|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
GeneticVariation |
BEFREE |
Our results of skeletal remodeling following this regenerative stem cell therapy with OPG variants indicated a significant protection against myeloma-induced osteolytic bone damage in areas of major myeloma skeletal dissemination, suggesting the potential of this therapy for treating osteolytic damage in myeloma patients.
|
29296887 |
2017 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Osteoprotegerin (OPG) is a glycoprotein that has multifaceted role and is associated with several cancer malignancies like that of bladder carcinoma, gastric carcinoma, prostate cancer, multiple myeloma and breast cancer.
|
26608463 |
2015 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
GeneticVariation |
BEFREE |
C950T and C1181G polymorphisms of the OPG gene were studied in 52 MM patients (36 with bone lesions and 16 without bone lesions) and in another 20 control subjects using DNA sequencing.
|
24074513 |
2014 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
GeneticVariation |
BEFREE |
In conclusion, rhTRAIL D269H/E195R is a potential therapy for multiple myeloma due to its high effectiveness and diminished binding to OPG.
|
24280212 |
2014 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Multiple myeloma (MM)-induced osteoclast (OC) formation is mainly due to an imbalance of the receptor activator NF-κB ligand (RANKL)-osteoprotegerin (OPG) ratio in favor of RANKL in the bone microenvironment and to the CCL3 production by MM cells.
|
23178378 |
2013 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Myeloma stimulates osteoclastogenesis, which is largely dependent on an increase in receptor activator of NF-κB ligand (RANKL) and a decrease in osteoprotegerin (OPG) within the bone marrow milieu.
|
23420490 |
2013 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Compared with osteoblasts incubated with MM cell supernatant alone, the mRNA levels of ALP, OC and OPG in osteoblasts co-treated with brucine and MM cell supernatant were higher (p<0.05), while the mRNA expression of RANKL was lower, and the ranges of the changes were all larger than those of the group treated with bortezomib (P<0.05).
|
22614932 |
2012 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Although disruption of the RANKL/OPG pathway has been shown to underlie formation of focal osteolytic lesions, its role in the development of osteoporosis in myeloma remains unclear.
|
22952578 |
2012 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Disturbances in the RANKL/OPG system are more profound in the BMSCs of MM patients than in those of control subjects after direct contact with RPMI8226 cells.
|
20157786 |
2010 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
These results suggest that DKK1 may play a key role in the development of MM-associated OBL by directly interrupting Wnt-regulated differentiation of osteoblasts and indirectly increasing osteoclastogenesis via a DKK1-mediated increase in RANKL-to-OPG ratios.
|
18305214 |
2008 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
AlteredExpression |
BEFREE |
A new xenograft model of myeloma bone disease demonstrating the efficacy of human mesenchymal stem cells expressing osteoprotegerin by lentiviral gene transfer.
|
17657224 |
2007 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Therefore, we hypothesized that specific agonists of TRAIL death receptors would not be inhibited by OPG released from osteoblasts and thus may represent a novel therapeutic approach in multiple myeloma.
|
17315027 |
2007 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
These results suggest that the combination of intermediate dose of Thal/Dex is effective in patients with refractory/relapsed myeloma and improves abnormal bone remodeling through the reduction of sRANKL/OPG ratio.
|
16079895 |
2005 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Osteoclast activity factors (in particular MIP1alpha) and imbalances between RANKL and osteoprotegerin are major factors for the development of myeloma bone disease.
|
12965277 |
2003 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
These data open new avenues for the treatment of bone disease in MM and highlight the promising therapeutical interest of RANKL inhibitors (OPG and RANK-Fc) and MIP-1 inhibitors in the management of myeloma-associated osteolysis, besides bisphosphonates.
|
14565645 |
2003 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
AlteredExpression |
BEFREE |
Patients with myeloma bone disease have inappropriately low serum and bone marrow levels of OPG.
|
12424190 |
2003 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
AlteredExpression |
BEFREE |
Together, our data strongly suggest that RANKL expression by MPC confers on them the ability to participate directly in the formation of osteoclast in vivo and extends our knowledge of the involvement of RANKL and OPG in the osteolysis characteristic of this disease.
|
14500379 |
2003 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
Our data identify TRANCE and OPG as key cytokines whose deregulation promotes bone destruction and supports myeloma growth.
|
11562486 |
2001 |
|
TNFRSF11B
|
Multiple Myeloma
|
0.100 |
Biomarker |
BEFREE |
In summary, these data indicate that myeloma cells affect the OPG/OPGL ratio in the BM environment and tend to confirm that the OPG/OPGL system is involved in the pathogenesis of MM-induced bone disease.
|
11739153 |
2001 |