INT196002

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Context Info
Confidence 0.22
First Reported 2006
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 4
Total Number 5
Disease Relevance 3.51
Pain Relevance 0.37

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

plasma membrane (Flt4) nucleus (Flt4) kinase activity (Flt4)
cytoplasm (Flt4)
Anatomy Link Frequency
endothelial cells 2
Flt4 (Mus musculus)
Pain Link Frequency Relevance Heat
cINOD 30 97.36 Very High Very High Very High
Kinase C 2 85.56 High High
Inflammation 34 79.60 Quite High
cytokine 15 48.48 Quite Low
Inflammatory response 2 33.12 Quite Low
cva 4 27.44 Quite Low
Inflammatory mediators 3 21.04 Low Low
metalloproteinase 1 8.80 Low Low
imagery 32 5.00 Very Low Very Low Very Low
positron emission tomography 22 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cancer 292 99.78 Very High Very High Very High
Metastasis 90 98.12 Very High Very High Very High
Lymphedema 45 85.04 High High
Hematological Disease 2 79.84 Quite High
INFLAMMATION 39 79.60 Quite High
Pressure And Volume Under Development 19 77.80 Quite High
Targeted Disruption 4 77.12 Quite High
Lymphatic Metastasis 2 75.20 Quite High
Lymphangioma 1 74.88 Quite High
Breast Cancer 7 68.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition, whether induction of the VEGF-C/VEGFR-3 axis results in increased lymphatic function, increased de novo development of lymphatics, or other alternative mechanisms of benefit is also not yet known and warrants intensive study.
Spec (whether) Positive_regulation (induction) of VEGFR-3
1) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2791214 Disease Relevance 0.76 Pain Relevance 0.33
The growth of blood vessels (angiogenesis) is primarily initiated by activation of VEGFR-1 and VEGFR-2 by VEGF-A, whereas lymphangiogenesis is predominantly driven by VEGF-C, which activates VEGFR-2 and VEGFR-3 expressed in lymphatic endothelial cells.
Positive_regulation (activates) of VEGFR-3 in endothelial cells
2) Confidence 0.21 Published 2010 Journal BMC Med Section Body Doc Link PMC2989928 Disease Relevance 1.19 Pain Relevance 0
There is also experimental evidence that VEGFR3 mediated activation of lymphatic endothelial cells is crucial for metastasis [29].
Positive_regulation (activation) of VEGFR3 in endothelial cells associated with metastasis
3) Confidence 0.10 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2902148 Disease Relevance 0.53 Pain Relevance 0.04
Immunohistochemically the tumor cells are positive for Von-Willebrand factor, CD31, CD34 and vascular endothelial growth factor receptor-3 (VEGFR-3).
Positive_regulation (positive) of vascular endothelial growth factor receptor-3 associated with cancer
4) Confidence 0.05 Published 2006 Journal Diagn Pathol Section Body Doc Link PMC1555613 Disease Relevance 0.84 Pain Relevance 0
point mutation and protein activation, superimposed on the original mutation in that gene. 2) KIT genomic amplification with overexpression of the KIT oncoprotein, without a new point mutation. 3) Target modulation – activation of an alternate receptor tyrosine kinase protein, accompanied by loss of KIT oncoprotein expression. 4) Functional resistance – KIT or PDGFR?
Positive_regulation (activation) of receptor tyrosine kinase protein
5) Confidence 0.04 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2503651 Disease Relevance 0.19 Pain Relevance 0

General Comments

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