To evaluate the role of vascular endothelial growth factor (VEGF) in the diagnosis of malignant pleural effusion, this study was carried out on thirty patients with exudative pleural effusion. They were divided into three groups, group I: included 10 patients with malignant pleural effusion, group II: included 10 patients with Tuberculous pleural effusion and group III included 10 patients with pneumonic pleural effusion. VEGF was estimated in both serum and pleural aspirates o all patients. The mean value of VEGF was significantly higher in pleural fluid of the malignant group as compared with the Tuberculous and the pneumonic groups. There was no statistically significant difference between the serums level of VEGF in the three groups although the serum level of VEGF in the malignant group was slightly higher as compared with the other groups. We concluded that estimation of pleural VEGF is very useful in the diagnosis of malignant pleural effusion.
INTRODUCTION
Vascular endothelial growth factor (VEGF) is a potent specific mutagen produced by endothelial cells and by macrophages. It is a member of a family of structurally related proteins. These proteins bind to the family of vascular endothelial growth factor receptors (VEGFRs), thereby stimulating various biologic processes. Placental growth factor (PIGF) and VEGF-B bind primarily to VEGFR-I.PIGH modulates angiogenesis and may also play a role in the inflammatory response VEGF-C and VEGF-D bind primarily to VEGFR-3 and stimulate lynphangiogenesis rather than angiogenesis.(Ferrara.1999)
VEGF exerts its effects by binding to and activating two structurally related membrane receptors tyrosine kinases, VEGFR-1 and VEGFR-2 which are expressed by endothelial cells within the blood vessel wall. VEGF also interacts with structurally distinct receptor neuropilin-1. Binding of VEGF to these receptors initiates a signaling cascade, resulting in the effects on gene expression and cell survival, proliferation, and migration (Ferrara. 1999).
VEGF stimulates vascular endothelial growth, survival and proliferation it plays a central role in the development of new blood vessels (angiogenesis) and also in survival of immature blood vessels (vascular maintenance) through preventing apoptosis of its vascular endothelial cells. VEGF is essential for establishing a functional vascular system during embryogenesis and early postnatal development. Many pro-angiogenetic factors stimulate VEGF expression, including epidermal growth factor, basic fibroblast growth factor, and platelet-derived growth factor and interleukin-la. VEGF levels are also directly regulated by environmental conditions such as pH, pressure and oxygen levels. VEGF can then stimulate the expression of factors important for angiogenesis, including antiapoptotic proteins, cell adhesion molecules, and matrix metalloproteinase. VEGF also stimulates vascular permeability in small blood vessels. The increased permeability causes the leakage of plasma proteins and the formation of an intravascular fibrin gel which provides a suitable environment for endothelial cell growth (Dvork, 2002).
In tumors, the high levels of VEGF result in vasculature that is extensively permeable and leaky, resulting in high interstitial pressure within the tumor and uneven delivery of nutrients, oxygen and therapeutic agents to the tumor which promotes its growth and metastasis (Ferrara, 1999).
Increased VEGF expression correlates with poor prognosis in many tumor types. Inhibition of VEFG represents a novel approach to anticancer therapy that may complement current therapeutic modalities (eg, radiation, chemotherapy, targeted biologic therapies) (Zhu et al., 2003
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