Tumor cell 6-Turn

Kushtai, G., Feldman, M. and Eisenbach, L. (1990) c-fos transfection of 3LL tumor cells turns on MHC gene expression and consequently reduces their metastatic competence. Int. J. Cancer, 45,1131-1136. 

In 1965 1967 a great interest has been attached to the possible role of free radicals in cancer after studies by Emanuel and his coworkers who reported the excessive production of free radicals in tumor cells (see, for example, Ref. [145]). On these grounds the authors suggested to apply antioxidant therapy for the treatment of cancer patients. Unfortunately, experimental proofs of overproduction of free radicals in cancer tissue turn out to be erroneous [146], A new interest in the role of free radicals in cancer development emerged after the discovery of superoxide and superoxide dismutases. 

One of the important relay stations in the immune system activation is the dendritic cell. Activation of these cells causes the most efficient stimulation of T-cells, which in turn attack tumor cells (9). This turned the dendritic cells (DCs) into the focus of modern immune research and therapy. However, another difficulty appeared that became a problem recently. In order to activate the dendritic cell, the antigen has to be present in the cytosol and has to be processed there further this is not an easy task to perform. 

Possible biochemical mechanisms of resistance to alkylating agents include changes in ceU DNA repair capability, increases in cell thiol content (which in turn can serve as alternative and benign targets of alkylation), decreases in ceU permeability, and increased activity of glutathione transferases. Increased metaUothionein content has been associated with tumor cell resistance to cisplatin. 

Bacillus Calmette-Guerin (BCG) is a viable attenuated strain of Mycobacterium bovis. Nonviable strains of the bacterium also have been shown to augment the immune response. The smallest active compound derived from BCG thus far has been identified as muramyl dipeptide. The T cell is a principal target for BCG. It also appears to stimulate natural killer cells, which in turn can kill malignant cells. It has been suggested that BCG cross-reacts immunologically with tumor cell antigens. 

Squalene supplementation is suggested to be accounted for tumor growth inhibition and prevention of normal cells to turn into tumor cells under oxidative stress. Although there is lack of evidence for human trials to show anticancer and antioxidant effects of squalene, animal models and in vitro experiments highlight a significant activity which urges for further exploration. 

Apart from the possible use of polymerized vesicles as stable models for biomembranes (Sect. 4) there may be a variety of different applications. Polymerized surfactant vesicles have been proposed to act as antitumor agents on a cellular level33 in analogy to the action of the immune system of mammals against tumor cells 85). Polymerized vesicles open the door to chemical membrane dissymmetry 22) which in turn, may lead to enhanced utility in photochemical energy transfer84 (solar energy conversion, artificial photosynthesis). The utilization of unpolymerized lipo-... 

Variations in the expression of angiogenic factors may modulate tumor vascularization and therefore oxygenation. This, in turn, may contribute to differing responsiveness to treatments between different tumor cell types. For example, increased radioresistance in pancreatic carcinoma cell lines was associated with an increased expression of angiopoietin (Ang)-2, which plays an important role in vascular maturation [56]. 

Fig. 2 Schematic illustration of the possible role of K+ channels in [Ca2+]j, cell volume regulation and intracellular alkalization in tumor cells. Activation of K+ channels causes membrane hyperpolarization that in turn increases Ca2+ entry by increasing the driving force for Ca2+ and causes H+ extrusion by enhancing Na+/H+ exchanger activity leading to intracellular alkalization increased Ca2+ entry and intracellular alkalization induce Ca2+ release from Ca2+ store, leading to an increase in [Ca2+]i. Activation of K+ channels also causes H2O outflow due to hypotonic cytoplasm as a result of K+ efflux, leading to cell volume regulation...

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