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Title
Cellular Mechanisms of Multiple Myeloma Bone Disease
Authors
Keywords
-
Journal
Clinical & Developmental Immunology
Volume 2013, Issue -, Pages 1-11
Publisher
Hindawi Limited
Online
2013-05-30
DOI
10.1155/2013/289458
References
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Note: Only part of the references are listed.- Circulating activin-A is elevated in patients with advanced multiple myeloma and correlates with extensive bone involvement and inferior survival; no alterations post-lenalidomide and dexamethasone therapy
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- The formation of osteoclasts in multiple myeloma bone disease patients involves the secretion of soluble decoy receptor 3
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- RANKL-independent human osteoclast formation with APRIL, BAFF, NGF, IGF I and IGF II
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- TNF-α's effects on proliferation and apoptosis in human mesenchymal stem cells depend on RUNX2 expression
- (2010) Olfa Ghali et al. JOURNAL OF BONE AND MINERAL RESEARCH
- Activin A promotes multiple myeloma-induced osteolysis and is a promising target for myeloma bone disease
- (2010) S. Vallet et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Increased Level of both CD4+FOXP3+ Regulatory T Cells and CD14+HLA-DR−/low Myeloid-Derived Suppressor Cells and Decreased Level of Dendritic Cells in Patients with Multiple Myeloma
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- A monoclonal gammopathy precedes multiple myeloma in most patients
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- Soluble decoy receptor 3 modulates the survival and formation of osteoclasts from multiple myeloma bone disease patients
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- Myeloma-derived Dickkopf-1 disrupts Wnt-regulated osteoprotegerin and RANKL production by osteoblasts: a potential mechanism underlying osteolytic bone lesions in multiple myeloma
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