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Lymphangiogenesis in human gynaecological cancers

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Abstract

The metastatic spread of tumor cells is responsible for the majority of cancer deaths, and with few exceptions, all cancers can metastasize. Clinical findings have for a long time suggested that by providing a pathway for tumor cell dissemination, tumor-associated lymphatics act as key components of metastatic spread. This is believed to occur principally via pre-existing and possibly also newly formed lymphatics (lymphangiogenesis). Increased expression of vascular endothelial growth factor-C (VEGF-C) and VEGF-D in primary tumors correlates with increased dissemination of tumor cells to regional lymph nodes (LNs) in a variety of human carcinomas. Here we will review the mechanisms of lymphangiogenesis, particularly in the context of metastatic tumor spread, and will critically examine the role of VEGF-C and VEGF-D in this process in gynaecological cancers. Potential anti-lymphangiogenic strategies are also discussed.

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Acknowledgements

Work in the authors’ laboratories was supported by grants from Cancer Research UK to Philippe O. Van Trappen and the Swiss National Science Foundation to Michael S. Pepper.

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Correspondence to Michael S. Pepper.

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Correspondence to: Prof. Michael S. Pepper, NetCare Institute of Molecular Medicine, Unitas Hospital, Clifton Avenue, P.O. Box 15123, 0140 Lyttelton, Pretoria, South Africa. Tel: +27-12-677-8504; Fax: +27-12-677-8505; E-mail: mpepper@doctors.netcare.co.za

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Trappen, P.O.V., Pepper, M.S. Lymphangiogenesis in human gynaecological cancers. Angiogenesis 8, 137–145 (2005). https://doi.org/10.1007/s10456-005-9008-7

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