The DOI matches its Crossref record; 60 of the 60 references it cites were found in a registry or an index.
Biology of Osteoclast Activation in Cancer
Abstract
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.
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Cites
Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.
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Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.
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A Parathyroid Hormone-Related Protein Implicated in Malignant Hypercalcemia: Cloning and Expression
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OSTEOBLASTIC CELLS ARE INVOLVED IN OSTEOCLAST FORMATION
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Severe osteoporosis in mice lacking osteoclastogenesis inhibitory factor/osteoprotegerin.
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Cited by
Roodman, G. D. (2004) · New England Journal of Medicine · doi:10.1056/nejmra030831 · Cited by 2,755
Self-citationMultiple myeloma: evolving genetic events and host interactions
Kuehl, W. M., & Bergsagel, P. L. (2002) · Nature Reviews Cancer · doi:10.1038/nrc746 · Cited by 818
RANK ligand and osteoprotegerin in myeloma bone disease.
Sezer, O., Heider, U., Zavrski, I., Kühne, C. A., & Hofbauer, L. C. (2003) · Blood · doi:10.1182/blood-2002-09-2684 · Cited by 258
Nabavi, N., Khandani, A., Camirand, A., & Harrison, R. E. (2011) · Bone · doi:10.1016/j.bone.2011.07.036 · Cited by 174
Human bone marrow myeloma cells express RANKL.
Sezer, O., Heider, U., Jakob, C., Eucker, J., Possinger, K., & Roodman, G. D. (2002) · Journal of Clinical Oncology · doi:10.1200/jco.2002.20.1.353 · Cited by 104
Self-citation
Metadata
- Authors
- Roodman, G. D.
- Venue
- Journal of Clinical Oncology
- Published
- 2001-08-01
- Volume
- 19
- Issue
- 15
- Pages
- 3562-3571
- ISSN
- 0732-183X (ISSN-L)
- 1527-7755
- OpenAlex
- W1944909911
- Cited by
- 306
- References
- 60
- FWCI
- 7.49
- Type
- journal article
- Language
- en
- Open access
- closed
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