Skip to Content

Vanderbilt-Ingram Cancer CenterVanderbilt-Ingram Cancer Center

Florent  Elefteriou

Florent Elefteriou, Ph.D.

Associate Professor of Pharmacology
Associate Professor of Cancer Biology
Associate Professor of Medicine (Clinical Pharmacology)

Contact Information:

MRB IV, Light Hall
room 1225E

  • Ph.D., Claude-Bernard University
  • Post doctoral training, Baylor College of Medicine
Research Description

Bone remodeling is regulated in vivo by a complex interplay between autocrine/paracrine and hormonal signals. Our studies, based on the use of mouse genetic models, demonstrated that this process is also regulated by the central nervous system, and that, as this finding implies, bone remodeling is an homeostatic process fully integrated to the regulation of the internal milieu via neurons, neuropeptides and hormones involved in the regulation of body weight, energy expenditure, reproduction or immunity. Our studies also identified the sympathetic nervous system as a critical regulator of bone remodeling. Our research currently focuses on the clinical implications of these findings from preclinical mouse models, with a special interest on osteoporosis and bone cancer metastasis.

The second main interest of our laboratory is to determine the role of Nf1 in bone cells and type I neurofibromatosis (NF1). Neurofibromatosis, caused by mutations in the Nf1 gene, is characterized by several skeletal complications including macrocephaly, scoliosis, bowing of the tibia and pseudo-arthrosis, but the origin of these skeletal dysplastic defects is unknown. By the use of mutant mouse models lacking Nf1 in osteoblasts, chondrocytes or mesenchymal stem cells, we are currently investigating the role of Nf1 signaling in the differentiation and function of bone cells, with the goal of identifying novel signaling pathways and transcription factors regulating bone growth, remodeling and repair, and to identify new therapeutic targets to treat bone diseases, including skeletal displasiae and fracture non-unions found in NF1 patients.