Linked Life Data

9581905

Source:http://linkedlifedata.com/resource/pubmed/id/9581905

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1998-7-9
pubmed:abstractText
Vascular endothelial growth factor (VEGF), a potent angiogenic mediator, is overexpressed in most solid tumors. On the basis of the knowledge that solid tumor growth beyond a small volume is critically dependent on angiogenesis, and that adenovirus (Ad) vectors can mediate efficient in vivo gene transfer and expression, we hypothesized that Ad-mediated transfer of a secreted form of the extracellular domain of the flt-1 VEGF receptor (Adsflt) would suppress tumor growth on a regional basis. To evaluate this concept, three tumor models were examined using a murine colon carcinoma cell line and syngeneic BALB/c mice. First, mice with preestablished splenic CT26.CL25 tumors and liver metastases were given Adsflt on AdNull intravenously and, after 15 days, spleens and livers were harvested to quantify tumor burden. Adslft-treated animals had minimal residual splenic tumors and liver metastases; in contrast, control animals had bulky splenic tumors and extensive liver metastases (p < 0.003). Second, mice with preestablished lung metastases showed a significant reduction in pulmonary metastases with regionally administered Adslft (intratracheal, p < 0.02) but not when the vector was systemically administered (intravenous, p > 0.9). Finally, mice with primary subcutaneous tumors treated with intratumoral administration of Adslft showed significant tumor suppression (p < 0.05) not observed in AdNull-treated mice or mice given Adslft intravenously (p > 0.3). We conclude that Ad-mediated in vivo regional delivery of a secreted form of the extracellular domain of the flt-1 VEGF receptor can effectively inhibit regional tumor growth, a strategy that may provide a means to control tumor growth within the treated organ without the risk of systemic antiangiogenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1043-0342
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
823-33
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9581905-Adenoviridae, pubmed-meshheading:9581905-Animals, pubmed-meshheading:9581905-Colonic Neoplasms, pubmed-meshheading:9581905-DNA, Complementary, pubmed-meshheading:9581905-Gene Therapy, pubmed-meshheading:9581905-Gene Transfer Techniques, pubmed-meshheading:9581905-Genetic Vectors, pubmed-meshheading:9581905-Liver Neoplasms, pubmed-meshheading:9581905-Lung Neoplasms, pubmed-meshheading:9581905-Mice, pubmed-meshheading:9581905-Mice, Inbred BALB C, pubmed-meshheading:9581905-Neoplasms, Experimental, pubmed-meshheading:9581905-Neovascularization, Pathologic, pubmed-meshheading:9581905-Proto-Oncogene Proteins, pubmed-meshheading:9581905-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:9581905-Skin Neoplasms, pubmed-meshheading:9581905-Tumor Cells, Cultured, pubmed-meshheading:9581905-Vascular Endothelial Growth Factor Receptor-1
pubmed:year
1998
pubmed:articleTitle
Regional suppression of tumor growth by in vivo transfer of a cDNA encoding a secreted form of the extracellular domain of the flt-1 vascular endothelial growth factor receptor.
pubmed:affiliation
Division of Pulmonary and Critical Care Medicine, The New York Hospital-Cornell Medical Center, New York 10021, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't