Biology of osteoclast activation in cancer

Research output: Contribution to journalArticle

238 Citations (Scopus)

Abstract

Bone is a frequent site of cancer metastasis. Bone metastases can result in bone destruction or new bone formation. Bone destruction is mediated by factors produced or induced by tumor cells that stimulate formation and activation of osteoclasts, the normal bone-resorbing cells. Local bone destruction also occurs in patients with osteoblastic metastases and may precede or occur simultaneously with increased bone formation. Several factors, including interleukin (IL)-1, IL-6, receptor activator of NF-kappaB (RANK) ligand, parathyroid hormone-related protein (PTHrP), and macrophage inflammatory protein-1-alpha (MIP-1α), have been implicated as factors that enhance osteoclast formation and bone destruction in patients with neoplasia. PTHrP seems to be the major factor produced by breast cancer cells that induces osteoclast formation through upregulation of RANK ligand. Enhanced RANK ligand expression also plays an important role in bone destruction in patients with myeloma. RANK ligand can act to enhance the effects of other factors produced by myeloma cells or in response to myeloma cells, such as MIP-1α and/or IL-6, to induce osteoclast formation. Understanding of the molecular mechanisms responsible for osteoclast activation in osteolytic metastases should lead to development of novel therapeutic approaches for this highly morbid and potentially fatal complication of cancer.

Original languageEnglish (US)
Pages (from-to)3562-3571
Number of pages10
JournalJournal of Clinical Oncology
Volume19
Issue number15
StatePublished - Aug 1 2001
Externally publishedYes

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Osteoclasts
Receptor Activator of Nuclear Factor-kappa B
Bone and Bones
Neoplasms
Osteogenesis
Neoplasm Metastasis
Ligands
Chemokine CCL3
Parathyroid Hormone-Related Protein
Interleukin-6 Receptors
Interleukin-1
Interleukin-6
Up-Regulation
Breast Neoplasms

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Biology of osteoclast activation in cancer. / Roodman, G. David.

In: Journal of Clinical Oncology, Vol. 19, No. 15, 01.08.2001, p. 3562-3571.

Research output: Contribution to journalArticle

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