Osteosarcoma development and stem cell differentiation

Clin Orthop Relat Res. 2008 Sep;466(9):2114-30. doi: 10.1007/s11999-008-0335-z. Epub 2008 Jun 18.

Abstract

Osteosarcoma is the most common nonhematologic malignancy of bone in children and adults. The peak incidence occurs in the second decade of life, with a smaller peak after age 50. Osteosarcoma typically arises around the growth plate of long bones. Most osteosarcoma tumors are of high grade and tend to develop pulmonary metastases. Despite clinical improvements, patients with metastatic or recurrent diseases have a poor prognosis. Here, we reviewed the current understanding of human osteosarcoma, with an emphasis on potential links between defective osteogenic differentiation and bone tumorigenesis. Existing data indicate osteosarcoma tumors display a broad range of genetic and molecular alterations, including the gains, losses, or arrangements of chromosomal regions, inactivation of tumor suppressor genes, and the deregulation of major signaling pathways. However, except for p53 and/or RB mutations, most alterations are not constantly detected in the majority of osteosarcoma tumors. With a rapid expansion of our knowledge about stem cell biology, emerging evidence suggests osteosarcoma should be regarded as a differentiation disease caused by genetic and epigenetic changes that interrupt osteoblast differentiation from mesenchymal stem cells. Understanding the molecular pathogenesis of human osteosarcoma could ultimately lead to the development of diagnostic and prognostic markers, as well as targeted therapeutics for osteosarcoma patients.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Bone Neoplasms / genetics*
  • Bone Neoplasms / physiopathology*
  • Cell Differentiation / physiology*
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Humans
  • Mesenchymal Stem Cells / cytology*
  • Neurofibromatosis 2 / genetics
  • Osteosarcoma / genetics*
  • Osteosarcoma / physiopathology*
  • Proto-Oncogenes / genetics
  • RecQ Helicases / genetics
  • Retinoblastoma Protein / genetics
  • Signal Transduction / genetics
  • Tumor Suppressor Protein p14ARF / genetics
  • Tumor Suppressor Protein p53 / genetics

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • Retinoblastoma Protein
  • Tumor Suppressor Protein p14ARF
  • Tumor Suppressor Protein p53
  • RecQ Helicases