| Literature DB >> 19878635 |
Allan Lipton1, Robert Uzzo, Robert J Amato, Georgiana K Ellis, Behrooz Hakimian, G David Roodman, Matthew R Smith.
Abstract
Cancer and its treatment can compromise bone health, leading to fracture, pain, loss of mobility, and hypercalcemia of malignancy. Bone metastasis occurs frequently in advanced prostate and breast cancers, and bony manifestations are commonplace in multiple myeloma. Osteoporosis and osteopenia may be consequences of androgen-deprivation therapy for prostate cancer, aromatase inhibition for breast cancer, or chemotherapy-induced ovarian failure. Osteoporotic bone loss and bone metastasis ultimately share a pathophysiologic pathway that stimulates bone resorption by increasing the formation and activity of osteoclasts. Important mediators of pathologic bone metabolism include substances produced by osteoblasts, such as RANKL, the receptor activator of nuclear factor kappa B ligand, which spurs osteoclast differentiation from myeloid cells. Available therapies are targeted to various steps in cascade of bone metastasis.Entities:
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Year: 2009 PMID: 19878635 PMCID: PMC3047391 DOI: 10.6004/jnccn.2009.0080
Source DB: PubMed Journal: J Natl Compr Canc Netw ISSN: 1540-1405 Impact factor: 11.908