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.
One or more of the authors have received funding from the American Cancer Society (TCH), The Brinson Foundation (RCH, TCH),
the Orthopaedic Research and Education Foundation (RCH), and the National Institutes of Health (RCH, TCH).