scholarly journals Effect of Anesthetic Technique on Serum Vascular Endothelial Growth Factor C and Transforming Growth Factor β in Women Undergoing Anesthesia and Surgery for Breast Cancer

2010 ◽  
Vol 113 (5) ◽  
pp. 1118-1125 ◽  
Author(s):  
Micheal Looney ◽  
Peter Doran ◽  
Donal J. Buggy

Background In breast cancer, vascular endothelial growth factor C, transforming growth factor β, placental growth factor, and fibroblast growth factor (acidic and basic) promote angiogenesis and metastases. We tested the hypothesis that a propofol-paravertebral anesthetic (PPA) technique would attenuate postoperative changes in these angiogenic factors to a greater extent than balanced general anesthesia (GA) and morphine analgesia in women undergoing surgery for primary breast cancer. Method Forty women with primary breast cancer undergoing surgical excision were randomized to receive either standard GA or PPA technique. Venous blood was sampled before and at 24 h after surgery and serum analyzed. The primary endpoint was a preoperative versus postoperative change in vascular endothelial growth factor C and transforming growth factor β concentrations. Results Using a visual analog scale (median [25-75% interquartile range]), PPA patients (1 [0-2]) had less pain at 2 h (P = 0.02) than did GA patients (3 [2-5]). The mean postoperative change in vascular endothelial growth factor C concentrations among GA patients was 733 versus 27 pg/ml for PPA patients (difference, 706 [97.5% CI, 280-1,130] pg/ml, P = 0.001). In contrast, the mean postoperative change in transforming growth factor β concentration among GA patients was -163 versus 146 pg/ml for PPA patients (difference, 309 [97.5% CI, -474 to -143] pg/ml, P = 0.005). Concentrations of placental growth factor and fibroblast growth factor, both acidic and basic, were undetectable in serum. Conclusion Anesthetic technique influences serum concentrations of factors associated with angiogenesis in primary breast cancer surgery.

CHEST Journal ◽  
2000 ◽  
Vol 118 (6) ◽  
pp. 1747-1753 ◽  
Author(s):  
Dong-sheng Cheng ◽  
Y. C. Gary Lee ◽  
Jeffrey T. Rogers ◽  
Elizabeth A. Perkett ◽  
J. Philip Moyers ◽  
...  

2002 ◽  
Vol 278 (8) ◽  
pp. 5750-5759 ◽  
Author(s):  
Pei-Wen Tsai ◽  
Shine-Gwo Shiah ◽  
Ming-Tsan Lin ◽  
Cheng-Wen Wu ◽  
Min-Liang Kuo

2004 ◽  
Vol 14 (1) ◽  
pp. 82-88
Author(s):  
M. SÖNMEZER ◽  
M. GÜNGÖR ◽  
A. Ensari ◽  
F. Ortaç

We aimed to evaluate the prognostic significance of microvessel density (MVD), vascular endothelial growth factor (VEGF), and transforming growth factor β (TGFβ), as well as to find out the relationship between MVD, and VEGF and TGFβ in epithelial ovarian cancer (EOC). Surgical specimens of 47 patients with stage I–IV primary EOC, who underwent extended surgical staging according to FIGO, were investigated. Five-μm thick tissue sections were immunostained with antibody to factor VIII-related antigen, and MVD was assessed at three separate areas of ×200 magnification. Expressions for VEGF and TGFβ were evaluated by immunohistochemical staining using related monoclonal antibodies. Results were correlated with clinicopathologic factors and survival. We did not find any correlation between MVD and clinicopathologic factors, or patient survival. Similarly, there was no association between the degree of VEGF staining and survival or clinicopathologic factors, except preoperative ascites volume, which was higher in patients showing moderate and intense VEGF staining than those with weak VEGF staining (P = 0.052). The expression of TGFβ was inversely correlated with preoperative CA-125 levels (P < 0.05). Furthermore, there was no correlation between MVD and the staining intensity of VEGF or TGFβ. In conclusion, angiogenesis does not appear as a prognostic factor in EOC. We suggest that VEGF is an important mediator of ascites formation, and that TGFβ, which is supposed to have tissue-specific actions in tumorigenesis, may have growth-inhibitory functions in EOC.


2014 ◽  
Vol 306 (6) ◽  
pp. H789-H796 ◽  
Author(s):  
Tieqiang Zhao ◽  
Wenyuan Zhao ◽  
Weixin Meng ◽  
Chang Liu ◽  
Yuanjian Chen ◽  
...  

Vascular endothelial growth factor (VEGF)-C is a key mediator of lymphangiogenesis. Our recent study shows that VEGF-C/VEGF receptors (VEGFR)-3 are significantly increased in the infarcted rat myocardium, where VEGFR-3 is expressed not only in lymph ducts but also in myofibroblasts, indicating that VEGF-C has an unrevealed role in fibrogenesis during cardiac repair. The current study is to explore the regulation and molecular mechanisms of VEGF-C in fibrogenesis. The potential regulation of VEGF-C on myofibroblast differentiation/growth/migration, collagen degradation/synthesis, and transforming growth factor (TGF)-β and ERK pathways was detected in cultured cardiac myofibroblasts. Our results showed that VEGF-C significantly increased myofibroblast proliferation, migration, and type I/III collagen production. Matrix metalloproteinase (MMP)-2 and -9 were significantly elevated in the medium of VEGF-C-treated cells, coincident with increased tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2. Furthermore, VEGF-C activated the TGF-β1 pathway and ERK phosphorylation, which was significantly suppressed by TGF-β or ERK blockade. This is the first study indicating that in addition to lymphangiogenesis, VEGF-C is also involved in fibrogenesis through stimulation of myofibroblast proliferation, migration, and collagen synthesis, via activation of the TGF-β1 and ERK pathways.


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