NFATc1 or RANKL.

Conclusions:

  • Melphalan promotes osteoclast formation via increased progenitor recruitment and differentiation, mediated by a CSR-dependent pathway.
  • Melphalan-induced osteoclast activity contributes to bone loss and reduced endosteal surface.
  • These findings suggest a mechanism by which melphalan may contribute to dormant MM cell reactivation, impacting therapeutic strategies.