Linked Life Data

9751633

Source:http://linkedlifedata.com/resource/pubmed/id/9751633

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
1998-10-1
pubmed:abstractText
Vascular endothelial growth factor (VEGF), also known as vascular permeability factor, has been investigated as a potent mediator of brain tumor angiogenesis and tumor growth. We evaluated the effect of VEGF expression on the pathophysiology of tumor growth in the brain. Human SK-MEL-2 melanoma cells, with minimal VEGF expression, were stably transfected with either sense or antisense mouse VEGF cDNA and used to produce intracerebral xenografts. Vascular permeability, blood volume, blood flow, and tumor fluorodeoxyglucose metabolism were assessed using tissue sampling and quantitative autoradiography. Tumor proliferation was assessed by measuring bromodeoxyuridine labeling indices. Tumor vascular density and morphological status of the blood-brain barrier were evaluated by immunohistochemistry. SK-MEL-2 cells transfected with sense VEGF (V+) expressed large amounts of mouse and human VEGF protein; V+ cells formed well-vascularized, rapidly growing tumors with minimal tumor necrosis. V+ tumors had substantial and significant increases in blood volume, blood flow, vascular permeability, and fluorodeoxyglucose metabolism compared to wild-type and/or V- (antisense VEGF) tumors. VEGF antisense transfected V- expressed no detectable VEGF protein and formed minimally vascularized tumors. V- tumors had a very low initial growth rate with central necrosis; blood volume, blood flow, vascular permeability, and glucose metabolism levels were low compared to wild-type and V+ tumors. A substantial inhibition of intracerebral tumor growth, as well as a decrease in tumor vascularity, blood flow, and vascular permeability may be achieved by down-regulation of endogenous VEGF expression in tumor tissue. VEGF-targeted antiangiogenic gene therapy could be an effective component of a combined strategy to treat VEGF-producing brain tumors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4185-92
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9751633-Animals, pubmed-meshheading:9751633-Blood Volume, pubmed-meshheading:9751633-Brain Neoplasms, pubmed-meshheading:9751633-Capillary Permeability, pubmed-meshheading:9751633-Cerebrovascular Circulation, pubmed-meshheading:9751633-Endothelial Growth Factors, pubmed-meshheading:9751633-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:9751633-Fluorodeoxyglucose F18, pubmed-meshheading:9751633-Humans, pubmed-meshheading:9751633-Lymphokines, pubmed-meshheading:9751633-Melanoma, pubmed-meshheading:9751633-Mice, pubmed-meshheading:9751633-Neoplasm Proteins, pubmed-meshheading:9751633-Neovascularization, Pathologic, pubmed-meshheading:9751633-RNA, Antisense, pubmed-meshheading:9751633-Transfection, pubmed-meshheading:9751633-Transplantation, Heterologous, pubmed-meshheading:9751633-Tumor Cells, Cultured, pubmed-meshheading:9751633-Vascular Endothelial Growth Factor A, pubmed-meshheading:9751633-Vascular Endothelial Growth Factors
pubmed:year
1998
pubmed:articleTitle
Tumor growth modulation by sense and antisense vascular endothelial growth factor gene expression: effects on angiogenesis, vascular permeability, blood volume, blood flow, fluorodeoxyglucose uptake, and proliferation of human melanoma intracerebral xenografts.
pubmed:affiliation
Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't