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Sarcoma
Volume 2011 (2011), Article ID 325238, 12 pages
http://dx.doi.org/10.1155/2011/325238
Review Article

Defective Osteogenic Differentiation in the Development of Osteosarcoma

1Molecular Oncology Laboratory, Department of Surgery, The University of Chicago Medical Center, 5841 South Maryland Avenue, MC3079, Chicago, IL 60637, USA
2Stem Cell Biology and Therapy Laboratory, The Children's Hospital of Chongqing Medical University, Chongqing 400014, China
3Key Laboratory of Diagnostic Medicine, Chinese Ministry of Education and Affiliated Hospitals, Chongqing Medical University, Chongqing 400016, China
4School of Bioengineering, Chongqing University, Chongqing 400044, China
5Department of Geriatrics, Xinhua Hospital, Shanghai Jiaotong University, Shanghai 200092, China
6Department of Cell Biology, Third Military Medical University, Chongqing 400030, China

Received 20 September 2010; Revised 19 December 2010; Accepted 20 December 2010

Academic Editor: H. Kovar

Copyright © 2011 Eric R. Wagner et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Osteosarcoma (OS) is associated with poor prognosis due to its high incidence of metastasis and chemoresistance. It often arises in areas of rapid bone growth in long bones during the adolescent growth spurt. Although certain genetic conditions and alterations increase the risk of developing OS, the molecular pathogenesis is poorly understood. Recently, defects in differentiation have been linked to cancers, as they are associated with high cell proliferation. Treatments overcoming these defects enable terminal differentiation and subsequent tumor inhibition. OS development may be associated with defects in osteogenic differentiation. While early regulators of osteogenesis are unable to bypass these defects, late osteogenic regulators, including Runx2 and Osterix, are able to overcome some of the defects and inhibit tumor propagation through promoting osteogenic differentiation. Further understanding of the relationship between defects in osteogenic differentiation and tumor development holds tremendous potential in treating OS.