scholarly journals A Case Report of Ischemic Stroke in a Patient with Metastatic Gastric Cancer Secondary to Treatment with the Vascular Endothelial Growth Factor Receptor-2 Inhibitor Ramucirumab

2016 ◽  
Vol 9 (2) ◽  
pp. 317-320 ◽  
Author(s):  
Michael E. Christiansen ◽  
Timothy Ingall ◽  
Edward C. Lew ◽  
Ramesh K. Ramanathan ◽  
Harshita R. Paripati
Keyword(s):  
Gastric Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Case Reports ◽  
Growth Factor Receptor ◽  
Metastatic Gastric Cancer ◽  
Vascular Endothelial ◽  
First Case ◽  
Endothelial Growth Factor

Ramucirumab is an antiangiogenesis agent targeting the vascular endothelial growth factor receptor-2 (VEGFR-2), approved to treat advanced gastric and colon cancer. In clinical trials, it was shown to cause a small increase in arterial thromboembolism compared to placebo, including cerebral and myocardial ischemia, which was not statistically significant. Detailed case reports are lacking and we here present one of the first case reports of stroke secondary to ramucirumab-induced in situ thrombosis.

scholarly journals Ramucirumab – egy új gyógyszer az onkológiában

2016 ◽  
Vol 157 (40) ◽  
pp. 1587-1594 ◽  
Author(s):  
András Telekes ◽  
Dániel Deme
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Progression Free Survival ◽  
Metastatic Gastric Cancer ◽  
Local Relapse ◽  
Vascular Endothelial ◽  
Previously Treated ◽  
And Migration ◽  
Endothelial Growth Factor

Ramucirumab is a humanized monoclonal antibody against vascular endothelial growth factor receptor-2, which inhibits the binding of vascular endothelial growth factor-A, -C and -D ligands. Furthermore it blocks the ligand stimulated activation of p44/p42 mitogen activated protein kinases, thus neutralizing the ligand induced proliferation and migration of human endothelial cells. Based on the results of the REGARD (Ramucirumab monotherapy for previously treated advanced gastric or gastro-oesophageal junction adenocarcinoma) and the RAINBOW (Ramucirumab plus paclitaxel versus placebo plus paclitaxel in patients with previously treated advanced gastric or gastro-oesophageal junction adenocarcinoma) studies ramucirumab was approved for 2nd line treatment as monotherapy and in combination with paclitaxel for patients with local relapse and unresectable or metastatic gastric cancer (including gastro-esophegal junction adenocarcinoma). Based on the results, in advanced solid malignancies, ramucirumab may prolong progression free survival and overall survival, although it may increase the risk of all adverse events (fatigue, neutropenia, haemorrhage, nausea, stomatitis). The authors review the clinical studies of ramucirumab. Orv. Hetil., 2016, 157(40), 1587–1594.

scholarly journals Role of vascular endothelial growth factor receptor in the pro-proliferation activity of CD40-CD40L in AGS gastric cancer cells

2010 ◽  
Vol 4 (5) ◽  
pp. 797-802 ◽  
Author(s):  
Yongling Ning ◽  
Keqing Qian ◽  
Chunjian Qi
Keyword(s):  
Gastric Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Line ◽  
Growth Factor Receptor ◽  
Cancer Cell Line ◽  
Vascular Endothelial ◽  
Ags Cells ◽  
Endothelial Growth Factor

Abstract Background: CD40 is a type α-membrane protein of the tumor necrosis factor receptor super-family, and CD40- induced responses may mediate growth and angiogenesis in carcinoma cells. Objectives: Define the effect of CD40 ligation on AGS gastric cancer cell line and the role of vascular endothelial growth factor/vascular endothelial growth factor receptor (VEGF/VEGFR) signals in this process. Methods: We treated AGS cells with 1 μg/mL soluble CD40 ligand (sCD40L) with or without pre-incubation of either anti-VEGF mAb (MAB293) or VEGFR tyrosine kinase inhibitor (SU5416). We determined the growth effects by cell counts or [3H]-thymidine incorporation assay and VEGF levels in cell-free supernatant using enzymelinked immunosorbent assays. Results: The engagement of CD40-induced AGS cells proliferation accompanied by a significant increase autocrine VEGF through PI3K activation (p <0.05), and exogenous VEGF alone had no effect on spontaneous cell growth. SU5416 with a concentration of 8 μM lead to a dramatic decrease in cell survival induced by sCD40L (p <0.05), whereas MAB293 did not have the similar effect (p >0.05). Conclusion: CD40-CD40L interaction promoted AGS cancer cell line proliferation through a VEGFR-dependent signal pathway in the presence of an internal autocrine loop.

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