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1 National Institute for Research on Cancer (IST), Genoa, Italy and 2 Università degli Studi dell'Insubria, Varese, Italy
Requests for reprints: Adriana Albini, Molecular Oncology Laboratory, National Cancer Research Institute, Largo Rosanna Benzi 10, 16132 Genoa, Italy. Phone: 39-105-737-7367; Fax: 39-105-737-7231; E-mail: adriana.albini{at}istge.it.
The importance of angiogenesis for the growth of tumors is widely recognized. Drugs that successfully target the endothelium, such as antivascular endothelial growth factor antibodies, are beginning to have an effect on the life expectancy of cancer patients. However, the endothelial cell is not the only possible target for antiangiogenic therapy or prevention of vascularization (angioprevention). It is evident from the literature that native immune cells recruited into tumors in turn stimulate the endothelium and are responsible for an indirect pathway of tumor vascularization. Inflammation-dependent angiogenesis seems to be a central force in tumor growth and expansion, a concept supported by the observation that the use of "classic" anti-inflammatory drugs, such as nonsteroidal anti-inflammatory drugs, leads to angiogenesis inhibition. The mechanisms of inflammatory angiogenesis provide new approaches to target, cure, or even better, prevent tumor angiogenesis by treatment with synthetic or natural agents with anti-inflammatory properties. We propose chemoprevention of inflammatory angiogenesis as a way of checking the cancer before it progresses.
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