Journal
MOLECULAR ONCOLOGY
Volume 1, Issue 3, Pages 288-302Publisher
WILEY
DOI: 10.1016/j.molonc.2007.10.003
Keywords
Vascular endothelial growth factor; Macrophages; Mammary; Tumor; Angiogenesis; Malignancy; Mouse; PyMT; Progression; Transgenic
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Funding
- NCI [CA RO1 94173, CA PO1 100324]
- Albert Einstein Cancer Center Core grant [P30 CA 13330]
- Betty and Sheldon Feinberg senior faculty scholar in cancer research
- Miriam Mandel Scholar for 2006-2007
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Genetic depletion of macrophages in Polyoma Middle T oncoprotein (PyMT)-induced mammary tumors in mice delayed the angiogenic switch and the progression to malignancy. To determine whether vascular endothelial growth factor A (VEGF-A) produced by tumor-associated macrophages regulated the onset of the angiogenic switch, a genetic approach was used to restore expression of VEGF-A into tumors at the benign stages. This stimulated formation of a high-density vessel network and in macrophage-depleted mice, was followed by accelerated tumor progression. The expression of VEGF-A led to a massive infiltration into the tumor of leukocytes that were mostly macrophages. This study suggests that macrophage-produced VEGF regulates malignant progression through stimulating tumor angiogenesis, leukocytic infiltration and tumor cell invasion. (C) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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