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Host microenvironment in breast cancer development: Inflammatory and immune cells in tumour angiogenesis and arteriogenesis

Breast cancer progression is associated with and dependent upon robust neovascularization. It is becoming clear that tumour-associated 'normal' cells, such as immune/inflammatory cells, endothelial cells and stromal cells, conspire with cancer cells in promoting this process. In particular...

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Detalles Bibliográficos
Autores principales: Yu, Joanne L, Rak, Janusz W
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC154151/
https://www.ncbi.nlm.nih.gov/pubmed/12631386
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author Yu, Joanne L
Rak, Janusz W
author_facet Yu, Joanne L
Rak, Janusz W
author_sort Yu, Joanne L
collection PubMed
description Breast cancer progression is associated with and dependent upon robust neovascularization. It is becoming clear that tumour-associated 'normal' cells, such as immune/inflammatory cells, endothelial cells and stromal cells, conspire with cancer cells in promoting this process. In particular, infiltrating immune/inflammatory cells secrete a diverse repertoire of growth factors and proteases that enable them to enhance tumour growth by stimulating angiogenesis and, as we suggest here, by promoting 'tumour arteriogenesis' – enlargement of feeding vessels supplying the expanding tumour capillary bed. Macrophages and their chemoattractants (e.g. macrophage chemoattractant protein-1) are critical for the arteriogenic process in ischaemia, and probably also in breast neoplasia. A better understanding of these various cellular and molecular constituents of breast cancer neovascularization may be useful in designing more effective therapies.
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spelling pubmed-1541512003-05-06 Host microenvironment in breast cancer development: Inflammatory and immune cells in tumour angiogenesis and arteriogenesis Yu, Joanne L Rak, Janusz W Breast Cancer Res Review Breast cancer progression is associated with and dependent upon robust neovascularization. It is becoming clear that tumour-associated 'normal' cells, such as immune/inflammatory cells, endothelial cells and stromal cells, conspire with cancer cells in promoting this process. In particular, infiltrating immune/inflammatory cells secrete a diverse repertoire of growth factors and proteases that enable them to enhance tumour growth by stimulating angiogenesis and, as we suggest here, by promoting 'tumour arteriogenesis' – enlargement of feeding vessels supplying the expanding tumour capillary bed. Macrophages and their chemoattractants (e.g. macrophage chemoattractant protein-1) are critical for the arteriogenic process in ischaemia, and probably also in breast neoplasia. A better understanding of these various cellular and molecular constituents of breast cancer neovascularization may be useful in designing more effective therapies. BioMed Central 2003 2003-02-03 /pmc/articles/PMC154151/ /pubmed/12631386 Text en Copyright © 2003 BioMed Central Ltd
spellingShingle Review
Yu, Joanne L
Rak, Janusz W
Host microenvironment in breast cancer development: Inflammatory and immune cells in tumour angiogenesis and arteriogenesis
title Host microenvironment in breast cancer development: Inflammatory and immune cells in tumour angiogenesis and arteriogenesis
title_full Host microenvironment in breast cancer development: Inflammatory and immune cells in tumour angiogenesis and arteriogenesis
title_fullStr Host microenvironment in breast cancer development: Inflammatory and immune cells in tumour angiogenesis and arteriogenesis
title_full_unstemmed Host microenvironment in breast cancer development: Inflammatory and immune cells in tumour angiogenesis and arteriogenesis
title_short Host microenvironment in breast cancer development: Inflammatory and immune cells in tumour angiogenesis and arteriogenesis
title_sort host microenvironment in breast cancer development: inflammatory and immune cells in tumour angiogenesis and arteriogenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC154151/
https://www.ncbi.nlm.nih.gov/pubmed/12631386
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