Pathophysiology of bone metastases

James R. Berenson, Lakshmi Rajdev, Michael Broder

Research output: Contribution to journalArticle

25 Citations (Scopus)

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
StatePublished - Sep 2006

Fingerprint

Neoplasm Metastasis
Bone and Bones
Osteoclasts
Bone Resorption
Osteoblasts
Osteogenesis
Neoplasms
Osteolysis
Bone Remodeling
Bone Development
Signal Transduction
Intercellular Signaling Peptides and Proteins
Growth

Keywords

  • Bone
  • Metastasis
  • Osteoblasts
  • Osteoclasts
  • Pathophysiology

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Berenson, J. R., Rajdev, L., & Broder, M. (2006). Pathophysiology of bone metastases. Cancer Biology and Therapy, 5(9), 1078-1081.

Pathophysiology of bone metastases. / Berenson, James R.; Rajdev, Lakshmi; Broder, Michael.

In: Cancer Biology and Therapy, Vol. 5, No. 9, 09.2006, p. 1078-1081.

Research output: Contribution to journalArticle

Berenson, JR, Rajdev, L & Broder, M 2006, 'Pathophysiology of bone metastases', Cancer Biology and Therapy, vol. 5, no. 9, pp. 1078-1081.
Berenson JR, Rajdev L, Broder M. Pathophysiology of bone metastases. Cancer Biology and Therapy. 2006 Sep;5(9):1078-1081.
Berenson, James R. ; Rajdev, Lakshmi ; Broder, Michael. / Pathophysiology of bone metastases. In: Cancer Biology and Therapy. 2006 ; Vol. 5, No. 9. pp. 1078-1081.
@article{ae5a0e8aada6465c9e9b815b1d597f91,
title = "Pathophysiology of bone metastases",
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.",
keywords = "Bone, Metastasis, Osteoblasts, Osteoclasts, Pathophysiology",
author = "Berenson, {James R.} and Lakshmi Rajdev and Michael Broder",
year = "2006",
month = "9",
language = "English (US)",
volume = "5",
pages = "1078--1081",
journal = "Cancer Biology and Therapy",
issn = "1538-4047",
publisher = "Landes Bioscience",
number = "9",

}

TY - JOUR

T1 - Pathophysiology of bone metastases

AU - Berenson, James R.

AU - Rajdev, Lakshmi

AU - Broder, Michael

PY - 2006/9

Y1 - 2006/9

N2 - 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.

AB - 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.

KW - Bone

KW - Metastasis

KW - Osteoblasts

KW - Osteoclasts

KW - Pathophysiology

UR - http://www.scopus.com/inward/record.url?scp=33751116804&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33751116804&partnerID=8YFLogxK

M3 - Article

C2 - 17012831

AN - SCOPUS:33751116804

VL - 5

SP - 1078

EP - 1081

JO - Cancer Biology and Therapy

JF - Cancer Biology and Therapy

SN - 1538-4047

IS - 9

ER -