Pathophysiology of bone metastases

James R. Berenson, Lakshmi Rajdev, Michael Broder

Research output: Contribution to journalReview article

26 Scopus citations

Abstract

Normal bone remodeling maintains an appropriate balance between the action of osteoclasts (bone-resorbing cells) and osteoblasts (bone-forming cells). Skeletal malignancies, including bone metastases, disrupt the OPG-RANKL-RANK signal transduction pathway and promote enhanced osteoclast formation, thereby accelerating bone resorption and inducing bone loss. This osteolysis in turn leads to the release of bone-derived growth factors, contributing to a "vicious cycle" in which interactions between tumor cells and osteoclasts not only lead to increased osteoclastogenesis and osteolytic activity, but also aggressive growth and behavior of the tumor cells. The osteolytic complications associated with bone metastases are caused by tumor-induced alterations of the OPG-RANKL-RANK system, which are accompanied by enhanced bone resorption and disassociated from counterbalancing bone formation by osteoblasts.

Original languageEnglish (US)
Pages (from-to)1078-1081
Number of pages4
JournalCancer Biology and Therapy
Volume5
Issue number9
DOIs
StatePublished - Sep 2006

Keywords

  • Bone
  • Metastasis
  • Osteoblasts
  • Osteoclasts
  • Pathophysiology

ASJC Scopus subject areas

  • Molecular Medicine
  • Oncology
  • Pharmacology
  • Cancer Research

Fingerprint Dive into the research topics of 'Pathophysiology of bone metastases'. Together they form a unique fingerprint.

  • Cite this

    Berenson, J. R., Rajdev, L., & Broder, M. (2006). Pathophysiology of bone metastases. Cancer Biology and Therapy, 5(9), 1078-1081. https://doi.org/10.4161/cbt.5.9.3306