author_facet Hou, Wen
Medynski, Dan
Wu, Shirley
Lin, Xinli
Li, Lu-Yuan
Hou, Wen
Medynski, Dan
Wu, Shirley
Lin, Xinli
Li, Lu-Yuan
author Hou, Wen
Medynski, Dan
Wu, Shirley
Lin, Xinli
Li, Lu-Yuan
spellingShingle Hou, Wen
Medynski, Dan
Wu, Shirley
Lin, Xinli
Li, Lu-Yuan
Clinical Cancer Research
VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
Cancer Research
Oncology
author_sort hou, wen
spelling Hou, Wen Medynski, Dan Wu, Shirley Lin, Xinli Li, Lu-Yuan 1078-0432 1557-3265 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/1078-0432.ccr-05-0384 <jats:title>Abstract</jats:title> <jats:p>Purpose: We determined the antiangiogenic and anticancer activity of VEGI-192, a new isoform of TNFSF15 (VEGI, TL1), with a Lewis lung cancer murine tumor model.</jats:p> <jats:p>Experimental Design: Recombinant human VEGI-192 was produced in Escherichia coli and purified to apparent homogeneity. The protein was given systemically via i.p., i.v., or s.c. injections to tumor-bearing C57BL/6 mice. Tumor growth rates, animal survival rates, and general toxicity were determined. Effect on endothelial cell/smooth muscle cell ratio of the tumor vasculature was analyzed.</jats:p> <jats:p>Results: Systemic administration of VEGI-192 gave rise to a marked inhibition of tumor growth. As much as 50% inhibition of the tumor growth rate was achieved with treatment initiated when the tumor volumes reached nearly 5% of the body weight. Inhibition of tumor formation was also observed when VEGI-192 was given at the time of tumor inoculation. Consistently, we observed an increased survival time of the treated animals. The VEGI-192-treated animals showed no liver or kidney toxicity. The treatment eliminated tumor endothelial cells but not vascular smooth muscle cells, which remained associated with a residual vascular structure consisting of the basement membrane. In addition, we carried out immunohistochemical analysis of rat kidneys and found that vascular endothelial cell growth inhibitor (VEGI) expression is largely limited to endothelial cells.</jats:p> <jats:p>Conclusions: Our findings indicate that VEGI is an endogenous inhibitor of angiogenesis, and that systemic administration of the VEGI-192 isoform resulted in inhibition of tumor angiogenesis and growth.</jats:p> VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth Clinical Cancer Research
doi_str_mv 10.1158/1078-0432.ccr-05-0384
facet_avail Online
Free
finc_class_facet Medizin
format ElectronicArticle
fullrecord blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OC8xMDc4LTA0MzIuY2NyLTA1LTAzODQ
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OC8xMDc4LTA0MzIuY2NyLTA1LTAzODQ
institution DE-Bn3
DE-Brt1
DE-Zwi2
DE-D161
DE-Gla1
DE-Zi4
DE-15
DE-Pl11
DE-Rs1
DE-105
DE-14
DE-Ch1
DE-L229
DE-D275
imprint American Association for Cancer Research (AACR), 2005
imprint_str_mv American Association for Cancer Research (AACR), 2005
issn 1078-0432
1557-3265
issn_str_mv 1078-0432
1557-3265
language English
mega_collection American Association for Cancer Research (AACR) (CrossRef)
match_str hou2005vegi192anewisoformoftnfsf15specificallyeliminatestumorvascularendothelialcellsandsuppressestumorgrowth
publishDateSort 2005
publisher American Association for Cancer Research (AACR)
recordtype ai
record_format ai
series Clinical Cancer Research
source_id 49
title VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_unstemmed VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_full VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_fullStr VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_full_unstemmed VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_short VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_sort vegi-192, a new isoform of tnfsf15, specifically eliminates tumor vascular endothelial cells and suppresses tumor growth
topic Cancer Research
Oncology
url http://dx.doi.org/10.1158/1078-0432.ccr-05-0384
publishDate 2005
physical 5595-5602
description <jats:title>Abstract</jats:title> <jats:p>Purpose: We determined the antiangiogenic and anticancer activity of VEGI-192, a new isoform of TNFSF15 (VEGI, TL1), with a Lewis lung cancer murine tumor model.</jats:p> <jats:p>Experimental Design: Recombinant human VEGI-192 was produced in Escherichia coli and purified to apparent homogeneity. The protein was given systemically via i.p., i.v., or s.c. injections to tumor-bearing C57BL/6 mice. Tumor growth rates, animal survival rates, and general toxicity were determined. Effect on endothelial cell/smooth muscle cell ratio of the tumor vasculature was analyzed.</jats:p> <jats:p>Results: Systemic administration of VEGI-192 gave rise to a marked inhibition of tumor growth. As much as 50% inhibition of the tumor growth rate was achieved with treatment initiated when the tumor volumes reached nearly 5% of the body weight. Inhibition of tumor formation was also observed when VEGI-192 was given at the time of tumor inoculation. Consistently, we observed an increased survival time of the treated animals. The VEGI-192-treated animals showed no liver or kidney toxicity. The treatment eliminated tumor endothelial cells but not vascular smooth muscle cells, which remained associated with a residual vascular structure consisting of the basement membrane. In addition, we carried out immunohistochemical analysis of rat kidneys and found that vascular endothelial cell growth inhibitor (VEGI) expression is largely limited to endothelial cells.</jats:p> <jats:p>Conclusions: Our findings indicate that VEGI is an endogenous inhibitor of angiogenesis, and that systemic administration of the VEGI-192 isoform resulted in inhibition of tumor angiogenesis and growth.</jats:p>
container_issue 15
container_start_page 5595
container_title Clinical Cancer Research
container_volume 11
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
_version_ 1792343557307105293
geogr_code not assigned
last_indexed 2024-03-01T16:51:16.116Z
geogr_code_person not assigned
openURL url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=VEGI-192%2C+a+New+Isoform+of+TNFSF15%2C+Specifically+Eliminates+Tumor+Vascular+Endothelial+Cells+and+Suppresses+Tumor+Growth&rft.date=2005-08-01&genre=article&issn=1557-3265&volume=11&issue=15&spage=5595&epage=5602&pages=5595-5602&jtitle=Clinical+Cancer+Research&atitle=VEGI-192%2C+a+New+Isoform+of+TNFSF15%2C+Specifically+Eliminates+Tumor+Vascular+Endothelial+Cells+and+Suppresses+Tumor+Growth&aulast=Li&aufirst=Lu-Yuan&rft_id=info%3Adoi%2F10.1158%2F1078-0432.ccr-05-0384&rft.language%5B0%5D=eng
SOLR
_version_ 1792343557307105293
author Hou, Wen, Medynski, Dan, Wu, Shirley, Lin, Xinli, Li, Lu-Yuan
author_facet Hou, Wen, Medynski, Dan, Wu, Shirley, Lin, Xinli, Li, Lu-Yuan, Hou, Wen, Medynski, Dan, Wu, Shirley, Lin, Xinli, Li, Lu-Yuan
author_sort hou, wen
container_issue 15
container_start_page 5595
container_title Clinical Cancer Research
container_volume 11
description <jats:title>Abstract</jats:title> <jats:p>Purpose: We determined the antiangiogenic and anticancer activity of VEGI-192, a new isoform of TNFSF15 (VEGI, TL1), with a Lewis lung cancer murine tumor model.</jats:p> <jats:p>Experimental Design: Recombinant human VEGI-192 was produced in Escherichia coli and purified to apparent homogeneity. The protein was given systemically via i.p., i.v., or s.c. injections to tumor-bearing C57BL/6 mice. Tumor growth rates, animal survival rates, and general toxicity were determined. Effect on endothelial cell/smooth muscle cell ratio of the tumor vasculature was analyzed.</jats:p> <jats:p>Results: Systemic administration of VEGI-192 gave rise to a marked inhibition of tumor growth. As much as 50% inhibition of the tumor growth rate was achieved with treatment initiated when the tumor volumes reached nearly 5% of the body weight. Inhibition of tumor formation was also observed when VEGI-192 was given at the time of tumor inoculation. Consistently, we observed an increased survival time of the treated animals. The VEGI-192-treated animals showed no liver or kidney toxicity. The treatment eliminated tumor endothelial cells but not vascular smooth muscle cells, which remained associated with a residual vascular structure consisting of the basement membrane. In addition, we carried out immunohistochemical analysis of rat kidneys and found that vascular endothelial cell growth inhibitor (VEGI) expression is largely limited to endothelial cells.</jats:p> <jats:p>Conclusions: Our findings indicate that VEGI is an endogenous inhibitor of angiogenesis, and that systemic administration of the VEGI-192 isoform resulted in inhibition of tumor angiogenesis and growth.</jats:p>
doi_str_mv 10.1158/1078-0432.ccr-05-0384
facet_avail Online, Free
finc_class_facet Medizin
format ElectronicArticle
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
geogr_code not assigned
geogr_code_person not assigned
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OC8xMDc4LTA0MzIuY2NyLTA1LTAzODQ
imprint American Association for Cancer Research (AACR), 2005
imprint_str_mv American Association for Cancer Research (AACR), 2005
institution DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275
issn 1078-0432, 1557-3265
issn_str_mv 1078-0432, 1557-3265
language English
last_indexed 2024-03-01T16:51:16.116Z
match_str hou2005vegi192anewisoformoftnfsf15specificallyeliminatestumorvascularendothelialcellsandsuppressestumorgrowth
mega_collection American Association for Cancer Research (AACR) (CrossRef)
physical 5595-5602
publishDate 2005
publishDateSort 2005
publisher American Association for Cancer Research (AACR)
record_format ai
recordtype ai
series Clinical Cancer Research
source_id 49
spelling Hou, Wen Medynski, Dan Wu, Shirley Lin, Xinli Li, Lu-Yuan 1078-0432 1557-3265 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/1078-0432.ccr-05-0384 <jats:title>Abstract</jats:title> <jats:p>Purpose: We determined the antiangiogenic and anticancer activity of VEGI-192, a new isoform of TNFSF15 (VEGI, TL1), with a Lewis lung cancer murine tumor model.</jats:p> <jats:p>Experimental Design: Recombinant human VEGI-192 was produced in Escherichia coli and purified to apparent homogeneity. The protein was given systemically via i.p., i.v., or s.c. injections to tumor-bearing C57BL/6 mice. Tumor growth rates, animal survival rates, and general toxicity were determined. Effect on endothelial cell/smooth muscle cell ratio of the tumor vasculature was analyzed.</jats:p> <jats:p>Results: Systemic administration of VEGI-192 gave rise to a marked inhibition of tumor growth. As much as 50% inhibition of the tumor growth rate was achieved with treatment initiated when the tumor volumes reached nearly 5% of the body weight. Inhibition of tumor formation was also observed when VEGI-192 was given at the time of tumor inoculation. Consistently, we observed an increased survival time of the treated animals. The VEGI-192-treated animals showed no liver or kidney toxicity. The treatment eliminated tumor endothelial cells but not vascular smooth muscle cells, which remained associated with a residual vascular structure consisting of the basement membrane. In addition, we carried out immunohistochemical analysis of rat kidneys and found that vascular endothelial cell growth inhibitor (VEGI) expression is largely limited to endothelial cells.</jats:p> <jats:p>Conclusions: Our findings indicate that VEGI is an endogenous inhibitor of angiogenesis, and that systemic administration of the VEGI-192 isoform resulted in inhibition of tumor angiogenesis and growth.</jats:p> VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth Clinical Cancer Research
spellingShingle Hou, Wen, Medynski, Dan, Wu, Shirley, Lin, Xinli, Li, Lu-Yuan, Clinical Cancer Research, VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth, Cancer Research, Oncology
title VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_full VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_fullStr VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_full_unstemmed VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_short VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
title_sort vegi-192, a new isoform of tnfsf15, specifically eliminates tumor vascular endothelial cells and suppresses tumor growth
title_unstemmed VEGI-192, a New Isoform of TNFSF15, Specifically Eliminates Tumor Vascular Endothelial Cells and Suppresses Tumor Growth
topic Cancer Research, Oncology
url http://dx.doi.org/10.1158/1078-0432.ccr-05-0384