Thursday, April 20, 2017 1:48:50 PM
http://www.medscape.com/viewarticle/582339
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Since angiogenesis is virtually absent in normal adults, antiangiogenic therapy is more tumor-specific and yields a low toxicity profile. Different antiangiogenic strategies have been developed: inhibition of proangiogenic factors and/or receptors and/or downstream cell signaling; inactivation of ECs; and inhibition of cellular adhesion molecules and/or ECM remodeling. Inhibitors of angiogenesis are separated into endogenous inhibitors, such as angiostatin, trombospondin or IFN-a; and natural or synthetic inhibitors, such as THD, antibodies against angiogenic growth factors or inhibitors of tyrosine kinase receptors.
No clear benefits for patients have been reported regarding the use of single antiangiogenic drugs. Interestingly, the levels of angiogenic molecules in circulating blood from patients with tumors have been shown to increase significantly in response to antiangiogenic treatment.[103] The mechanisms involved in this phenomenon are not known. The role of the third compartment (i.e., pericytes, microglia and astrocytes) as well as endothelial and tumor cells remains unclear. Furthermore, several mechanisms are involved in angiogenesis, and the targeting of one molecule or pathway may lead to the increased activity of other pathways, which may then sustain angiogenesis. It seems likely that a combination of these antiangiogenic agents with chemotherapy seems to be more efficient.
Antiangiogenic therapy has been demonstrated to represent a promising novel approach to the treatment of malignant brain tumors. It seems likely that a combination of antiangiogenic agents with other cytotoxic therapies will be required to achieve maximal efficacy. Antiangiogenic compounds are not expected to reduce the tumor burden but, rather, to exert a cytostatic effect. A crucial issue is, therefore, the search for end points and surrogate markers as indicators of biological response and anti-tumor activity.
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