rdf:type |
|
lifeskim:mentions |
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0026255,
umls-concept:C0237477,
umls-concept:C0290149,
umls-concept:C0332281,
umls-concept:C0598934,
umls-concept:C1515655,
umls-concept:C1517499,
umls-concept:C1655807,
umls-concept:C1706968
|
pubmed:issue |
11
|
pubmed:dateCreated |
1998-6-22
|
pubmed:abstractText |
The antitumoral effects that follow the local delivery of the N-terminal fragment of human plasminogen (angiostatin K3) have been studied in two xenograft murine models. Angiostatin delivery was achieved by a defective adenovirus expressing a secretable angiostatin K3 molecule from the cytomegalovirus promoter (AdK3). In in vitro studies, AdK3 selectively inhibited endothelial cell proliferation and disrupted the G2/M transition induced by M-phase-promoting factors. AdK3-infected endothelial cells showed a marked mitosis arrest that correlated with the down-regulation of the M-phase phosphoproteins. A single intratumoral injection of AdK3 into preestablished rat C6 glioma or human MDA-MB-231 breast carcinoma grown in athymic mice was followed by a significant arrest of tumor growth, which was associated with a suppression of neovascularization within and at the vicinity of the tumors. AdK3 therapy also induced a 10-fold increase in apoptotic tumor cells as compared with a control adenovirus. Furthermore, we showed that systemic injection of AdK3 delayed C6 tumor establishment and growth, confirming that angiostatin can function in a paracrin manner. Our data support the concept that targeted antiangiogenesis, using adenovirus-mediated gene transfer, represents a promising alternative strategy for delivering antiangiogenic factors as their bolus injections present unsolved pharmacological problems.
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-1279432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-1503910,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-1644927,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-1688381,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-1701519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-1703548,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-1718597,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-2502207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-479157,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-6574461,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-7525077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-7584949,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-7644496,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-7683111,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-7689950,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-7954823,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-8538748,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-8640562,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-8647630,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-8756718,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-8910613,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-8978404,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-9008168,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-9041178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-9102221,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-9118223,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9600971-9240963
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
0027-8424
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
26
|
pubmed:volume |
95
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
6367-72
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:9600971-Adenoviridae,
pubmed-meshheading:9600971-Angiostatins,
pubmed-meshheading:9600971-Animals,
pubmed-meshheading:9600971-Cell Division,
pubmed-meshheading:9600971-Endothelium, Vascular,
pubmed-meshheading:9600971-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:9600971-Gene Transfer Techniques,
pubmed-meshheading:9600971-Genetic Vectors,
pubmed-meshheading:9600971-Humans,
pubmed-meshheading:9600971-Mice,
pubmed-meshheading:9600971-Mitosis,
pubmed-meshheading:9600971-Neoplasms, Experimental,
pubmed-meshheading:9600971-Neovascularization, Pathologic,
pubmed-meshheading:9600971-Peptide Fragments,
pubmed-meshheading:9600971-Plasminogen,
pubmed-meshheading:9600971-Rats
|
pubmed:year |
1998
|
pubmed:articleTitle |
Angiostatin gene transfer: inhibition of tumor growth in vivo by blockage of endothelial cell proliferation associated with a mitosis arrest.
|
pubmed:affiliation |
le Centre National de la Recherche Scientifique Unite de Recherche Associée 1301/Rhône-Poulenc Rorer Gencell, Institut Gustave Roussy, 94805 Villejuif, France. grisceli@igr.fr
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|