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Targeting lymphangiogenesis to prevent tumour metastasis

Recent studies involving animal models of cancer and clinicopathological analyses of human tumours suggest that the growth of lymphatic vessels (lymphangiogenesis) in or nearby tumours is associated with the metastatic spread of cancer. The best validated molecular signalling system for tumour lymph...

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Detalles Bibliográficos
Autores principales: Achen, M G, Mann, G B, Stacker, S A
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361285/
https://www.ncbi.nlm.nih.gov/pubmed/16641900
http://dx.doi.org/10.1038/sj.bjc.6603120
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author Achen, M G
Mann, G B
Stacker, S A
author_facet Achen, M G
Mann, G B
Stacker, S A
author_sort Achen, M G
collection PubMed
description Recent studies involving animal models of cancer and clinicopathological analyses of human tumours suggest that the growth of lymphatic vessels (lymphangiogenesis) in or nearby tumours is associated with the metastatic spread of cancer. The best validated molecular signalling system for tumour lymphangiogenesis involves the secreted proteins vascular endothelial growth factor-C (VEGF-C) and VEGF-D that induce growth of lymphatic vessels via activation of VEGF receptor-3 (VEGFR-3) localised on the surface of lymphatic endothelial cells. In this review, we discuss the evidence supporting a role for this signalling system in the spread of cancer and potential approaches for blocking this system to prevent tumour metastasis.
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spelling pubmed-23612852009-09-10 Targeting lymphangiogenesis to prevent tumour metastasis Achen, M G Mann, G B Stacker, S A Br J Cancer Review Recent studies involving animal models of cancer and clinicopathological analyses of human tumours suggest that the growth of lymphatic vessels (lymphangiogenesis) in or nearby tumours is associated with the metastatic spread of cancer. The best validated molecular signalling system for tumour lymphangiogenesis involves the secreted proteins vascular endothelial growth factor-C (VEGF-C) and VEGF-D that induce growth of lymphatic vessels via activation of VEGF receptor-3 (VEGFR-3) localised on the surface of lymphatic endothelial cells. In this review, we discuss the evidence supporting a role for this signalling system in the spread of cancer and potential approaches for blocking this system to prevent tumour metastasis. Nature Publishing Group 2006-05-22 2006-04-25 /pmc/articles/PMC2361285/ /pubmed/16641900 http://dx.doi.org/10.1038/sj.bjc.6603120 Text en Copyright © 2006 Cancer Research UK https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Review
Achen, M G
Mann, G B
Stacker, S A
Targeting lymphangiogenesis to prevent tumour metastasis
title Targeting lymphangiogenesis to prevent tumour metastasis
title_full Targeting lymphangiogenesis to prevent tumour metastasis
title_fullStr Targeting lymphangiogenesis to prevent tumour metastasis
title_full_unstemmed Targeting lymphangiogenesis to prevent tumour metastasis
title_short Targeting lymphangiogenesis to prevent tumour metastasis
title_sort targeting lymphangiogenesis to prevent tumour metastasis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361285/
https://www.ncbi.nlm.nih.gov/pubmed/16641900
http://dx.doi.org/10.1038/sj.bjc.6603120
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