A short account of metastatic bone disease

Metastases to bone may have either an osteolytic or an ostoblastic phenotype. The interaction in the bone microenvironment between biological factors secreted by metastatic cells, and by osteoblasts and osteoclasts, and the osteolytic and osteoblastic factors released from the organic matrix mediate a vicious cycle characterized by metastatic growth and by ongoing progressive bone destruction. This interaction determines the phenotype of the metastatic bone disease.If primary cancer cells penetrate the walls of blood or lymphatic vessels and gain access to the blood or lymph stream, they may spread to remote sites, where depending upon their interaction with stromal, endothelial and immune cells in their new microenvironment, they may either die, or survive in a dormant state, or undergo clonal expansion to form a metastatic growth [1]. It is probable that those cells that do form a metastatic growth are cells which possess the cytogenetic profile conferring upon them the potential to initiate and sustain growth in a favourable microenvironment [2].The gene profile that conveys the potential for metastatic growth may be expressed in certain primary cancer cells early in carcinogenesis, or may be acquired only later in the course of primary cancer progression, as a result of evolution of subclones of cancer cells that have undergone multiple episodes of cytogenetic and epigenetic alteration [1-7].Cells with a cancer stem cell phenotype which disseminate early in the course of the primary cancer, often remain dormant in their new location for a long time, and become active only if or when their new microenvironment favours growth of the metastatic cancer cells. If the primary cancer is large, it can be not only a source of metastasizing cells, but also of biologically active mediators that promote development of favourable prematastatic niches, where colonization by dormant or newly-arrived metastatic cells, will be supported [2,5,6].Primary cancers of lung, breast, t