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Local chronic inflammation can act as a high cancer risk factor. The basis of this pathogenic effect is under investigation. This review examines the evidence that chronic inflammation is capable of inducing the complex of microenvironmental changes similar to those seen around growing cancer cells. The changes include: enhanced oxidative cell resistance against apoptosis; switch to glycolytic metabolism, neovasculogenesis and vasorelaxation which provide nutrient delivery but restrict the immune/inflammatory cell recruiting. These synergistic changes can act as a counter balancing force to self-limit the cytotoxic response by normally acute inflammation. However, the duration and intensity of this force can become insufficient to restrict the prolonged cytotoxic response by chronic inflammation. The hypothetic model of the latter effects is presented as a result of discoordinated feedback regulation among heme-, prostaglandin E2-, nitric oxide-, carbon monoxide-, and polyamine-dependent enzymatic pathways in the growth inhibiting (cytotoxic) and growth promoting (regenerative) stages of acute or chronic inflammatory response. According to this model, chronic inflammation is capable of generating a potentially 'vicious self-sustaining loop(s)' which are resulted in the pro-cancer microenvironment favorable for survival of tumor cells and their growth. |
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