Annals of Oncology Advance Access originally published online on May 31, 2005
Annals of Oncology 2005 16(8):1223-1231; doi:10.1093/annonc/mdi235
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© 2005 European Society for Medical Oncology
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Myeloma bone disease: pathophysiology and management
1 Department of Hematology, 251 General Airforce Hospital, Athens, Greece; 2 Department of Hematology, Faculty of Medicine Imperial College London, Hammersmith Hospital, London, UK; 3 Department of Clinical Therapeutics and Internal Medicine, University of Athens School of Medicine, Athens, Greece
* Correspondence to: Dr E. Terpos, 5 Marathonomahon street, Drossia Attikis, 14572, Greece. Tel:+30-210-7463803; Fax:+30-210-7464648; Email: e.terpos{at}imperial.ac.uk
Bone disease is a major feature of multiple myeloma. Myeloma-induced bone destruction is the result of an increased activity of osteoclasts, which is not accompanied by a comparable increase of osteoblast function. Recent studies have revealed that new molecules such as the receptor activator of nuclear factor-kappa B (RANK), its ligand (RANKL), osteoprotegerin (OPG), and macrophage inflammatory protein-1
are implicated in osteoclast activation and differentiation, while proteins such as dickkopf-1 inhibit osteoblastic bone formation. These new molecules seem to interfere not only with the biology of myeloma bone destruction but also with tumour growth and survival, creating novel targets for the development of new antimyeloma treatment. Currently, bisphosphonates play a major role in the management of myeloma bone disease. Clodronate, pamidronate and zoledronic acid are the most effective bisphosphonates in symptomatic myeloma patients. Biochemical markers of bone remodeling have been used in an attempt to identify patients more likely to benefit from early treatment with bisphosphonates. Furthermore, using microarray techniques, myeloma patients may be subdivided into molecular subgroups with certain clinical characteristics, such as propensity for lytic lesions that may need early prophylactic treatment. Recent phase I studies with recombinant OPG and monoclonal antibodies to RANKL appear promising.
Key words:
bone disease, bisphosphonates, macrophage inflammatory protein-1 alpha (MIP-1), multiple myeloma, osteoprotegerin, receptor activator of nuclear factor-kappa B ligand (RANKL)
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