Pathophysiological consequences of VEGF-induced vascular permeability

By Sara M Weis, D. Cheresh. Nature, 2005

901 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/ab4196d130b2ec9c789328a278e0f5d414d109bb

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Rakesh K. Jain
2. Dai Fukumura
3. N. Ferrara
4. Sara M Weis
5. K. Alitalo
6. D. Duda
7. D. Cheresh
8. P. Steeg

In Molecular Biology

1. Rakesh K. Jain
2. N. Ferrara
3. Dai Fukumura
4. K. Alitalo
5. J. Massagué
6. D. Duda
7. Sara M Weis
8. D. Cheresh

In Oncology

1. Rakesh K. Jain
2. N. Ferrara
3. J. Massagué
4. Dai Fukumura
5. K. Alitalo
6. P. Steeg
7. T. Tammela
8. Jeremy N. Rich

Citations in the corpus

• Phase II Trial of Bevacizumab and Irinotecan in Recurrent Malignant Glioma (2007, background): “Age (y) Median (range) 49 ( 27-66 ) Gender”
• Astrocyte-derived VEGF-A drives blood-brain barrier disruption in CNS inflammatory disease. (2012, positive): “Although VEGF-A–induced vascular permeability has previously been implicated in pathogenesis of disorders, including myocardial infarction, CNS hypoxia/reperfusion injury, and tumor growth and metastasis (49), and we and others have previously speculated on its role in BBB breakdown (12, 26), this s”
• VEGF controls endothelial-cell permeability by promoting the β-arrestin-dependent endocytosis of VE-cadherin (2006, background): “In adults, deregulated expression of VEGF is involved in a variety of disease states, ranging from inflammation, oedema and thrombotic reactions to cancer and metastasi”
• Tumor microenvironment abnormalities: Causes, consequences, and strategies to normalize (2007, background): “A better understanding of the molecular mechanisms of permeability regulation in tumors is likely to yield strategies for improved delivery of molecular medicine to tumors as discussed in the following [ Weis and Cheresh, 2005 ].”
• AZD2171, a pan-VEGF receptor tyrosine kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma patients. (2007, background): “Preclinical studies have demonstrated that VEGF blockade can reduce edema due to ischemic injury (Weis and Cheresh, 2005).”
• Tumor metastasis: mechanistic insights and clinical challenges (2006, background): “VEGF-induced vascular permeability involves both intraendothelial macromoleulcar transport, resulting from caveolae and chains of vesiculovacuolar organelles, as well as interendothelial leakage resulting from reduced endothelial cell-cell adherenc”
• The role of adherens junctions and VE-cadherin in the control of vascular permeability (2008, background): “In addition, the association of VEGFR2 with VE-cadherin might facilitate the phosphorylation of AJ components by SRC (Weis and Cheresh, 2005), and might thereby impair endothelial-barrier function.”
• Cancer metastasis: building a framework. (2006, background): “Are there signals emanating from metastatic cells that actively induce changes in the vascular permeability of blood vessels in target organs? VEGF—initially identified as a potent vascular permeability factor—is one prime candidate (Weis and Cheresh, 2005).”
• Tumor angiogenesis: molecular pathways and therapeutic targets (2011, background): “Although the induction of angiogenesis may initially provide the tumor with more oxygen and nutrients, the ultimate response is poor, as the continuously remodeled tumor vasculature is leaky and tortuous, causing irregular blood flo”
• Lymphangiogenesis in development and human disease (2005, background): “The pathophysiology of vascular permeability has been recently reviewed elsewher”