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. 2019 Nov 7;9:1185. doi: 10.3389/fonc.2019.01185

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Copyright © 2019 Langsten, Kim, Sarver, Dewhirst and Modiano.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic of the interaction between tumor cells and endothelial cells, including the associated recruitment of inflammatory cells by endothelium. Through hypoxia, HIF-1 is upregulated, increasing PDGF, FGF, TGFβ, and VEGF-A expression. VEGF-A binds to its receptors, VEGFR-1 and VEGFR-2, leading to angiogenesis (through VEGFR-2 signaling), immune cell invasion (through VEGFR-1 signaling), and promotion of epithelial-mesenchymal transition (EMT) in tumor cells (created with Biorender.com).