Abstract
When tumor cells are injected into a syngeneic recipient, an inflammatory response occurs at the site of injection (1). The sequence of events and the types of cells entering the lesion are fairly typical of that seen during wound healing (2). Both tumor growth and wound healing involve changes in blood vessel permeability, as well as proliferation of vascular endothelial cells, influx of leukocytes and plasma constituents, and proliferation of cells such as fibroblasts and epithelial cells. In both situations these reactions probably involve the release of vasoactive amines (by platelets and mast cells), arachidonic acid or prostaglandins (by macrophages, mast cells and perhaps tumor cells), activation of the complement, coagulation, fibrinolytic and kinin systems, and the release of mediators controlling or stimulating cellular proliferation. It has been reported in tumor model systems (3) and during wound healing (2) that prevention of macrophage infiltration at the site may result in impaired growth or repair, implying an important role for macrophages in these reactions.
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References
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Evans, R., Brit. J. Cancer 37:1086, 1978.
Evans, R., and Eidlen, D. M., J. Reticuloendothelial Soc. 301:425, 1981.
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© 1982 Plenum Press, New York
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Evans, R., Eidlen, L.G. (1982). The Role of the Inflammatory Response During Tumor Growth. In: Normann, S.J., Sorkin, E. (eds) Macrophages and Natural Killer Cells. Advances in Experimental Medicine and Biology, vol 155. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4394-3_39
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DOI: https://doi.org/10.1007/978-1-4684-4394-3_39
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4684-4396-7
Online ISBN: 978-1-4684-4394-3
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