Download Eicosanoids, Lipid Peroxidation and Cancer by V. Ullrich, M. Hecker, R. Nüsing, T. Rosenbach (auth.), PDF

By V. Ullrich, M. Hecker, R. Nüsing, T. Rosenbach (auth.), Santosh K. Nigam Ph.D., M.B., B.Ch., David C. H. McBrien Ph.D., Trevor F. Slater Ph.D., D.Sc., M.D.(Hon.) (eds.)

This quantity will give you up to date, specialist experiences of this fast-moving field.The major subject matters are according to the interrelationships among arachidonate metabolism, platelet-activating issue, lipid peroxidation and melanoma. The stories supply important details for the professional and also will be of price to a large viewers attracted to advancements in cellphone biology, pharmacology, pathology, biochemistry and melanoma.

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Extra info for Eicosanoids, Lipid Peroxidation and Cancer

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The mechanism of platelet facilitated metastasis is unknown, although several hypotheses have been set forth. Honn et al. (1984) have suggested that platelets staNigam et al. ), Eicosanoids, Lipid Peroxidation and Cancer © Springer-Verlag Berlin Heidelberg 1988 30 K. V. Honn et al. bilize the attachment of tumour cells to endothelial cells and subendothelial matrix. Evidence for this mechanism has been demonstrated by Menter et al. (1987 a, b). The participation of platelets in tumour cell arrest has suggested that some form of antiplatelet therapy may be efficacious in reducing tumour cell metastasis.

Averdunk ity for regressive tumours but not for progressive ones. Further evidence supporting this assumption comes from our investigations with the inoculation of subcellular fractions of tumour cells into the rats (Table 5). The 150000g membrane fraction stimulated eicosanoid synthesis in the rats 2 h after the inoculation, suggesting that host cells are activated in a manner similar to tumour cells. Thus, these findings rule out in vivo elevation of plasma eicosanoids due to increased overall metabolism of arachidonic acid in tumour cells.

Submitted). Mehta and coworkers (1983, 1984) determined in vitro that the PGI 2 biosynthetic capability of vessels removed from patients with osteogenic sarcoma was less than that of vessels removed from patients without cancer. 1. Effect of TXSI (CGS 14854) and LOX (quercetin) inhibitors on Walker 256 carcinosarcoma-induced platelet aggregation. Aggregation of homologous plateletrich plasma was induced by 5 x 105 tumour cells. c g> 20 CGS14854 + QUERCETIN 10 O~---T/-d~------·5 o 5 10 15 time (min) normal controls.

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