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Alterations of certain genes and proteins seem to be essential for development of bone cancer. The cellular pathways regulated by the p53 and by Rb genes are extremely important in preventing tumor formation, and inactivation of one or both of these the pathways is virtually an absolute requirement for the formation of bone cancer. Other pathways that contribute to progression of bone cancer include those regulated by PTEN and PIK3, c-MET, c-MYC, and RUNX2, among others. Mutations of these genes in individual bone cells (“somatic mutations”) are common and play an important role in the development of bone cancer. However, mutations in these genes do not contribute to risk at the population level.

It is thought that risk is related to the number of cell divisions required to form bone. More cell divisions are required to form larger bones, accounting for the association between size and risk. Any process that accelerates cell division can also lead to mutations that increase cancer risk, and this might account for the risk associated with rapid growth and traumatic fractures.