scholarly journals Expression of Soluble Vascular Endothelial Growth Factor Receptor-1 in Human Monocyte-Derived Mature Dendritic Cells Contributes to Their Antiangiogenic Property

2009 ◽  
Vol 183 (12) ◽  
pp. 8176-8185 ◽  
Author(s):  
Masatoshi Kishuku ◽  
Yasuhiko Nishioka ◽  
Shinji Abe ◽  
Jun Kishi ◽  
Hirokazu Ogino ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Dendritic Cells ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Human Monocyte ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Defective Differentiation of Myeloid and Plasmacytoid Dendritic Cells in Advanced Cancer Patients is not Normalized by Tyrosine Kinase Inhibition of the Vascular Endothelial Growth Factor Receptor

2007 ◽  
Vol 2007 ◽  
pp. 1-9 ◽  
Author(s):  
H. van Cruijsen ◽  
K. Hoekman ◽  
A. G. M. Stam ◽  
A. J. M. van den Eertwegh ◽  
B. C. Kuenen ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Dendritic Cells ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Cancer Patients ◽  
Advanced Cancer ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Advanced Cancer Patients ◽  
Endothelial Growth Factor

Tumor-derived vascular endothelial growth factor (VEGF) has previously been identified as a causative factor in the disturbed differentiation of myeloid dendritic cells (DC) in advanced cancer patients. Here, we investigated the potential of vascular endothelial growth factor receptor (VEGFR) tyrosine kinase (TK) inhibition to overcome this defective DC differentiation. To this end, peripheral blood DC (PBDC) precursor and subset frequencies were measured in 13 patients with advanced cancer before and after treatment with AZD2171, a TK inhibitor (TKI) of VEGFR, coadministered with gefitinib, and an epidermal growth factor receptor (EGFR) TKI. Of note, not only myeloid DC but also plasmacytoid DC frequencies were significantly reduced in the blood of the cancer patients prior to treatment, as compared to healthy controls. Moreover, besides an accumulated population of immature myeloid cells (ImC), a population of myeloid suppressor cells (MSC) was significantly increased. Upon systemic VEGFR TK inhibition, DC frequencies did not increase, whereas the rate of circulating MSC showed a slight, but not significant, decrease. In conclusion, TK inhibition of VEGFR with AZD2171 does not restore the defective PBDC differentiation observed in advanced cancer patients.

Fortgeschrittenes medulläres Schilddrüsenkarzinom: Vandetanib verbessert das progressionsfreie Überleben

2012 ◽  
Vol 03 (02) ◽  
pp. 93-92
Author(s):  
Alexander Kretzschmar
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Phase Iii ◽  
Vascular Endothelial ◽  
Medulläres Schilddrüsenkarzinom ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

Vandetanib ist ein oraler Hemmer des RET-Kinase-, VEGF (Vascular Endothelial Growth Factor Receptor)- und EGFR (Epidermal Growth Factor Receptor)-Signalwegs. In einer zulassungsrelevanten, randomisierten, doppelblinden, placebokontrollierten Phase- III-Studie verlängerte der Tyrosinkinasehemmer das progressionsfreie Überleben (PFS) signifikant länger als Placebo.

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