Vascular endothelial growth factor (VEGF) is a potent proangiogenic protein that activates VEGF receptor (VEGFR) tyrosine kinases expressed by vascular endothelial cells. We previously showed that one of these receptors, VEGFR-2, has a truncated soluble form (sVEGFR-2) that can be detected in mouse and human plasma. Because activation of VEGFR-2 plays an important role in tumor angiogenesis, clinical interest in monitoring plasma sVEGFR-2 levels in cancer patients has focused on its potential exploitation as a surrogate biomarker for disease progression as well as assessing efficacy/activity of antiangiogenic drugs, particularly those that target VEGF or VEGFR-2. However, no preclinical studies have been done to study sVEGFR-2 during tumor growth or the mechanisms involved in its modulation. Using spontaneously growing tumors and both localized and metastatic human tumor xenografts, we evaluated the relationship between sVEGFR-2 and tumor burden as well as underlying factors governing
%0 Journal Article
%1 Ebos.2008
%A Ebos, J. M.
%A Lee, C. R.
%A Bogdanovic, E.
%A Alami, J.
%A Van, Slyke P.
%A Francia, G.
%A Xu, P.
%A Mutsaers, A. J.
%A Dumont, D. J.
%A Kerbel, R. S.
%D 2008
%J Cancer Res.
%K A Adenocarcinoma Adenoviridae Animals BALB Biological Burden C C57BL Cell Cells Cultured Disease Endothelial Experimental Factor Female Genetic Growth HT29 Heterologous Human Humans Inbred Male Mammary Markers Mice Neoplasm Neoplasms Progression Proliferation Prostatic Receptor-2 Research Solubility Transduction Transfection Transgenic Transplantation Tumor Tyrosine Vascular blood cells genetics metabolism methods pathology physiology protein
%N 2
%P 521-529
%T Vascular endothelial growth factor-mediated decrease in plasma soluble vascular endothelial growth factor receptor-2 levels as a surrogate biomarker for tumor growth
%U PM:18199548
%V 68
%X Vascular endothelial growth factor (VEGF) is a potent proangiogenic protein that activates VEGF receptor (VEGFR) tyrosine kinases expressed by vascular endothelial cells. We previously showed that one of these receptors, VEGFR-2, has a truncated soluble form (sVEGFR-2) that can be detected in mouse and human plasma. Because activation of VEGFR-2 plays an important role in tumor angiogenesis, clinical interest in monitoring plasma sVEGFR-2 levels in cancer patients has focused on its potential exploitation as a surrogate biomarker for disease progression as well as assessing efficacy/activity of antiangiogenic drugs, particularly those that target VEGF or VEGFR-2. However, no preclinical studies have been done to study sVEGFR-2 during tumor growth or the mechanisms involved in its modulation. Using spontaneously growing tumors and both localized and metastatic human tumor xenografts, we evaluated the relationship between sVEGFR-2 and tumor burden as well as underlying factors governing
@article{Ebos.2008,
abstract = {Vascular endothelial growth factor (VEGF) is a potent proangiogenic protein that activates VEGF receptor (VEGFR) tyrosine kinases expressed by vascular endothelial cells. We previously showed that one of these receptors, VEGFR-2, has a truncated soluble form (sVEGFR-2) that can be detected in mouse and human plasma. Because activation of VEGFR-2 plays an important role in tumor angiogenesis, clinical interest in monitoring plasma sVEGFR-2 levels in cancer patients has focused on its potential exploitation as a surrogate biomarker for disease progression as well as assessing efficacy/activity of antiangiogenic drugs, particularly those that target VEGF or VEGFR-2. However, no preclinical studies have been done to study sVEGFR-2 during tumor growth or the mechanisms involved in its modulation. Using spontaneously growing tumors and both localized and metastatic human tumor xenografts, we evaluated the relationship between sVEGFR-2 and tumor burden as well as underlying factors governing },
added-at = {2010-02-05T11:28:39.000+0100},
author = {Ebos, J. M. and Lee, C. R. and Bogdanovic, E. and Alami, J. and Van, Slyke P. and Francia, G. and Xu, P. and Mutsaers, A. J. and Dumont, D. J. and Kerbel, R. S.},
biburl = {https://www.bibsonomy.org/bibtex/271956b27a8f21b1b822b52d005ae329f/kanefendt},
interhash = {e9064ce3c5ea9d32691b0145526d01b9},
intrahash = {71956b27a8f21b1b822b52d005ae329f},
journal = {Cancer Res.},
keywords = {A Adenocarcinoma Adenoviridae Animals BALB Biological Burden C C57BL Cell Cells Cultured Disease Endothelial Experimental Factor Female Genetic Growth HT29 Heterologous Human Humans Inbred Male Mammary Markers Mice Neoplasm Neoplasms Progression Proliferation Prostatic Receptor-2 Research Solubility Transduction Transfection Transgenic Transplantation Tumor Tyrosine Vascular blood cells genetics metabolism methods pathology physiology protein},
number = 2,
pages = {521-529},
timestamp = {2010-02-05T11:28:51.000+0100},
title = {Vascular endothelial growth factor-mediated decrease in plasma soluble vascular endothelial growth factor receptor-2 levels as a surrogate biomarker for tumor growth},
url = {PM:18199548},
volume = 68,
year = 2008
}