scholarly journals Relationship between the expression of vascular endothelial growth factor and the density of dendritic cells in gastric adenocarcinoma tissue

1998 ◽  
Vol 78 (12) ◽  
pp. 1573-1577 ◽  
Author(s):  
H Saito ◽  
S Tsujitani ◽  
M Ikeguchi ◽  
M Maeta ◽  
N Kaibara
Blood ◽  
1998 ◽  
Vol 92 (11) ◽  
pp. 4150-4166 ◽  
Author(s):  
Dmitry Gabrilovich ◽  
Tadao Ishida ◽  
Tsunehiro Oyama ◽  
Sophia Ran ◽  
Vladimir Kravtsov ◽  
...  

Abstract Defective function of dendritic cells (DC) in cancer has been recently described and may represent one of the mechanisms of tumor evasion from immune system control. We have previously shown in vitro that vascular endothelial growth factor (VEGF), produced by almost all tumors, is one of the tumor-derived factors responsible for the defective function of these cells. In this study, we investigated whether in vivo infusion of recombinant VEGF could reproduce the observed DC dysfunction. Continuous VEGF infusion, at rates as low as 50 ng/h (resulting in serum VEGF concentrations of 120 to 160 pg/mL), resulted in a dramatic inhibition of dendritic cell development, associated with an increase in the production of B cells and immature Gr-1+ myeloid cells. Infusion of VEGF was associated with inhibition of the activity of the transcription factor NF-κB in bone marrow progenitor cells. Experiments in vitro showed that VEGF itself, and not factors released by VEGF-activated endothelial cells, affected polypotent stem cells resulting in the observed abnormal hematopoiesis. These data suggest that VEGF, at pathologically relevant concentrations in vivo, may exert effects on pluripotent stem cells that result in blocked DC development as well as affect many other hematopoietic lineages.


2012 ◽  
Vol 84 (7) ◽  
Author(s):  
Jarosław Bury ◽  
Justyna Szumiło ◽  
Andrzej Dąbrowski ◽  
Aleksander Ciechański ◽  
Justyna Śliwińska ◽  
...  

2005 ◽  
Vol 334 (1) ◽  
pp. 193-198 ◽  
Author(s):  
Sreenivas Laxmanan ◽  
Stuart W. Robertson ◽  
Enfeng Wang ◽  
Julie S. Lau ◽  
David M. Briscoe ◽  
...  

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