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      Inhibition of tumour invasion and angiogenesis by epigallocatechin gallate (EGCG), a major component of green tea.

      International Journal of Experimental Pathology

      Angiogenesis Inhibitors, therapeutic use, Anticarcinogenic Agents, Catechin, analogs & derivatives, Humans, Neoplasm Invasiveness, prevention & control, Neoplasms, blood supply, Neovascularization, Pathologic, Phytotherapy, Plant Extracts, Tea, chemistry

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          Abstract

          Epidemiological studies have suggested that consumption of green tea may decrease cancer risk. In addition, abundant pre-clinical data from several laboratories have provided convincing evidence that polyphenols present in green tea afford protection against cancer in both in vivo and in vitro studies. Recently, epigallocatechin gallate (EGCG), a putative chemopreventive agent and a major component of green tea, was reported to inhibit tumour invasion and angiogenesis, processes that are essential for tumour growth and metastasis. Understanding the basic principles by which EGCG inhibits tumour invasion and angiogenesis may lead to the development of new therapeutic strategies, in addition to supporting the role of green tea as a cancer chemopreventive agent.

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          Most cited references 37

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          Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo.

           G Breier,  H Weich,  W Risau (1992)
          Clinical and experimental studies suggest that angiogenesis is a prerequisite for solid tumour growth. Several growth factors with mitogenic or chemotactic activity for endothelial cells in vitro have been described, but it is not known whether these mediate tumour vascularization in vivo. Glioblastoma, the most common and most malignant brain tumour in humans, is distinguished from astrocytoma by the presence of necroses and vascular proliferations. Here we show that expression of an endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), is induced in astrocytoma cells but is dramatically upregulated in two apparently different subsets of glioblastoma cells. The high-affinity tyrosine kinase receptor for VEGF, flt, although not expressed in normal brain endothelium, is upregulated in tumour endothelial cells in vivo. These observations strongly support the concept that tumour angiogenesis is regulated by paracrine mechanisms and identify VEGF as a potential tumour angiogenesis factor in vivo.
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            The implications of angiogenesis for the biology and therapy of cancer metastasis.

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              Angiogenesis inhibited by drinking tea.

               Yu Cao,  Zhirong Cao (1999)
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                Author and article information

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                11846837
                2517785

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