The prognostic value of vascular endothelial growth factor, urokinase plasminogen activator and plasminogen activator inhibitor-1 in node-negative breast cancer

2004 ◽  
Vol 19 (4) ◽  
pp. 282-288 ◽  
Author(s):  
S. Meo ◽  
Ruggero Dittadi ◽  
L. Peloso ◽  
M. Gion
Keyword(s):  
Breast Cancer ◽  
Plasminogen Activator ◽  
Prognostic Value ◽  
Plasminogen Activator Inhibitor ◽  
Vascular Endothelial ◽  
Plasminogen Activator Inhibitor 1 ◽  
Node Negative ◽  
Node Negative Breast Cancer ◽  
Endothelial Growth Factor ◽  
Activator Inhibitor

The Prognostic Value of Vascular Endothelial Growth Factor, Urokinase Plasminogen Activator and Plasminogen Activator Inhibitor-1 in Node-Negative Breast Cancer

2004 ◽  
Vol 19 (4) ◽  
pp. 282-288 ◽  
Author(s):  
S. Meo ◽  
R. Dittadi ◽  
L. Peloso ◽  
M. Gion
Keyword(s):  
Breast Cancer ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Vascular Endothelial ◽  
Plasminogen Activator Inhibitor 1 ◽  
Node Negative ◽  
Node Negative Breast Cancer ◽  
Endothelial Growth Factor ◽  
The Relationship ◽  
Pai 1

The vascular endothelial growth factor (VEGF) and the plasminogen activator system play an essential role in solid tumor angiogenesis and in tumor invasion and metastasis. In the present study we investigated the relationship between patient outcome and levels of VEGF, urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) in tumor cytosols of 196 node-negative primary invasive breast cancer patients who did not receive any adjuvant therapy. The median follow-up was 65 months. VEGF, uPA and PAI-1 were measured by commercially available enzyme-linked immunosorbent assays. Cox's univariate analysis showed that pT (p=0.0007), uPA (p=0.0156) and PAI-1 (p=0.0015) had a significant impact on relapse-free survival, whereas VEGF did not have any prognostic value (p=0.18). Bivariate analysis showed significant interactions between uPA and PAI-1 (p=0.0035) and between VEGF and PAI-1 (p=0.006). Our study confirms that uPA and PAI-1 cytosol levels can be considered as prognostic factors for relapse-free survival in node-negative breast cancer. Moreover, the interaction between VEGF and PAI-1 warrants further investigation into the relationship between the biomarkers of angiogenesis and those of the protease cascade.

scholarly journals Plasminogen activator inhibitor-1 (PAI-1) gene 4G/5G promoter polymorphism is not associated with breast cancer.

2000 ◽  
Vol 47 (1) ◽  
pp. 191-199 ◽  
Author(s):  
J Błasiak ◽  
B Smolarz
Keyword(s):  
Breast Cancer ◽  
Plasminogen Activator ◽  
Pcr Amplification ◽  
Plasminogen Activator Inhibitor ◽  
Cancer Tissue ◽  
Plasminogen Activator Inhibitor 1 ◽  
Node Negative ◽  
Node Positive ◽  
Activator Inhibitor ◽  
Pai 1

The antigen content of plasminogen activator inhibitor-1 (PAI-1) in primary breast cancer tissue extracts may be of strong prognostic value: high levels of PAI-1 in tumors predict poor prognosis for patients. The gene encoding PAI-1 is highly polymorphic and an insertion (5G)/deletion (4G) polymorphism in the PAI-1 gene promoter (the 4G/5G polymorphism), may have functional significance in PAI-1 expression. In the present work the distribution of genotypes and frequency of alleles of the 4G/5G polymorphism in subjects with breast cancer were investigated. Tumor tissues were obtained from 100 postmenopausal women with node-negative and node-positive ductal breast carcinoma with uniform tumor size. Blood samples from age matched healthy women served as control. The 4G/5G polymorphism was determined by PCR amplification using the allele specific primers. The distribution of the genotypes of the 4G/5G polymorphism in both control and patients did not differ significantly (P > 0.05) from those predicted by the Hardy-Weinberg distribution. There were no differences in the genotype distributions and allele frequencies between node-positive and node-negative patients. The 4G/5G polymorphism may not be linked with elevated level of PAI-1 observed in breast cancer and therefore may not be associated with appearance and/or progression of breast cancer.

Prognostic value of pre-surgical plasma PAI-1 (plasminogen activator inhibitor-1) levels in breast cancer

2009 ◽  
Vol 124 (4) ◽  
pp. 403-408 ◽  
Author(s):  
Raffaele Palmirotta ◽  
Patrizia Ferroni ◽  
Annalisa Savonarola ◽  
Francesca Martini ◽  
Filippo Ciatti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Plasminogen Activator ◽  
Prognostic Value ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor ◽  
Pai 1

Increased vascular endothelial growth factor may account for elevated level of plasminogen activator inhibitor-1 via activating ERK1/2 in keloid fibroblasts

2004 ◽  
Vol 286 (4) ◽  
pp. C905-C912 ◽  
Author(s):  
Yidi Wu ◽  
Qunzhou Zhang ◽  
David K. Ann ◽  
Anita Akhondzadeh ◽  
Hai S. Duong ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Normal Skin ◽  
Plasminogen Activator Inhibitor ◽  
Vascular Endothelial ◽  
Plasminogen Activator Inhibitor 1 ◽  
Keloid Formation ◽  
Endothelial Growth Factor ◽  
Activator Inhibitor ◽  
Pai 1 ◽  
Keloid Fibroblasts

Keloids are characterized as an “overexuberant” healing response in which disequilibrium between production and catabolism of extracellular matrix (ECM) occurs. Previous studies from our laboratory and others demonstrate an intrinsically higher level of plasminogen activator inhibitor-1 (PAI-1) expression in keloid tissues and cultured fibroblasts compared with normal bordering skin. These findings support the concept that an altered balance of activator and inhibitor activities in the plasminogen system, in particular, an overexpression of PAI-1, may partly contribute to keloid formation and tissue fibrosis. Vascular endothelial growth factor (VEGF) has been implicated as a critical factor in regulating angiogenesis and inflammation under both physiological and pathological conditions. This study was designed to assess whether VEGF plays a role in keloid fibrosis. We report that VEGF was expressed at higher levels in keloid tissues and their derived fibroblasts compared with their associated normal skin. We have further demonstrated that VEGF stimulated the expression of PAI-1, but not urokinase plasminogen activator (uPA), in keloid fibroblasts at both mRNA and protein levels, in a dose- and time-dependent manner. However, treatment of normal skin fibroblasts with VEGF exerted little effects on PAI-1 gene expression. Additionally, we have characterized for the first time that the extracellular signal-regulated kinase (ERK)1/2 signaling pathway is mainly involved in VEGF-induced PAI-1 expression and have demonstrated its potential as a target molecule for modulation of scar fibrosis. These findings suggest that VEGF may play an important role in keloid formation by altering ECM homeostasis toward a state of impaired degradation and excessive accumulation.

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