scholarly journals Genetic variants in the plasminogen activator inhibitor-1 gene are associated with an increased risk of radiation pneumonitis in lung cancer patients

2017 ◽  
Vol 6 (3) ◽  
pp. 681-688 ◽  
Author(s):  
Bo Liu ◽  
Yang Tang ◽  
Minxiao Yi ◽  
Qingxu Liu ◽  
Huihua Xiong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Plasminogen Activator ◽  
Genetic Variants ◽  
Radiation Pneumonitis ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Lung Cancer Patients ◽  
Increased Risk ◽  
Activator Inhibitor

The association between the 4G/5G polymorphism in the promoter of the plasminogen activator inhibitor-1 gene and deep venous thrombosis in young people

2005 ◽  
Vol 20 (1) ◽  
pp. 48-52 ◽  
Author(s):  
A Mansilha ◽  
F Araújo ◽  
M Severo ◽  
S M Sampaio ◽  
T Toledo ◽  
...  
Keyword(s):  
Young People ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Control Group ◽  
Plasminogen Activator Inhibitor 1 ◽  
Increased Risk ◽  
Activator Inhibitor ◽  
Pai 1

Objective: To evaluate the association between the 4G/5G polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene and deep venous thrombosis (DVT) in young people. Methods: Prevalence of the 4G/5G polymorphism was investigated using DNA analysis in a population of 81 consecutive and unrelated patients with an objectively documented first episode of DVT under 40 years old and in a control group of 88 healthy subjects. Results: The frequency of genotypes among patients was 0.27 4G/4G, 0.49 4G/5G and 0.23 5G/5G, corresponding to a frequency of 0.52 for the 4G allele. In the control group the results were, respectively, 0.24, 0.44 and 0.32, corresponding to a frequency of 0.46 for the 4G allele. The odds ratio (OR) for homozygous 4G genotype was 1.5 (95% confidence interval: 0.7–3.6), which was not statistically significant ( P = 0.51). Conclusion: In this study, the 4G/5G polymorphism in the promoter of the PAI-1 gene, including the homozygous 4G genotype, was not associated with a significantly increased risk of DVT in young people.

Fibrinogen, Plasminogen Activator Inhibitor-1, and Carotid Intima-Media Wall Thickness in the NHLBI Family Heart Study

1998 ◽  
Vol 79 (02) ◽  
pp. 400-404 ◽  
Author(s):  
James Pankow ◽  
Roger Williams ◽  
Gregory Evans ◽  
Michael Province ◽  
John Eckfeldt ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Carotid Atherosclerosis ◽  
Intima Media Thickness ◽  
Plasminogen Activator Inhibitor ◽  
Carotid Intima Media Thickness ◽  
Family Type ◽  
Plasminogen Activator Inhibitor 1 ◽  
Increased Risk ◽  
Activator Inhibitor ◽  
Pai 1

SummarySeveral studies have linked higher plasma fibrinogen and plasminogen activator inhibitor (PAI-1) concentrations with increased risk of cardiovascular disease. We studied whether members of families with increased occurrence of coronary heart disease (CHD) have increased levels of fibrinogen and PAI-1 and whether subclinical carotid atherosclerosis is associated with these two hemostatic factors. Contrary to our hypothesis, fibrinogen and PAI-1 antigen levels were not different between high CHD risk families versus random families. Adjusted for age and family type, fibrinogen and PAI-1 were both associated positively with carotid intima-media thickness assessed by B-mode ultrasound. However, adjustment for lifestyle and medical covariates essentially eliminated these associations. These data suggest 1) elevated fibrinogen and PAI-1 do not explain clustering of CHD in families and 2) fibrinogen and PAI-1 may partly mediate the effects of other risk factors on carotid atherosclerosis, though the data are also consistent with them playing no causal role.

Plasminogen activator inhibitor-1 polymorphism is associated with increased risk for oral cancer

Oral Oncology ◽  
2006 ◽  
Vol 42 (9) ◽  
pp. 888-892 ◽  
Author(s):  
E. Vairaktaris ◽  
C. Yapijakis ◽  
Z. Serefoglou ◽  
A. Vylliotis ◽  
J. Ries ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Increased Risk ◽  
Activator Inhibitor

scholarly journals Plasminogen activator inhibitor 1 and venous thrombosis in pancreatic cancer

2021 ◽  
Vol 5 (2) ◽  
pp. 487-495
Author(s):  
Yohei Hisada ◽  
Kenison B. Garratt ◽  
Anaum Maqsood ◽  
Steven P. Grover ◽  
Tomohiro Kawano ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Venous Thrombosis ◽  
Cancer Patients ◽  
Plasminogen Activator ◽  
Cell Lines ◽  
Plasminogen Activator Inhibitor ◽  
Pancreatic Tumors ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor ◽  
Pai 1

Abstract Pancreatic cancer patients have a high risk of venous thromboembolism (VTE). Plasminogen activator inhibitor 1 (PAI-1) inhibits plasminogen activators and increases the risk of thrombosis. PAI-1 is expressed by pancreatic tumors and human pancreatic cell lines. However, to date, there are no studies analyzing the association of active PAI-1 and VTE in pancreatic cancer patients. We investigated the association of active PAI-1 in plasma and VTE in pancreatic cancer patients. In addition, we determined if the presence of human pancreatic tumors expressing PAI-1 impairs venous thrombus resolution in mice. Plasma levels of active PAI-1 in patients with pancreatic cancer and mice bearing human tumors were determined by enzyme-linked immunosorbent assay. We measured PAI-1 expression in 5 different human pancreatic cancer cell lines and found that PANC-1 cells expressed the highest level. PANC-1 tumors were grown in nude mice. Venous thrombosis was induced by complete ligation of the inferior vena cava (IVC). Levels of active PAI-1 were independently associated with increased risk of VTE in patients with pancreatic cancer (subdistribution hazard ratio per doubling of levels: 1.39 [95% confidence interval, 1.09-1.78], P = .007). Mice bearing PANC-1 tumors had increased levels of both active human and active mouse PAI-1 and decreased levels of plasmin activity. Importantly, mice bearing PANC-1 tumors exhibited impaired venous thrombus resolution 8 days after IVC stasis compared with nontumor controls. Our results suggest that PAI-1 contributes to VTE in pancreatic cancer.

scholarly journals Failure to Lyse Venous Thrombi Because of Elevated Plasminogen Activator Inhibitor 1 (PAI-1) and 4G Polymorphism of Its Promotor Genome (The PAI-1/4G Syndrome)

2010 ◽  
Vol 16 (5) ◽  
pp. 574-578 ◽  
Author(s):  
Murray M. Bern ◽  
Nancy McCarthy
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activators ◽  
Plasminogen Activator Inhibitor 1 ◽  
Genomic Changes ◽  
Increased Risk ◽  
High Prevalence ◽  
Residual Thrombus ◽  
Activator Inhibitor ◽  
Pai 1

Plasminogen activator Inhibitor 1 (PAI-1) inhibits plasminogen activators leading to decreased fibrinolysis and increased risk of thromboembolic disease (TED). Shifts in PAI-1 promoter genome from normal 5G>5G to 4G>5G or 4G>4G alleles are associated with overexpression of PAI-1. In this study patients with residual venous thrombi were observed to have increased PAI-1 levels and more frequent shifts to 4G alleles. Of the 26, 20 (76.9%) patients with unresolved thrombus had elevated PAI-1 values. 4G genomic shifts were found in 92.9% patients studied. Normal PAI-1 levels were found in 5 patients with 4G polymorphisms. Thus, PAI-1 is often elevated among patients with residual thrombus, with an unexpectedly high prevalence of the 4G polymorphism of the promoter genome. Patients with persistent thrombus should be considered at risk of having constituently increased PAI-1 due to genomic changes in the PAI-1 promoter genome. Hypotheses are proposed to explain those with normal PAI-1, despite having 4G polymorphisms.

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