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| Bone, Joint & Cancer |
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 Bone, Joint & Cancer Group leader A/Professor Matthew Gillespie Our skeleton provides a structural support for our bodies and as a source of nutrients for the blood and immune system. Bone diseases such as osteoporosis, arthritis and most cancers of bone all result in a reduction in bone mass, that can lead to fractures. We seek to identify the pathways that are required to build bone and/or limit bone destruction, and how the cells in the bone microenvironment communicate with each other. Ultimately, we aim to identify new factors or ways to promote bone formation. Communication between the cells of bone The internal structure of our skeleton constantly changes as a result of the applied stresses and strains. Extenbone sive communication is required between the cells that detect these changes with the cells that destroy (osteoclasts) and rebuild (osteoblasts) bone. The only known therapy that can reliably increase the amount of bone is daily injection of parathyroid hormone (PTH), which is an expensive treatment. We are working on new approaches to treatments that build bone. By investigating pathways of PTH action, we have identified new PTH targets and we are investigating their potential in treatment of osteoporosis. We have also determined that there is considerable overlap between the skeleton and immune cell function. In particular, many of the cytokines and growth factors required for immune cell differentiation modulate bone formation or bone destruction. This has led to the emergence of a new field of “osteoimmunology” that recognises this pivotal interaction, and aims to determine the interdependence and interrelationships between the immune system and the skeleton. Cancer One of the focus areas of the Bone, Joint and Cancer Unit is the spread of primary cancers to other sites in the body that results in secondary cancer. This process, known as metastasis, is a serious and unfortunately common complication of many cancers including breast cancer, which often spreads to bone. We have shown that a protein called osteoprotegerin inhibits the process of bone breakdown. Osteoprotegerin is commonly expressed by the bone forming cells, and we provided some of the first evidence that it is also produced by a number of cancers. We explored the consequences of regulating osteoprotegrin levels in breast cancers and determined that this factor can regulate tumour growth both in bone and in the breast. This identified a new role for this protein and indicated that high levels of osteoprotegerin in a tumour might be a poor prognostic indicator for patients. We are now determining how this protein affects tumour growth and whether we can counteract its activity.
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