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© 2015 Elsevier Inc. All rights reserved.. Tumor-induced osteolysis is achieved through the usurpation of the osteoclast, the only specialized bone resorbing cell within the body. The recruitment of the osteoclast by invading cancer cells is a central feature of the bone-tumor niche, where tumor metastases hijack the host environment, coercing cellular machinery normally used to remove old or damaged bone to instead degrade healthy viable bone. The consequent release of bone matrix proteins fuels tumor cell growth, thereby creating a cycle of bone destruction and tumor proliferation which is driven by excessive osteoclast formation and activity. The osteoclast derives from hematopoietic stem cells after commitment to a myeloid lineage. Key differentiation factors have been identified within the bone microenvironment, which stimulate osteoclastogenesis and now form effective targets for anti-resorptive therapies. However, a wide range of additional factors and tumor-derived products have been demonstrated to act directly upon precursor cells (e.g. interlukins) or indirectly through osteoblast/stromal populations (e.g. parathyroid hormone-related protein) to manipulate the bone-tumor niche and positively regulate osteoclast formation and sustained osteoclast activity.

Original publication





Book title

Bone Cancer: Primary Bone Cancers and Bone Metastases: Second Edition

Publication Date



55 - 63