ABSTRACT
Tumor progression is a multistep process. Neoplastic clones are usually generated by a series of somatic and/or inherited mutations. Those genetic changes allow cells to bypass programmed cell death, avoid the need for growth factors (positive regulators), ignore restraining signals (negative regulators), escape from immunological surveillance, stimulate the formation of their own blood supply (angiogenesis), breach surrounding tissues (invasion), and often colonize distant sites (metastasis). Malignant tumor cells generally metastasize via lymphatic and/or vascular systems. During the hematogenous phase of metastasis, tumor cells undergo extensive cell-cell (such as tumor cell-tumor cell, tumor cell-stromal cell, tumor cell-platelet, tumor cell-EC) and cell-ECM interactions. 1 - 3 These interactions are mediated by a wide spectrum of surface adhesion molecules 4 present on both tumor cells and host cells, in particular target organ microvascular endothelial cells. 5 - 7 Therefore, adhesions are involved essentially, although at different levels, in all of the tumor cell-host cell interactions. In fact, cell adhesion is the fundamental process of all biological systems. Altered adhesion could result in a loss of cell-cell contact, an increase in cell motility, and a commitment to the first step of invasion. Also, altered adhesion could enhance tumor cell interaction with platelets, augment tumor cell lodgement in the microvasculature and adhesion to endothelium, establish tumor cell linkage with subendothelial matrix, and lead to tumor cell extravasation.
