Organ-Specific Requirements for Cell Adhesion Molecules During Lymphoma Cell Dissemination
The malignant process is, in many aspects, a distorted image of normal physiological activities. In this respect, the dissemination mechanism of malignant lymphomas may display a hazy reflection of normal cell migration, an essential function of the lymphoid system. The successful response of the individual’s defense machinery against invading microorganisms is largely due to its ability to rapidly mobilize leukocytes to the site of infection. Cell motility in blood, lymph, lymphoid organs and tissues is highly dependent on the coordinated activity of different cell adhesion molecules. These are implicated in the transendothelial migration of intravasated and extravasated cells, the capture of cells by the luminal surface of the endothelium, cell rolling and cell arrest in the vasculature, binding of lymphocytes to the high endothelial venule (HEV) of the lymph node, as well as subsequent cell lodgment in organ parenchyma (a process known as cell homing), and cell migration on extracellular matrix (ECM) (Parkhurst and Saltzman 1992; Picker and Butcher 1992; Thomas et al. 1992; Springer 1994; Ley and Tedder 1995). Three pairs of adhesion receptor and counterreceptor families are implicated in the interaction between leukocytes and their target cells in the endothelium and tissues: (1) integrins, which target molecules of the immunoglobulin superfamily (IgSF) or ECM components, (2) selectins, which interact with sialylated carbohydrate determinants O-linked to mucin-like molecules (also known as addressins), and (3) CD44 receptors with binding affinity for matrix and cell surface constituents (Ruoslahti 1991; Yamada 1991; Picker and Butcher 1992; Lesley et al. 1993; Springer 1994; Naor et al. 1997).
KeywordsMigration Heparin Oncol Lysine Arginine
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