![]() ![]() Li Z, Mathew P, Yang J, Starbuck M-W, Zurita AJ, Liu J et al (2008) Androgen receptor–negative human prostate cancer cells induce osteogenesis through FGF9-mediated mechanisms. Lee YC, Cheng CJ, Bilen MA, Lu JF, Satcher RL, Yu-Lee LY et al (2011) BMP4 promotes prostate tumor growth in bone through osteogenesis. Lee YP, Schwarz EM, Davies M, Jo M, Gates J, Zhang X et al (2002) Use of zoledronate to treat osteoblastic versus osteolytic lesions in a severe-combined-immunodeficient mouse model. Khodavirdi AC, Song Z, Yang S, Zhong C, Wang S, Wu H et al (2006) Increased expression of osteopontin contributes to the progression of prostate cancer. Jacob K, Webber M, Benayahu D, Kleinman HK (1999) Osteonectin promotes prostate cancer cell migration and invasion: a possible mechanism for metastasis to bone. (2011) Randomized, double-blind study of denosumab versus zoledronic acid in the treatment of bone metastases in patients with advanced cancer (excluding breast and prostate cancer) or multiple myeloma. Henry DH, Costa L, Goldwasser F, Hirsh V, Hungria V, Prausova J, et al. Heidenreich A, Elert A, Hofmann R (2002) Ibandronate in the treatment of prostate cancer associated painful osseous metastases. Gordon JA, Sodek J, Hunter GK, Goldberg HA (2009) Bone sialoprotein stimulates focal adhesion-related signaling pathways: role in migration and survival of breast and prostate cancer cells. Lancet Oncol 10:872–876įizazi K, Carducci M, Smith M, Damião R, Brown J, Karsh L et al (2011) Denosumab versus zoledronic acid for treatment of bone metastases in men with castration-resistant prostate cancer: a randomised, double-blind study. Cancer Res 65:8274–8285ĭearnaley DP, Mason MD, Parmar MK, Sanders K, Sydes MR (2009) Adjuvant therapy with oral sodium clodronate in locally advanced and metastatic prostate cancer: long-term overall survival results from the MRC PR04 and PR05 randomised controlled trials. Cancer Res 64:994–999ĭai J, Keller J, Zhang J, Lu Y, Yao Z, Keller ET (2005) Bone morphogenetic protein-6 promotes osteoblastic prostate cancer bone metastases through a dual mechanism. Br J Urol 68:74–80ĭai J, Kitagawa Y, Zhang J, Yao Z, Mizokami A, Cheng S et al (2004) Vascular endothelial growth factor contributes to the prostate cancer-induced osteoblast differentiation mediated by bone morphogenetic protein. Cancer Metastasis Rev 25:601–609Ĭlarke NW, McClure J, George NJ (1991) Morphometric evidence for bone resorption and replacement in prostate cancer. Cancer Res 67:6544–6548Ĭhoueiri M, Tu S-M, Yu-Lee LY, Lin SH (2006) The central role of osteoblasts in the metastasis of prostate cancer. Cancer 107:289–298Ĭhen N, Ye XC, Chu K, Navone NM, Sage EH, Yu-Lee LY et al (2007) A secreted isoform of ErbB3 promotes osteonectin expression in bone and enhances the invasiveness of prostate cancer cells. Cancer 51:918–924Ĭhen G, Sircar K, Aprikian A, Potti A, Goltzman D, Rabbani SA (2006) Expression of RANKL/RANK/OPG in primary and metastatic human prostate cancer as markers of disease stage and functional regulation. Clin Prostate Cancer 2:34–40Ĭharhon SA, Chapuy MC, Delvin EE, Valentin-Opran A, Edouard CM, Meunier PJ (1983) Histomorphometric analysis of sclerotic bone metastases from prostatic carcinoma with special reference to osteomalacia. KeywordsĬereceda LE, Flechon A, Droz JP (2003) Management of vertebral metastases in prostate cancer: a retrospective analysis in 119 patients. These observations suggest that osteolytic and osteoblastic bone metastases are not the same and tumor-induced osteoblastic and osteolytic activity play different roles in supporting their growth and survival. Thus, while osteolytic components are present in both osteoblastic and osteolytic bone lesions, inhibition of the osteolytic component is not sufficient to alter the vicious cycle leading to tumors with an osteoblastic phenotype. The recent development of agents that target the osteolytic components of bone metastasis, including bisphosphonates and denosumab, showed promising results in osteolytic bone diseases such as multiple myeloma but were less effective in improving the osteoblastic bone disease found in prostate cancer. Therapies that can restore the balance may limit the growth of cancer cells in the bone. These cancer-induced bone responses favor the survival and growth of cancer cells in their new environment. Thus, osteoclast activity is activated in a predominantly osteoblastic lesion and vice versa. Tumor-induced bone lesions usually exhibit disturbances of both cell types. Invasion of the bone compartment by cancer cells causes an imbalance in their activities and results in predominantly bone lysing or bone forming phenotypes depending on the origin of the cancer. Normal bone development and maintenance are sustained through a balanced communication between osteoclasts and osteoblasts. ![]()
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