Biography and Research Information
OverviewAI-generated summary
Cecile Bustamante-Gomez's research focuses on bone biology and remodeling, particularly in the context of animal models. Her work investigates the role of specific molecular pathways, such as RANKL signaling, in bone loss and healing. She has studied the effects of therapeutic agents like denosumab and romosozumab on bone turnover and has explored the potential of sclerostin inhibition for restoring bone health in models of multiple myeloma. Additionally, her research has involved characterizing different types of mesenchymal cells associated with bone, contributing to a deeper understanding of skeletal development and repair mechanisms. Bustamante-Gomez has published seven papers and has a citation count of 41, with an h-index of 2. She collaborates with several researchers at the University of Arkansas for Medical Sciences, including Charles A. O’Brien, Visanu Wanchai, Jinhu Xiong, and Melda Onal.
Metrics
- h-index: 2
- Publications: 7
- Citations: 50
Selected Publications
-
Healing of lytic lesions and restoration of bone health in multiple myeloma through sclerostin inhibition (2025)
-
Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice (2025)
-
RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis (2024)
-
Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone (2024)
-
A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone (2023)
Collaboration Network
Top Collaborators
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Healing of lytic lesions and restoration of bone health in multiple myeloma through sclerostin inhibition
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- RANKL-mediated osteoclast formation is required for bone loss in a murine model of Staphylococcus aureus osteomyelitis
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
Similar Researchers
Based on overlapping research topics