Breast cancer metastasis to the bone: Mechanisms of bone loss

Yu Chi Chen, Donna M. Sosnoski, Andrea M. Mastro

Research output: Contribution to journalReview article

128 Citations (Scopus)

Abstract

Breast cancer frequently metastasizes to the skeleton, interrupting the normal bone remodeling process and causing bone degradation. Osteolytic lesions are the end result of osteoclast activity; however, osteoclast differentiation and activation are mediated by osteoblast production of RANKL (receptor activator for NFκB ligand) and several osteoclastogenic cytokines. Osteoblasts themselves are negatively affected by cancer cells as evidenced by an increase in apoptosis and a decrease in proteins required for new bone formation. Thus, bone loss is due to both increased activation of osteoclasts and suppression of osteoblasts. This review summarizes the current understanding of the osteolytic mechanisms of bone metastases, including a discussion of current therapies.

Original languageEnglish (US)
Article number215
JournalBreast Cancer Research
Volume12
Issue number6
DOIs
StatePublished - Dec 16 2010

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Osteoclasts
Osteoblasts
Breast Neoplasms
Neoplasm Metastasis
Bone and Bones
Bone Remodeling
Osteogenesis
Skeleton
Apoptosis
Cytokines
Ligands
Neoplasms
Proteins
Therapeutics

All Science Journal Classification (ASJC) codes

  • Cancer Research
  • Oncology
  • Medicine(all)

Cite this

Chen, Yu Chi ; Sosnoski, Donna M. ; Mastro, Andrea M. / Breast cancer metastasis to the bone : Mechanisms of bone loss. In: Breast Cancer Research. 2010 ; Vol. 12, No. 6.
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Breast cancer metastasis to the bone : Mechanisms of bone loss. / Chen, Yu Chi; Sosnoski, Donna M.; Mastro, Andrea M.

In: Breast Cancer Research, Vol. 12, No. 6, 215, 16.12.2010.

Research output: Contribution to journalReview article

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T2 - Mechanisms of bone loss

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AU - Sosnoski, Donna M.

AU - Mastro, Andrea M.

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AB - Breast cancer frequently metastasizes to the skeleton, interrupting the normal bone remodeling process and causing bone degradation. Osteolytic lesions are the end result of osteoclast activity; however, osteoclast differentiation and activation are mediated by osteoblast production of RANKL (receptor activator for NFκB ligand) and several osteoclastogenic cytokines. Osteoblasts themselves are negatively affected by cancer cells as evidenced by an increase in apoptosis and a decrease in proteins required for new bone formation. Thus, bone loss is due to both increased activation of osteoclasts and suppression of osteoblasts. This review summarizes the current understanding of the osteolytic mechanisms of bone metastases, including a discussion of current therapies.

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