Genetic polymorphism of the plasminogen activator inhibitor-1 is associated with an increased risk of endometrial cancer

2011 ◽  
Vol 104 (7) ◽  
pp. 755-759 ◽  
Author(s):  
Chung-Kuang Su ◽  
Kun-Tu Yeh ◽  
Chao-Bin Yeh ◽  
Po-Hui Wang ◽  
Esther Shih-Chu Ho ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Genetic Polymorphism ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
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 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.

Plasminogen Activator Inhibitor-1 Levels and Polymorphisms

2002 ◽  
Vol 126 (11) ◽  
pp. 1401-1404
Author(s):  
Charles W. Francis
Keyword(s):  
Venous Thromboembolism ◽  
Plasminogen Activator ◽  
Plasma Levels ◽  
Plasminogen Activator Inhibitor ◽  
Case Control Studies ◽  
Plasminogen Activator Inhibitor 1 ◽  
Published Evidence ◽  
Increased Risk ◽  
Activator Inhibitor ◽  
Pai 1

Abstract Objective.—To review the published evidence of a relationship between levels of plasminogen activator inhibitor-1 (PAI-1) or the 4G/5G polymorphism of the PAI-1 gene and the occurrence of venous thromboembolic disease. Methods.—Review of the medical literature using computerized databases and a review of secondary sources identified through bibliographies. Data Synthesis.—Plasminogen activator inhibitor-1 is an important inhibitor of the fibrinolytic system, so it is biologically plausible that elevated levels could suppress fibrinolysis and result in an increased risk of thrombosis. Several small studies reported associations between PAI-1 levels and venous thromboembolism, some of which appear to be familial. Problems with these studies include variations in PAI-1 plasma levels due to circadian changes and the acute phase response, as well as alterations due to common comorbid disease states. More recent investigations have focused on genetic polymorphisms, particularly the 4G/5G insertion/deletion in the promoter region, affecting transcription rates. The relation of 4G/5G to venous thrombosis has been investigated primarily in case-control studies, which have produced inconsistent findings. Most studies, however, have reported higher PAI-1 plasma levels in individuals with 4G/4G. Conclusions.—The evidence regarding the relationship between an elevated PAI-1 plasma level or PAI-1 genetic polymorphism and the risk of venous thromboembolism is conflicting. There is insufficient information to recommend use of PAI-1 levels or genotype in evaluating thrombophilia.

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