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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2002-3-4
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pubmed:abstractText |
The brain-specific angiogenesis inhibitor 1 gene has been isolated in an attempt to find fragments with p53 "functional" binding sites. As reported herein and by others, brain-specific angiogenesis inhibitor 1 expression is present in some normal tissues, but is reduced or lost in tumour tissues. Such data and its particular structure prompted the hypothesis that brain-specific angiogenesis inhibitor 1 may act as a mediator in the local angiogenesis balance. We herein demonstrate that brain-specific angiogenesis inhibitor 1 over-expression suppresses tumour angiogenesis, delaying significantly the human tumour growth in immunodeficient mice. The inhibitory effect of brain-specific angiogenesis inhibitor 1 was documented using our intravital microscopy system, strongly implicating brain-specific angiogenesis inhibitor 1 as a mediator in the control of tumour angiogenesis. In contrast, in vitro tumour cell proliferation was not inhibited by brain-specific angiogenesis inhibitor 1 transfection, whereas some level of cytotoxicity was assessed for endothelial cells. Immunohistochemical analysis of tumour samples confirmed a reduction in the microvessel density index in brain-specific angiogenesis inhibitor 1-overexpressing tumours. At messenger level, moderate changes could be detected, involving the down-regulation of vascular endothelial growth factor and collagenase-1 expression. Furthermore, brain-specific angiogenesis inhibitor 1 expression that was lost in a selection of human cancer cell lines could be restored by wild-type p53 adenoviral transfection. Brain-specific angiogenesis inhibitor 1 should be considered for gene therapy and development of efficient drugs based on endogenous antiangiogenic molecules.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10048576,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10206959,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10343108,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10353734,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10438512,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10446996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10568831,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10639598,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10655109,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10692390,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-10706132,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-3547771,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-4938153,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-7521539,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-7531056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-7686555,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-7692730,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-8952701,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-9221813,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-9393972,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-9407320,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-9533023,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-9647739,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-9772287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-9790924,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11875720-9791730
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0007-0920
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pubmed:author |
pubmed-author:BRUCKM AMA,
pubmed-author:DotyR CRC,
pubmed-author:HorieMM,
pubmed-author:LozonschiLL,
pubmed-author:MatsunoSS,
pubmed-author:MotoiFF,
pubmed-author:NakamuraYY,
pubmed-author:SunamuraMM,
pubmed-author:TaneGG,
pubmed-author:YatsuokaTT,
pubmed-author:YokoyamaTT
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pubmed:copyrightInfo |
Copyright 2002 The Cancer Research Campaign
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
86
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
490-6
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11875720-Adenocarcinoma,
pubmed-meshheading:11875720-Angiogenesis Inhibitors,
pubmed-meshheading:11875720-Angiogenic Proteins,
pubmed-meshheading:11875720-Animals,
pubmed-meshheading:11875720-Cell Division,
pubmed-meshheading:11875720-Genes, p53,
pubmed-meshheading:11875720-Humans,
pubmed-meshheading:11875720-Mice,
pubmed-meshheading:11875720-Mice, SCID,
pubmed-meshheading:11875720-Neovascularization, Pathologic,
pubmed-meshheading:11875720-Pancreatic Neoplasms,
pubmed-meshheading:11875720-Proteins,
pubmed-meshheading:11875720-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11875720-Transfection,
pubmed-meshheading:11875720-Transplantation, Heterologous,
pubmed-meshheading:11875720-Tumor Cells, Cultured
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pubmed:year |
2002
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pubmed:articleTitle |
Overexpression of the p53-inducible brain-specific angiogenesis inhibitor 1 suppresses efficiently tumour angiogenesis.
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pubmed:affiliation |
First Department of Surgery, Tohoku University Medical School, 1-1 Seiryomachi, Aoba-ku, 980-8574 Sendai, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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