The Expression Of MMP-2 And VEGF In Intracranial Hemangiopericytoma And The Relationship And Significance With Vasculogenic Mimicry

BackgroundBoth acranial hemangiopericytoma and meningioma originated from the mesoderm.The clinical manifestations and imaging findings of intracranial hemangiopericytoma are difficult to be distinguished from meningioma, however the prognosis and perioperative treatment are different form those of meningioma. Intracranial Hemangiopericytoma recurrence rate is higher and survival time is short and continue treatment have poor result. Intracranial hemangiopericytoma can infiltrate to surrounding tissues. The disease advance very fast and the blood supply become insufficient and generate a lot of neovascularizations. But now,the commonly used medications therapy targeted of angiogenesis to treat intracranial hemangiopericytoma is disappointing. Tumors invasion and metastasis are closely related to vessel and there are lots of ways of tumor blood.When studying microcirculation of human eye uveal melanoma, Maniotis found a new angiogenesis mechanism that was completely different from classical angiogenesis and didn't rely on vascular endothelial cells. The new mechanism was called "Tumor vasculogenic mimicry (VM)". Since then, the importance of VM in high-invasive cancer is gradually emphasized. Now VM has been found in a variety of high malignant tumors, such as melanoma, inflammatory breast cancer, liver cancer, prostate cancer. But there is no reseach and reports about the existence of VM in intracranial hemangiopericytoma in home and aborad. There are lots of regulated factors of tumor angiogenesis,of which VEGF and MMP-2 are very important.Matrix metalloproteinase 2 (MMP-2) is a zinc-dependent endopeptidase and is considered the most important matrix metalloproteinases in the process of tumor invasion. Vascular endothelial growth factor (VEGF) is a highly specific endothelial cell mitogen and the most important factor in the regulation of angiogenesis. VEGF expression level reflects vascular endothelial cell proliferation in tumor and tumor migration. In our study we will investigate the expression of MMP-2 and VEGF in intracranial hemangiopericytoma and the relationship and significance with vasculogenic mimicry by immunohistochemistry and immunofluorescence technique.This dissertation consisits of two parts:ⅠThe expression and significance of vasculogenic mimicry in intracranial hemangiopericytomaObjective To explore whether there was vasculogenic mimicry(VM) in intracranial hema-ngiopericytoma and its significance. Methods Select twelve intracranial hemangiopericytoma specimens to undergo HE staining and double staining of CD34 and PAS to observe the existence of VM. Results Typical vasculogenic mimicry expressed canal structures formed by tumor cells, canals are cord-like or beam-like, and red blood cells exist in the cannals; CD34-PAS double staining show PAS-positive material formed a base membrane like structure and exist between tumor cell and red blood cells. Tumor cells formed canal like structures outside the PAS-positive material. Conclusion VM existed in intracranial hemangiopericytoma tissues, VM participated the invasion mechanism of intracranial hemangiopericytomaⅡThe expression of MMP2 and VEGF in intracranial hemangiopericytoma and the relationship and significance with vasculogenic mimicry Objective To explore the expression of MMP-2 and VEGF in intracranial hemangiopericytoma and its relationship and significance with VM. Methods Select fifty mingioma specimens and twelve intracranial hemangiopericytoma specimens, detect the expression of MMP-2 and VEGF by the means of immunohistochemistry and immunofluorescence technique and semiquantitative analysis the fluorescence optical density of MMP-2 and VEGF by Image-Pro Plus software and determinate its microvascular density (MVD). Results In two kinds of specimens above mentioned, the expression of MMP2 and VEGF advance gradually,theirs disparity have statistical significance (P＜0.01),the expression of MMP-2 in the intracranial hemangiopericytoma tissues which observed VM is higher than that which not observed VM (P＜0.01), the expression of VEGF and MVD in the intracranial hemangiopericytoma tissues which observed VM is lower than that which not observed VM (P＜0.01). Conclusion MMP2 and VEGF are associated with the degree of malignancy of tumor, and participate in the formation of VM. VM and MMP-2 may be the new target of intracranial hemangiopericytoma on the aspect of anti-angiogenic cancer therapy.