Direct evidence that the VEGF-specific antibody bevacizumab has antivascular effects in human rectal cancer

By C. Willett, Y. Boucher, E. Tomaso, D. Duda, Lance L. Munn, Ricky T. Tong, D. Chung, D. Sahani, S. Kalva, S. Kozin and 13 more. Nature Medicine, 2004

2,071 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/08355df47540821e8060652cb6acbc355208316b

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Citations in the corpus

Antiangiogenic agents can increase lymphocyte infiltration into tumor and enhance the effectiveness of adoptive immunotherapy of cancer (2010, positive): “Inhibition of the VEGF/VEGFR-2 axis has been reported to normalize tumor vasculature, decrease interstitial fluid pressure, enhance oncotic pressure gradient, decrease hydrostatic pressure gradient across the tumor vasculature (21), and increase deeper penetration of high molecular weight tetramethy”
AZD2171, a pan-VEGF receptor tyrosine kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma patients. (2007, background): “Indeed, we have found that bevacizumab decreases the number of viable CECs and CPCs in rectal carcinoma patients (Willett et al., 2004, 2005).”
Angiogenesis as a therapeutic target (2005, background): “reported that a single infusion of bevacizumab to patients with rectal carcinoma rapidly decreased tumour perfusion, vascular volume, microvascular density and interstitial fluid pressure as well as the number of viable, circulating endothelial cells in six colorectal cancer patient”
Tumor microvasculature and microenvironment: targets for anti-angiogenesis and normalization. (2007, methodology): “At the same time, tumor blood perfusion determined by functional CT as well as microvessel density in the biopsy specimen decreased by 30% and 50%, respectively while PET scans showed no change in the tumor FDG uptake (Willett et al., 2004; Willett et al., 2005).”
Factors controlling the pharmacokinetics, biodistribution and intratumoral penetration of nanoparticles. (2013, background): “However, the majority of the studies were performed with small molecules [121, 122], and the relevance to nanoparticles is yet to be confirmed.”
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.”
VEGF as a Key Mediator of Angiogenesis in Cancer (2005, background): “It has been proposed that inhibiting VEGF may result in the remodeling of the tumor vasculature, leading to decreases in tumor perfusion, microvascular density, vascular volume and interstitial fluid pressure in patients with colorectal cancer [”
AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer. (2005, background): “An additional small preoperative biomarker study has also suggested antivascular effects in rectal carcinoma patients, following bevacizumab treatment (62).”
Vascular Normalization by Vascular Endothelial Growth Factor Receptor 2 Blockade Induces a Pressure Gradient Across the Vasculature and Improves Drug Penetration in Tumors (2004, background): “We have recently shown that an anti-VEGF antibody can lower interstitial fluid pressure (IFP) in transplanted tumors in mice (3) and in rectal carcinomas in patients (4).”