INT173097

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Context Info
Confidence 0.73
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 20
Total Number 20
Disease Relevance 12.73
Pain Relevance 0.31

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

extracellular region (KDR) cytoplasmic membrane-bounded vesicle (KDR) plasma membrane (KDR)
nucleus (KDR) cytoplasm (KDR)
Anatomy Link Frequency
endothelial cell 2
endothelium 2
platelet 1
KDR (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 45 95.92 Very High Very High Very High
Chronic pancreatitis 9 82.44 Quite High
cytokine 42 55.36 Quite High
nud 1 53.44 Quite High
agonist 43 50.00 Quite Low
addiction 13 32.56 Quite Low
Potency 2 24.12 Low Low
pain flank 1 14.48 Low Low
metalloproteinase 29 5.00 Very Low Very Low Very Low
dexamethasone 17 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Pancreatic Cancer 244 99.80 Very High Very High Very High
Disease 99 99.72 Very High Very High Very High
Toxicity 44 99.54 Very High Very High Very High
Carcinoma 196 99.26 Very High Very High Very High
Cancer 744 98.68 Very High Very High Very High
Myocardial Infarction 24 98.04 Very High Very High Very High
Coronary Artery Disease 54 97.76 Very High Very High Very High
Leukemia 82 96.28 Very High Very High Very High
INFLAMMATION 48 95.92 Very High Very High Very High
Lymphatic System Cancer 94 95.68 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Given the exploratory pilot nature of this study, it is hoped that future studies will validate these results and provide a mechanism by which toxicity is related to PFS and VEGFR2 genotypic variation is related to toxicity.


Localization (variation) of VEGFR2 associated with toxicity
1) Confidence 0.73 Published 2010 Journal J Exp Clin Cancer Res Section Body Doc Link PMC2913951 Disease Relevance 0.76 Pain Relevance 0
However, this assumption needs to be thoroughly re-evaluated, in light of recent VEGFR2-immunostaining that localized VEGFR2 equally on luminal and abluminal surfaces of tumor- and adenoVEGF-induced microvascular endothelium, as well as significantly on transendothelial vesiculovaculolar organelles (VVOs) and luminally-attached caveolae [162].
Localization (localized) of VEGFR2 in endothelium associated with cancer
2) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.10 Pain Relevance 0
An inverse correlation of CD45dimCD34+KDR+ with disease activity (r?
Localization (correlation) of KDR associated with disease
3) Confidence 0.64 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2972200 Disease Relevance 0.90 Pain Relevance 0
Sensitivity to VEGF-binding affinity of VEGFR1 and VEGFR2
Localization (affinity) of VEGFR2
4) Confidence 0.61 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Among the major endothelial cell surface receptor targets for these VEGF isoforms are: the tyrosine kinases VEGFR1 (Flt-1; UniProt accession P17948-1) and VEGFR2 (mouse Flk-1; human KDR; UniProt accession P35968); as well as the co-receptor neuropilin-1 (NRP1; UniProt accession O14786), which couples directly with VEGFR1, and indirectly with VEGFR2 through non-overlapping binding sites on VEGF165 [7].


Localization (targets) of VEGFR2 in endothelial cell
5) Confidence 0.61 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.47 Pain Relevance 0.03
Our results confirmed the presence of VEGF, VEGFR-1, and VEGFR-2 mRNA and reinforced VEGF's mitogenic effect in multiple human pancreatic cancer cell lines [84].
Localization (presence) of VEGFR associated with pancreatic cancer
6) Confidence 0.58 Published 2003 Journal Mol Cancer Section Body Doc Link PMC150383 Disease Relevance 0.98 Pain Relevance 0.06
Our results confirmed the presence of VEGF, VEGFR-1, and VEGFR-2 mRNA and reinforced VEGF's mitogenic effect in multiple human pancreatic cancer cell lines [84].
Localization (presence) of VEGFR associated with pancreatic cancer
7) Confidence 0.58 Published 2003 Journal Mol Cancer Section Body Doc Link PMC150383 Disease Relevance 0.98 Pain Relevance 0.06
However, this assumption needs to be thoroughly re-evaluated, in light of recent VEGFR2-immunostaining that localized VEGFR2 equally on luminal and abluminal surfaces of tumor- and adenoVEGF-induced microvascular endothelium, as well as significantly on transendothelial vesiculovaculolar organelles (VVOs) and luminally-attached caveolae [162].
Localization (localized) of VEGFR2 in endothelium associated with cancer
8) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.10 Pain Relevance 0
In this study, multiple cell lines of human pancreatic cancer actively secreted VEGF, and treatment of VEGFR-positive cells with VEGF produced significant enhancement of pancreatic cancer cell growth [83].
Localization (secreted) of VEGFR associated with pancreatic cancer
9) Confidence 0.51 Published 2003 Journal Mol Cancer Section Body Doc Link PMC150383 Disease Relevance 0.80 Pain Relevance 0.08
Additionally, two small-molecule inhibitors targeting VEGFR and other kinases, sorafenib (Nexavar, Bayer and Onyx pharmaceuticals) and sunitinib (Sutent, Pfizer), have been approved based on their efficacy in treating renal cell- and hepatocellular carcinoma [27, 28].
Localization (targeting) of VEGFR associated with hepatocellular cancer
10) Confidence 0.44 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2875768 Disease Relevance 0.73 Pain Relevance 0
The major classes of antiangiogenic therapy include (1) direct anti-VEGF acting molecules (anti-VEGF antibodies, VEGF-antisense nucleotides), (2) immunomodulatory drugs (IMIDs) with antiangiogenic properties, (3) receptor tyrosine kinase inhibitors that target VEGFR signaling as well as receptors of other (proangiogenic) factors, (4) the antiendothelial approach of metronomic therapy, and (5) other new compounds targeting signaling downstream to proangiogenic growth factors, such as mammalian target of rapamycin (mTOR) inhibitors, histone deacetylases' (HDAC) inhibitors, and proteasome inhibitors.
Localization (targeting) of VEGFR
11) Confidence 0.44 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2875768 Disease Relevance 0.88 Pain Relevance 0
In 1997, eEPCs were the first putative endothelial progenitors isolated in vitro by culturing CD34+ VEGFR2+ mononuclear blood cells on fibronectin [25] and confirming a subsequent increase in expression of endothelial cell-associated markers such as CD34, CD31, VEGFR2, Tie2, and E-selectin.
Localization (blood cells) of VEGFR2 in endothelial cell
12) Confidence 0.37 Published 2010 Journal BMC Med Genomics Section Body Doc Link PMC2881111 Disease Relevance 0.18 Pain Relevance 0.05
After blocking cells were labelled for 45 minutes at 37°C in the presence of a mouse monoclonal antibody (dilution of 1:50) directed against vWF (DakoCytomation, Denmark), a goat polyclonal antibody (diluition of 1:50) direct against FLT-1 (Santa Cruz Biotechnology-USA), a mouse monoclonal antibody (diluition of 1:50) directed against KDR (SigmaAldrich, Italy).
Localization (directed) of KDR
13) Confidence 0.33 Published 2007 Journal BMC Dev Biol Section Body Doc Link PMC1810523 Disease Relevance 0 Pain Relevance 0
In contrary, knockdown of Mcl-1 slightly sensitized HCC cells towards inhibition of mTOR by rapamycin (5 nM, 24 h, p < 0.01), selective inhibition of VEGF (Flk-1) and PDGF receptor tyrosine kinases by SU5614 (15 ?
Localization (rapamycin) of Flk-1 associated with carcinoma
14) Confidence 0.30 Published 2006 Journal BMC Cancer Section Body Doc Link PMC1601962 Disease Relevance 0.95 Pain Relevance 0
HCCs are vascularized tumors with high expression of VEGF raising the possibility that agents targeting VEGFR might be of therapeutic value.
Localization (targeting) of VEGFR associated with cancer
15) Confidence 0.30 Published 2006 Journal BMC Cancer Section Body Doc Link PMC1601962 Disease Relevance 1.20 Pain Relevance 0
Combination approaches targeting the VEGF/VEGFR and the PDGF/PDGFR axes are thus very appealing [67].


Localization (targeting) of VEGFR
16) Confidence 0.26 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2804796 Disease Relevance 0.91 Pain Relevance 0.03
There are reports demonstrating use of VEGF and VEGFR antisense RNA in preclinical models.
Localization (use) of VEGFR
17) Confidence 0.24 Published 2004 Journal J Transl Med Section Body Doc Link PMC455695 Disease Relevance 0.83 Pain Relevance 0
Upon activation of VEGFR2 by VEGF, VEGFR2 binds to dimeric PDCD10, translocates to the membrane, and becomes activated.
Localization (translocates) of VEGFR2
18) Confidence 0.21 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2909203 Disease Relevance 0 Pain Relevance 0
In addition to agents targeting VEGF-VEGFR signaling directly, a number of agents have been developed to target the tumor microenvironment (reviewed in [99–102]), including ECM modulators, tyrosine kinase inhibitors, and immunomodulators, many of which indirectly target cancer angiogenesis.
Localization (targeting) of VEGFR associated with cancer
19) Confidence 0.19 Published 2010 Journal PPAR Research Section Body Doc Link PMC2829627 Disease Relevance 1.33 Pain Relevance 0
In addition, the targets of sunitinib involve vascular endothelial growth factor receptors (VEGFR1, VEGFR2 and VEGFR3), platelet-derived growth factor receptors (PDGFR?
Localization (receptors) of VEGFR2 in platelet
20) Confidence 0.10 Published 2010 Journal World J Surg Oncol Section Body Doc Link PMC2890518 Disease Relevance 0.63 Pain Relevance 0

General Comments

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