Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
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: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