Inhibition of vascular endothelial growth factor (VEGF) signaling in cancer causes loss of endothelial fenestrations, regression of tumor vessels, and appearance of basement membrane ghosts.

By T. Inai, Michael R. Mancuso, H. Hashizume, F. Baffert, A. Haskell, P. Baluk, D. Hu-Lowe, D. Shalinsky, Gavin Thurston, G. Yancopoulos and 1 more. American Journal of Pathology, 2004

759 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f959f75d6d8aa0fbdfd4428f047a48e651f4264f

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Citations in the corpus

High interstitial fluid pressure — an obstacle in cancer therapy (2004, background): “Interestingly, treatment of islet-cell tumours of RIP-Tag2 transgenic mice with an antibody against VEGF led to decreased fenestration of endothelial cells, consistent with a decreased vessel permeabilit”
Autocrine VEGF signaling is required for vascular homeostasis. (2007, neutral): “VEGF is an integral component of tumor angiogenesis and its inhibition results in reduction of tumor burden subsequent to the regression of some tumor vessels and improved drug delivery (Inai et al., 2004; Jain, 2001).”
Tumor angiogenesis and vascular normalization: alternative therapeutic targets (2017, background): “the perivascular basement membrane can also present profound structural abnormalities with irregular thickness and some perforations [41, 42].”
Improving Conventional Enhanced Permeability and Retention (EPR) Effects; What Is the Appropriate Target? (2013, background): “(23-25) Perivascular smooth muscle is often lacking in these vessels making them poorly reactive to stimuli.”
AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer. (2005, background): “These include regression of existing tumor vessels with a VEGFR-Fc fusion construct in tumor bearing RIP-Tag2 transgenic mice (58), a KDR blocking antibody in squamous cell tumor xenografts (59), and a VEGF-neutralizing antibody in LS174T colon tumor xenografts (60).”
VEGF-dependent plasticity of fenestrated capillaries in the normal adult microvasculature. (2006, methodology): “The organs and tumors used for immunohistochemistry were rinsed several times with PBS, infiltrated with 30% sucrose, and frozen in optimal cutting temperature compound (30).”
Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation. (2005, neutral): “cryostat sections with 1 or more primary antibodies (52): (a) lymphatic ves-”
Kinetics of vascular normalization by VEGFR2 blockade governs brain tumor response to radiation: role of oxygenation, angiopoietin-1, and matrix metalloproteinases. (2004, background): “…those of tumor hypoxia.man tumors, that VEGF signal blockade increases the fraction The mechanisms responsible for the increase in pericyteof vessels that are covered with closely attached perivascular cells (Tong et al., 2004; Willett et al., 2004; Inai et al., 2004), coverage are largely unknown.”
Axitinib is an active treatment for all histologic subtypes of advanced thyroid cancer: results from a phase II study. (2008, result): “Concomitant studies producing similar results by VEGF-Trap support the contention that axitinib exerts its antiangiogenic activity by inhibiting VEGF receptor signaling.(17) A phase I trial of 36 patients with advanced solid tumors identified axitinib 5 mg twice daily as the starting clinical dose a”
Mechanisms of adverse effects of anti-VEGF therapy for cancer (2007, methodology): “Vascular endothelial growth factor (VEGF) not only drives angiogenesis, but also serves as a survival factor for endothelial cells and promotes the abnormal phenotype of blood vessels in tumours (Inai et al, 2004).”
Tumor microenvironment abnormalities: Causes, consequences, and strategies to normalize (2007, background): “More recently, seven independent laboratories have published data that support our findings on vascular normalization using a variety of anti-angiogenic drugs and animal models [Wildiers et al., 2003; Inai et al., 2004; Ansiaux et al., 2005; Bang et al., 2005; Huber et al., 2005; Salnikov et al., ”
Cellular abnormalities of blood vessels as targets in cancer. (2005, background): “Inhibition of VEGF signaling causes robust and rapid changes in all components of the wall of tumor vessels (Figure 1c) [46 ].”
Disrupting tumour blood vessels (2005, background): “html">Pfizer compound AG013736, a broad-spectrum receptor tyrosine kinase inhibito”