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Abstract

The development of a tumor is dependent on a number of genetic and epigenetic changes. An important step for the propagation and progression of many solid tumors is the induction of a tumor vasculature, i.e., “the angiogenic switch” (1,2). This ensures an adequate supply of oxygen and metabolites for tumor growth and metastasis. This switch is activated when the angiogenic balance tips in favor of proangiogenesis; this results in the increased production of proangiogenic factors and/or downregulation of antiangiogenic factors. The angiogenic switch may occur at any stage of tumor progression, depending on the nature of the tumor and the microenvironment. However, tumor angiogenesis differs from physiological angiogenesis in several respects: the vascular structure, the endothelial cell and pericyte interactions, blood flow, increased permeability, and delayed maturation (36; Table 1).

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