Tumor angiogenesis: molecular pathways and therapeutic targets

Vascular Endothelial Growth Factor C Disrupts the Endothelial Lymphatic Barrier to Promote Colorectal Cancer Invasion

“…However, while the role of the vascular endothelium in cancer progression is well described 26 , the contribution of tumoral LVs is still unclear. In many types of human cancers, including CRC 3-5 , the expression of VEGFC 2 and its receptor, VEGFR3 25,27 , correlates with lymphangiogenic sprouting, metastases and poor prognosis.…”

Carcinogenesis of renal cell carcinoma reflected in HLA ligands: A novel approach for synergistic peptide vaccination design

“…These included LOX and PLOD2, with high potential in engaging metastasis, [36][37][38] GRB2, ITPR3, and BCAR1, all of which are part of the EGFR pathway 39 and other growth factor receptor pathways, plus ENPEP, NRP2, TGFBI, THBS1, and THBS2, which are essential for angiogenesis. 40 It is notable that 16 out of 24 peptides listed in Table 3 were only found in one tissue sample each. Network analysis suggests that other proteins involved in the pathway could also be active in the same tissue sample but were not detected due to lack of sensitivity or the selectivity of antigen processing.…”

The biology of personalized cancer medicine: Facing individual complexities underlying hallmark capabilities

“…Furthermore, the endothelial cells of tumor blood vessels can display features –fenestration patterns, pericyte and inflammatory‐cell association, proliferation and apoptosis rates, and gene expression profiles – that vary not only among different tumor types or individual tumors, but also in a local–regional manner within a given tumor. Such heterogeneity may be influenced by the site in which a tumor arises (i.e., the specific organ or tissue microenvironment), the tumor growth stage, the biophysical properties of the surrounding stroma (e.g., interstitial pressure, collagen cross‐linking and extra‐cellular matrix tension), and many other ill‐defined spatiotemporal differences such as angiogenic gene expression by tumor and stromal cells (Carmeliet and Jain, 2011a; Chung and Ferrara, 2011; Hanahan and Weinberg, 2011; Kerbel, 2008; Leite de Oliveira et al., 2011; McDonald and Choyke, 2003; Nagy et al., 2010; Potente et al., 2011; Weis and Cheresh, 2011). As a consequence of these many variables affecting vascular phenotypes, experimental tumors growing subcutaneously in mice may differ significantly from spontaneous tumors in terms of vascular density, functionality, phenotype, and gene expression.…”