The Retinoblastoma Protein in Osteoblast Differentiation and Osteosarcoma

Authors: Deshpande, Amit; Hinds, Philip W.

Source: Current Molecular Medicine, Volume 6, Number 7, November 2006 , pp. 809-817(9)

Publisher: Bentham Science Publishers

Buy & download fulltext article:

Price: $63.10 plus tax (Refund Policy)

Abstract:

Osteogenic sarcoma (osteosarcoma) is the most common primary tumor of bone. It accounts for approximately 19% of all malignant tumors of the bone. Of all the molecular targets altered during the genesis of osteosarcoma, the retinoblastoma gene (RB1) shows the highest frequency of inactivation. Published data from human osteosarcoma tumors and in vivo and in vitro model systems support a role for the retinoblastoma gene family in bone development and tumorigenesis. Although a variety of bone tumors, depending on the cell of origin, including osteoclasts or osteoclast-like cells, chondroblasts, and fibroblasts, are described, for the purpose of this review we will focus primarily on the tumors arising from the osteoblast lineage.

Keywords: Retinoblastoma tumor suppressor; osteosarcoma; osteoblast differentiation

Document Type: Research article

Affiliations: 1: Molecular Oncology Research Institute, Department of Radiation Oncology, Tufts-New England Medical Center, 750 Washington Street #5609, Boston, MA 02111, USA.

Publication date: 2006-11-01

More about this publication?

Current Molecular Medicine is an interdisciplinary journal focused on providing the readership with current and comprehensive reviews on fundamental molecular mechanisms of disease pathogenesis, the development of molecular-diagnosis and/or novel approaches to rational treatment. The reviews should be of significant interest to basic researchers and clinical investigators in molecular medicine. Periodically the journal will invite guest editors to devote an issue on a basic research area that shows promise to advance our understanding of the molecular mechanism(s) of a disease or has potential for clinical applications.