VEGFR2 Cancer Research Results

VEGFR2, Vascular Endothelial Growth Factor Receptor 2: Click to Expand ⟱
Source:
Type: receptor tyrosine kinase
VEGFR2 is a receptor tyrosine kinase that plays a crucial role in angiogenesis, the process of new blood vessel formation. In cancer, VEGFR2 is often overexpressed, promoting the growth of new blood vessels that supply the tumor with oxygen and nutrients, facilitating its growth and metastasis.
Inhibiting VEGFR2 signaling has been shown to be an effective strategy in cancer therapy, and several VEGFR2 inhibitors have been approved for the treatment of various types of cancer, including renal cell carcinoma, colorectal cancer, and non-small cell lung cancer. These inhibitors work by blocking the binding of VEGF to VEGFR2, thereby inhibiting angiogenesis and tumor growth.


Scientific Papers found: Click to Expand⟱
3482- MF,    Pulsed Electromagnetic Fields Increase Angiogenesis and Improve Cardiac Function After Myocardial Ischemia in Mice
- in-vitro, NA, NA
*cardioP↑, *VEGF↑, *VEGFR2↑, *Hif1a↑, *FGF↑, *ITGB1↑, *angioG↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Proliferation, Differentiation & Cell State

FGF↑, 1,  

Migration

ITGB1↑, 1,  

Angiogenesis & Vasculature

angioG↑, 1,   Hif1a↑, 1,   VEGF↑, 1,   VEGFR2↑, 1,  

Functional Outcomes

cardioP↑, 1,  
Total Targets: 7

Scientific Paper Hit Count for: VEGFR2, Vascular Endothelial Growth Factor Receptor 2
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:768  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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