Rosuvastatin- and Heparin-Loaded Poly(l-lactide-co-caprolactone) Nanofiber Aneurysm Stent Promotes Endothelialization via Vascular Endothelial Growth Factor Type A Modulation

2018 ◽  
Vol 10 (48) ◽  
pp. 41012-41018 ◽  
Author(s):  
Peixi Liu ◽  
Yingjun Liu ◽  
Peiliang Li ◽  
Yingjie Zhou ◽  
Yaying Song ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Type A ◽  
Vascular Endothelial ◽  
Factor Type ◽  
Endothelial Growth Factor

Clinical Relevance of Vascular Endothelial Growth Factor Type A (VEGFA) and VEGF Receptor Type 2 (VEGFR2) Gene Polymorphism In Chronic Lymphocytic Leukemia

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4467-4467
Author(s):  
Joanna Gora-Tybor ◽  
Krzysztof Jamroziak ◽  
Zofia Szemraj ◽  
Janusz Szemraj ◽  
Ewa Lech-Maranda ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Chronic Lymphocytic Leukemia ◽  
Research Funding ◽  
Lymphocytic Leukemia ◽  
Allele Frequencies ◽  
Vascular Endothelial ◽  
Factor Type ◽  
Endothelial Growth Factor

Abstract Abstract 4467 Vascular endothelial growth factor type A (VEGFA) is a key regulator of angiogenesis and vascular permeability. Given that chronic lymphocytic leukemia (CLL) cells secrete VEGFA, express VEGFA receptors and circulate in blood with increased VEGFA level it is likely that VEGFA-mediated signaling may influence CLL clone survival. In this case-control study we verified the hypothesis that inherited differences in activities of VEGFA and its main receptor in CLL, vascular endothelial growth factor receptor type 2 (VEGFR2, also known as kinase insert domain-containing receptor/fetal liver kinase-1, Flk/1/KDR) impact predisposition to CLL or the course of the disease. Four functional single nucleotide polymorphisms (SNPs) including two SNPs in VEGFA gene, namely +405G>C (rs2010963) and +936C>T (rs3025039) and two SNPs in VEGFR2 gene, namely -271G>A and +1719A>T (rs1870377) were genotyped using PCR-based assays in 175 Caucasian CLL patients and 133 ethnically, geographically, age and sex matched controls. The minor allele frequencies in CLL patients were found as follows: 0.36 for +405C VEGFA allele, 0.17 for +936T VEGFA allele, 0.46 for -271 VEGFR2 allele and 0.35 for +1719A VEGFR2 allele. The genotype and allele frequencies of all tested SNPS in VEGFA and VEGFR2 genes did not differ significantly between cases and controls (p>0.05). No genotype or allele was significantly associated with important prognostic factors in CLL including clinical stage, IgVH mutational status, ZAP-70 expression and FISH cytogenetic abnormalities. Furthermore, the carriers of different VEGFA and VEGFR2 genetic variants had comparable time to CLL treatment initiation. In conclusion, the results of our study do not support major involvement of genetic polymorphisms in VEGFA mediated pathway in susceptibility to CLL or its outcome. Disclosures: Robak: GlaxoSmithKline: Consultancy, Honoraria, Research Funding; Genmab: Consultancy, Research Funding; Roche: Consultancy, Honoraria, Research Funding.

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