Vascular endothelial growth factor single‐nucleotide polymorphism in gall bladder cancer

2013 ◽  
Vol 28 (10) ◽  
pp. 1678-1685 ◽  
Author(s):  
Kumudesh Mishra ◽  
Anu Behari ◽  
Vinay Kumar Kapoor ◽  
M. Salman Khan ◽  
Swayam Prakash ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Bladder Cancer ◽  
Single Nucleotide Polymorphism ◽  
Growth Factor ◽  
Gall Bladder ◽  
Gall Bladder Cancer ◽  
Vascular Endothelial ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Endothelial Growth Factor

A vascular endothelial growth factor A genetic variant is associated with improved ventricular function and transplant-free survival after surgery for non-syndromic CHD

2017 ◽  
Vol 28 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Constantine D. Mavroudis ◽  
Daniel Seung Kim ◽  
Nancy Burnham ◽  
Alexandra H. Morss ◽  
Jerry H. Kim ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Single Nucleotide Polymorphism ◽  
Growth Factor ◽  
Ventricular Function ◽  
Vascular Endothelial ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Free Survival ◽  
Endothelial Growth Factor

AbstractBackgroundWe have previously shown that the minor alleles of vascular endothelial growth factor A (VEGFA) single-nucleotide polymorphism rs833069 and superoxide dismutase 2 (SOD2) single-nucleotide polymorphism rs2758331 are both associated with improved transplant-free survival after surgery for CHD in infants, but the underlying mechanisms are unknown. We hypothesised that one or both of these minor alleles are associated with better systemic ventricular function, resulting in improved survival.MethodsThis study is a follow-up analysis of 422 non-syndromic CHD patients who underwent neonatal cardiac surgery with cardiopulmonary bypass. Echocardiographic reports were reviewed. Systemic ventricular function was subjectively categorised as normal, or as mildly, moderately, or severely depressed. The change in function was calculated as the change from the preoperative study to the last available study. Stepwise linear regression, adjusting for covariates, was performed for the outcome of change in ventricular function. Model comparison was performed using Akaike’s information criterion. Only variables that improved the model prediction of change in systemic ventricular function were retained in the final model.ResultsGenetic and echocardiographic data were available for 335/422 subjects (79%). Of them, 33 (9.9%) developed worse systemic ventricular function during a mean follow-up period of 13.5 years. After covariate adjustment, the presence of the VEGFA minor allele was associated with preserved ventricular function (p=0.011).ConclusionsThese data support the hypothesis that the mechanism by which the VEGFA single-nucleotide polymorphism rs833069 minor allele improves survival may be the preservation of ventricular function. Further studies are needed to validate this genotype–phenotype association and to determine whether this mechanism is related to increased vascular endothelial growth factor production.

scholarly journals A Single-Nucleotide Polymorphism in a Half-Binding Site Creates p53 and Estrogen Receptor Control of Vascular Endothelial Growth Factor Receptor 1

2007 ◽  
Vol 27 (7) ◽  
pp. 2590-2600 ◽  
Author(s):  
Daniel Menendez ◽  
Alberto Inga ◽  
Joyce Snipe ◽  
Oliver Krysiak ◽  
Gilbert Schönfelder ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Single Nucleotide Polymorphism ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Regulatory Pathways ◽  
Flt1 Expression ◽  
Endothelial Growth Factor ◽  
Half Site

ABSTRACT Interactions between master regulatory pathways provide higher-order controls for cellular regulation. Recently, we reported a C→T single-nucleotide polymorphism (SNP) in the vascular endothelial growth factor receptor 1 (VEGFR-1/Flt1) promoter that merges human VEGF and p53 pathways. This finding suggested a new layer in environmental controls of a pathway relevant to several diseases. The Flt1-T SNP created what appeared to be a half-site p53 target response element (RE). The absence of information about p53 gene responsiveness mediated by half-site REs led us to address how it influences Flt1 expression. We now identify a second regulatory sequence comprising a partial RE for estrogen receptors (ERs) upstream of the p53 binding site. Surprisingly, this provides for synergistic stimulation of transcription specifically at the Flt1-T allele through the combined action of ligand-bound ER and stress-induced p53. In addition to demonstrating direct control of Flt1 expression by ER and p53 proteins acting as sequence-specific transcription factors at half-site REs, we establish a new interaction between three master regulatory pathways, p53, ER, and VEGF. The mechanism of joint regulation through half-sites is likely relevant to transcriptional control of other targets and expands the number of genes that may be directly controlled in master regulatory networks.

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