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Tumor necrosis factor (TNF , TNF -a , cachectin ) is a pleiotropic pro-inflammatory cytokine produced mainly by activated macrophages and monocytes. In addition to functioning immonomodulacyjnego TNF also has antitumor effect by inhibiting the growth of certain tumors , and even causing regression . TNF Therefore , in spite of its toxicity , is used in cancer therapy , mainly non-operative limb sarcomas and melanomas . Analysis of the data obtained in different experimental models allowed to distinguish three main mechanisms of action of TNF for modulating tumor growth : 1 ) a direct toxic effect on tumor cells , 2 ) an indirect effect caused by the influence on the immune system , and 3 ) an indirect effect caused by affecting the vascular tumor . This paper presents the mechanisms of antitumor action of TNF , focusing on the effects exerted on the tumor vascular bed . TNF acts directly cytostatic or cytotoxic effect on the vascular endothelial cells , or indirectly by modulation of neutrophil function . TNF also affect angiogenesis leading to the development of the tumor vasculature . TNF also influences blood coagulation and fibrinolysis , modifying blood flow to the tumor tissue . TNF increases tumor tissue infiltration by immune cells at the same time modulating the activity of these cells. By influencing the expression of adhesion molecules on endothelial cells and tumor cells modified TNF metastatic process . Action exerted by TNF against tumor vascular are most likely independent of the sensitivity of tumor cells to direct the TNF toxicity . Detailed knowledge of the impact of TNF on vascular tumors is therefore of great practical importance , because the tumor vessels may be universal destination therapy.
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The Editorial Board
Andrzej Łukaszyk - przewodniczący, Zofia Bielańska-Osuchowska, Szczepan Biliński, Mieczysław Chorąży, Aleksander Koj, Włodzimierz Korochoda, Leszek Kuźnicki, Aleksandra Stojałowska, Lech Wojtczak

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