Abstract
Tumor neovascularization plays critical roles for the development, progression and metastasis of cancers via utilizing blood flow to supply nutrients and oxygen. Recent cumulative information on biology of tumor neovascularization from both laboratory and clinical studies has opened us to develop new therapeutic approaches to treat malignancies by controlling angiogenic activities; i.e., a humanized monoclonal antibody bevacizumab specifically targeting VEGF (vascular endothelial growth factor), as well as several tyrosine kinase inhibitors targeting VEGF-related pathways. It is obvious that VEGF is a key molecule for tumor neovascularization, however, strategies targeting VEGF may be a milestone and not a goal for antiangiogenic approach, because it has been elucidated the complexity of cancer microenvironments that mediate neovascularization and blood-borne metastasis. Specific subsets of chemoattractants recruit hematopoietic cells from the BM (bone marrow) that support tumor neovascularization in the primary lesion, and these mobilized cells are suggested to participate in pre-metastatic niche formation for circulating tumor cells. To establish safe and effective antiangiogenic therapies, it is important to understand the cross-communication between tumors and hosts that mediate proinflammatory milieu of both primary and metastatic lesions. This review discusses special features of tumor angiogenic vessels and their microenvironments, and in addition, recent topics including contribution of BM-derived cells, special mesenchymal cells and their chemoattractants that activate tumor vascular beds are summarized.
Keywords: Neovascularization, angiogenesis, tumor, endothelial cells, endothelial progenitor cells, hematopoietic cells, mesenchymal cells, chemokines
Current Cancer Drug Targets
Title: Cancer Neovascularization and Proinflammatory Microenvironments
Volume: 8 Issue: 4
Author(s): Mitsuko Furuya and Yoshikazu Yonemitsu
Affiliation:
Keywords: Neovascularization, angiogenesis, tumor, endothelial cells, endothelial progenitor cells, hematopoietic cells, mesenchymal cells, chemokines
Abstract: Tumor neovascularization plays critical roles for the development, progression and metastasis of cancers via utilizing blood flow to supply nutrients and oxygen. Recent cumulative information on biology of tumor neovascularization from both laboratory and clinical studies has opened us to develop new therapeutic approaches to treat malignancies by controlling angiogenic activities; i.e., a humanized monoclonal antibody bevacizumab specifically targeting VEGF (vascular endothelial growth factor), as well as several tyrosine kinase inhibitors targeting VEGF-related pathways. It is obvious that VEGF is a key molecule for tumor neovascularization, however, strategies targeting VEGF may be a milestone and not a goal for antiangiogenic approach, because it has been elucidated the complexity of cancer microenvironments that mediate neovascularization and blood-borne metastasis. Specific subsets of chemoattractants recruit hematopoietic cells from the BM (bone marrow) that support tumor neovascularization in the primary lesion, and these mobilized cells are suggested to participate in pre-metastatic niche formation for circulating tumor cells. To establish safe and effective antiangiogenic therapies, it is important to understand the cross-communication between tumors and hosts that mediate proinflammatory milieu of both primary and metastatic lesions. This review discusses special features of tumor angiogenic vessels and their microenvironments, and in addition, recent topics including contribution of BM-derived cells, special mesenchymal cells and their chemoattractants that activate tumor vascular beds are summarized.
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Cite this article as:
Furuya Mitsuko and Yonemitsu Yoshikazu, Cancer Neovascularization and Proinflammatory Microenvironments, Current Cancer Drug Targets 2008; 8 (4) . https://dx.doi.org/10.2174/156800908784533481
DOI https://dx.doi.org/10.2174/156800908784533481 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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