Abstract
Leukocyte infiltration into inflamed or injured tissues is regulated by a variety of cell-associated and soluble factors that mediate the communications between circulating leukocytes and vascular endothelial cells. Since the late 1980s, a superfamily of polypeptide leukocyte chemoattractants known as chemokines has been identified and demonstrated to selectively induce rapid endothelial cell adhesion and transmigration of leukocyte subpopulations (1). Chemokines are produced by virtually every mammalian somatic cell type in response to inflammatory and immunologic stimuli, and have been detected in tissues of numerous disease states characterized by infiltration of distinct leukocyte subsets. Chemokines bind and activate cell-surface receptors that belong to the seven-transmembrane, G protein—coupled receptor superfamily (2). Several chemokine receptors have been identified as fusion cofactors for human immunodeficiency virus. Chemokines have also been shown to play a critical role in the host interaction with malignant tumors via recruitment of immune cells into the tumor tissue, induction of angiogenesis or angiostasis, or through their direct effect on tumor cell migration and proliferation. As chemokine research is a rapidly expanding area, this chapter reviews the available information concerning the role of chemokines in tumor growth and metastasis.
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Wang, J.M., Shen, W., Chertov, O., Van Damme, J., Oppenheim, J.J. (1999). Chemokine Modulation of Tumor Cell Physiology. In: Rollins, B.J. (eds) Chemokines and Cancer. Contemporary Cancer Research. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-701-7_8
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DOI: https://doi.org/10.1007/978-1-59259-701-7_8
Publisher Name: Humana Press, Totowa, NJ
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