Biologic and Therapeutic Implications of Osteomimicry and Epithelial-Mesenchymal Transition in Prostate Cancer

DOI: 10.1385/1-59259-892-7:075


Death from prostate cancer is usually attributable to the development of bone and visceral organ metastases. The spine, pelvic
bones, and ribs are among the most frequent sites of prostate cancer bone metastases. The peripheral skeleton and skull are
less frequent sites (1,2). There are two hypotheses for the preferential homing of prostate cancer cells to bone. The first is that the mechanical
hemodynamics of blood flow from prostate to bone favor the spread of prostate cancer cells to specific anatomical sites (3). A second theory holds that prostate cancer cells have a specific affinity to bone, which attracts and colonizes prostate
cancer cells in a relationship like the “seed” (cancer cell) and “soil” (bone microenvironment) hypothesis originally proposed
by Paget (4). Understanding the molecular mechanism underlying prostate cancer tropism to bone and the evolutionary process leading to
androgen independence and invasiveness will allow us to develop better therapies for the management of prostate cancer bone

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