Source:http://linkedlifedata.com/resource/pubmed/id/16557578
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2006-6-8
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| pubmed:abstractText |
The Ewing's sarcoma cell line TC71 overexpresses vascular endothelial growth factor isoform 165 (VEGF165), a potent proangiogenic molecule that induces endothelial cell proliferation, migration, and chemotaxis. CD34+ bone marrow stem cells can differentiate into endothelial and hematopoietic cells. We used a transplant model to determine whether CD34+ cells migrate from the bone marrow to Ewing's sarcoma tumors and participate in the neovascularization process that supports tumor growth. We also examined the role of VEGF165 in CD34+ cell migration. Human umbilical cord CD34+ cells were transplanted into sublethally irradiated severe combined immunodeficient mice. Seven days later, the mice were injected subcutaneously with TC71 tumor cells. Tumors were excised 2 weeks later and analyzed by immunohistochemistry. The tumor sections expressed both human VE-cadherin and mouse CD31, indicating involvement of donor-derived human cells in the tumor vessels. To determine the role of VEGF165 in the chemoattraction of CD34+ cells, we generated two VEGF165-deficient TC71 clones, a stable anti-sense VEGF165 cell line (Clone 17) and a VEGF165 siRNA-inhibited clone (TC/siVEGF(7-1)). The resulting VEGF165-deficient tumor cells had normal growth rates in vitro, but had delayed growth when implanted into mice. Immunohistochemical analysis revealed decreased infiltration of CD34+ cells into both VEGF165-deficient tumors. These data show that bone marrow stem cells contribute to the growing tumor vasculature in Ewing's sarcoma and that VEGF165 is critical for the migration of CD34+ cells from the bone marrow into the tumor.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD34,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Antisense,
http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations,
http://linkedlifedata.com/resource/pubmed/chemical/Laminin,
http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/VEGFA protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A,
http://linkedlifedata.com/resource/pubmed/chemical/matrigel
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| pubmed:status |
MEDLINE
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| pubmed:month |
Aug
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| pubmed:issn |
0020-7136
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2006 Wiley-Liss, Inc.
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| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
119
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
839-46
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:16557578-Animals,
pubmed-meshheading:16557578-Antigens, CD34,
pubmed-meshheading:16557578-Cell Movement,
pubmed-meshheading:16557578-Collagen,
pubmed-meshheading:16557578-DNA, Antisense,
pubmed-meshheading:16557578-Drug Combinations,
pubmed-meshheading:16557578-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16557578-Humans,
pubmed-meshheading:16557578-Laminin,
pubmed-meshheading:16557578-Mice,
pubmed-meshheading:16557578-Neoplasm Transplantation,
pubmed-meshheading:16557578-Proteoglycans,
pubmed-meshheading:16557578-Recombinant Proteins,
pubmed-meshheading:16557578-Sarcoma, Ewing,
pubmed-meshheading:16557578-Stem Cells,
pubmed-meshheading:16557578-Vascular Endothelial Growth Factor A
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| pubmed:year |
2006
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| pubmed:articleTitle |
Production of VEGF165 by Ewing's sarcoma cells induces vasculogenesis and the incorporation of CD34+ stem cells into the expanding tumor vasculature.
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| pubmed:affiliation |
Division of Pediatrics, University of Texas, MD Anderson Cancer Center, Houston, TX 77030, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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