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The Osteoblastic and Osteoclastic Interactions in Spinal Metastases Secondary to Prostate Cancer
Author(s) -
Sathana Dushyanthen,
Davina A. F. Cossigny,
Gerald M. Y. Quan
Publication year - 2013
Publication title -
cancer growth and metastasis
Language(s) - English
Resource type - Journals
ISSN - 1179-0644
DOI - 10.4137/cgm.s12769
Subject(s) - medicine , spinal cord compression , bone metastasis , prostate cancer , metastasis , rankl , prostate , pathological , cancer , spinal cord , oncology , pathology , receptor , psychiatry , activator (genetics)
Prostate cancer (PC) is one of the most common cancers arising in men and has a high propensity for bone metastasis, particularly to the spine. At this stage, it often causes severe morbidity due to pathological fracture and/or metastatic epidural spinal cord compression which, if untreated, inevitably leads to intractable pain, neurological deficit, and paralysis. Unfortunately, the underlying molecular mechanisms driving growth of secondary PC in the bony vertebral column remain largely unknown. Further investigation is warranted in order to identify therapeutic targets in the future. This review summarizes the current understanding of PC bone metastasis in the spine, highlighting interactions between key tumor and bone-derived factors which influence tumor progression, especially the functional roles of osteoblasts and osteoclasts in the bone microenvironment through their interactions with metastatic PC cells and the critical pathway RANK/RANKL/OPG in bone destruction.

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