Abstract |
Figure 5 is a proposed model for MIP-1alpha's effects on myeloma bone disease. MIP-1alpha is produced by myeloma cells and directly stimulates OCL formation. In addition MIP-1alpha enhances adhesive interactions between myeloma cells and marrow stromal cells increasing expression of RANKL and IL-6, which further increase bone destruction and tumor burden. The recent evidence from our group and others lead to the conclusion that MIP-1alpha is an important mediator in the debilitating bone destruction in multiple myeloma. Blocking MIP-1alpha expression may have profound effects on myeloma cell growth, homing, and bone destruction in this in vivo model of myeloma. These data suggest that antagonists that decrease MIP-1alpha activity in vivo or blocking MIP-1alpha signaling by neutralizing its receptor may provide therapeutic alternatives for treating patients with myeloma to decrease both their tumor burden and bone destruction.
|
Authors | G David Roodman, Sun Jin Choi |
Journal | Cancer treatment and research
(Cancer Treat Res)
Vol. 118
Pg. 83-100
( 2004)
ISSN: 0927-3042 [Print] United States |
PMID | 15043189
(Publication Type: Journal Article, Review)
|
Chemical References |
- Biomarkers, Tumor
- Chemokine CCL3
- Chemokine CCL4
- Lymphokines
- Macrophage Inflammatory Proteins
- osteoclast activating factor
|
Topics |
- Animals
- Biomarkers, Tumor
(metabolism)
- Bone Diseases
(pathology)
- Chemokine CCL3
- Chemokine CCL4
- Humans
- Lymphokines
(metabolism)
- Macrophage Inflammatory Proteins
(metabolism)
- Models, Biological
- Multiple Myeloma
(metabolism)
- Osteoclasts
(physiology)
- Prognosis
|