Brain Edema in Meningiomas Is Associated with Increased Vascular Endothelial Growth Factor Expression

Goldman, Corey K.; Bharara, Suman; Palmer, Cheryl A.; Vitek, Jiri J.; Tsai, Jui‐Chang; Weiss, Heidi L.; Gillespie, G. Yancey

doi:10.1097/00006123-199706000-00029

Cited by 167 publications

(96 citation statements)

References 34 publications

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“…Meningiomas with edema contained significantly higher levels of vascular endothelial growth factor messenger RNA than those without edema in 16 tumors analyzed by Kalkanis and associates [22] and in 18 tumors analyzed by Provias and colleagues. [31] Increased vascular endothelial growth factor detected by immunostaining correlated with the degree of edema in 37 tumors examined by Goldman, et al [14] The volume of peritumoral edema in 15 meningiomas correlated with tumor plasminogen activator content in a study by Quindlen and Bucher. [32] Hirashima and coworkers [15] found that platelet-activating factor immunostaining correlated with peritumoral edema in 31 patients.…”

Section: Discussionmentioning

confidence: 92%

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

Mantle¹,

Lach²,

Delgado³

et al. 1999

FOC

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Object The goal of this study was to determine whether the quantity of peritumoral brain edema displayed on computerized tomography (CT) scanning could be correlated with brain invasion and subsequent recurrence of meningiomas. Methods One hundred thirty-five patients who underwent resection of intracranial meningiomas at the Ottawa Civic Hospital were followed during the period 1980 to 1998. A complete resection was defined as one in which tumor, invaded bone, and involved dura were removed. Tumors were examined microscopically for evidence of brain invasion. The mean follow-up period was 9 years (± 4 years, standard deviation [SD]) and the mean time to recurrence was 5 years (± 4 years, SD). The authors used a simple grading system based on the average thickness (in centimeters) of edema seen on an axial CT slice showing the most tumor. Edema grade was linearly related to edema volume determined by digitizing the scans (r = 0.96; 29 cases). The chance of brain invasion increased by 20% for each centimeter of edema (rs = 1, p < 0.0001; 124 cases). The presence of brain invasion was predictive of recurrence after complete resection with an accuracy of 83%, a sensitivity of 89%, and a specificity of 82%. The chance of recurrence within 10 years after complete resection was given by the equation: percentage chance of recurrence = (centimeter of edema)3 X 0.7, which can be used to predict the chance of recurrence based on findings on CT scans (rs = 1.00, p < 0.0001; 86 patients). Statistical significance was confirmed using Kaplan-Meier and univariate and multivariate analyses. Completeness of resection was the most powerful predictor of recurrence (p < 0.00001, r = 0.6), followed by edema grade and brain invasion (both p = 0.02, r = 0.1). Patient age and gender and tumor location, size, and histological subtype were nonsignificant factors. Conclusions Brain invasion causes peritumoral edema. Invaded brain tissue is also the source of residual cells in cases of tumor recurrence after gross-total resection.

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Section: Discussionmentioning

confidence: 92%

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

Mantle¹,

Lach²,

Delgado³

et al. 1999

FOC

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“…for the development of ischemia-and tumor-induced vasogenic brain edema (13). To examine whether rVEGF affects the ZO-2 protein level, we exposed HBMECs to rVEGF (50 ng/ml) for 3 h (Fig.…”

Section: Zo-2 Reduction By Rvegf Is Recovered By Combination Treatmenmentioning

confidence: 99%

“…Vascular endothelial growth factor (VEGF), known as vascular permeability factor, is a possible candidate for the development of ischemia-and tumor-induced vasogenic brain edema (13,14). During development, VEGF and Ang-1 collaborate to regulate vascular formation (15).…”

Section: Introductionmentioning

confidence: 99%

Angiopoietin-1 reduces vascular endothelial growth factor-induced brain endothelial permeability via upregulation of ZO-2

Lee

Kim²,

Jun³

et al. 1998

Int J Mol Med

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Abstract. Brain microvessels possess barrier structures comprising tight junctions which are critical for the maintenance of central nervous system homeostasis. Brain vascular diseases, such as ischemic stroke damage to blood-brain barrier, increase the vascular permeability, and then lead to vasogenic brain edema. Herein, we examined whether angiopoietin-1 (Ang-1) could regulate zonula occludens-2 (ZO-2) expression and counteract vascular endothelial growth factor (VEGF)-induced vascular permeability. When we treated brain microvascular endothelial cells with Ang-1, Ang-1 caused a time-and dosedependent increase of ZO-2 and down-regulation in endothelial permeability. VEGF, one of the key regulators of ischemiainduced vascular permeability, increased endothelial cell permeability in vitro, whereas, Ang-1 reversed this VEGF effect by up-regulating ZO-2 expression. Additionally, the recovery effect of Ang-1 on permeability was strongly blocked by siRNA against ZO-2. Collectively, our results suggest that Ang-1 shows anti-permeability activity through up-regulation of ZO-2.

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“…The VEGF-A mRNA is expressed by meningioma cells, and several studies demonstrated that VEGF-A levels in meningiomas are associated with the extent of peritumoral edema. 10 Meningiomas with high VEGF-A expression also tend to recruit pial arterial supply and are associated with increased edema. 11 Although some groups have suggested that VEGF-A transcription is associated with tumor vascularity, and that VEGF-A mRNA expression may correlate with meningioma vascularity, 12 no study has confirmed the relationship between vessel density, VEGF level, and histologic grade.…”

Section: Factors Related To Meningioma Invasion and Growthmentioning

confidence: 99%

Molecular Biology of Unreresectable Meningiomas: Implications for New Treatments and Review of the Literature

et al. 2008

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Even though meningiomas are most often benign tumors, they can be locally invasive and can develop in locations that prevent surgical treatment. The molecular and biologic factors underlying meningioma development are only now beginning to be understood. Genetic factors such as mutations in the neurofibromatosis-2 gene and in chromosomes 1, 9, and 10 play important roles in meningioma development and may be responsible for atypical tumors in some cases. Cellular factors such as telomerase activation and tyrosine kinase receptor mutations may also play an important role. Finally, autocrine and paracrine factors including epidermal growth factor receptor, platelet-derived growth factor-1, and fibroblast growth factor have been implicated in the development of some tumors. Although the relationship between the various factors implicated in tumor development is unknown, understanding these factors will be critical in the treatment of malignant or surgically inaccessible tumors.

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Brain Edema in Meningiomas Is Associated with Increased Vascular Endothelial Growth Factor Expression

Abstract: These data suggest that meningioma-associated edema may be a result of the capacity of meningioma cells to produce VPF/VEGF locally, leading to increased tumor neovascularization and enhanced vascular permeability.

Cited by 167 publications

References 34 publications

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

Predicting the probability of meningioma recurrence based on the quantity of peritumoral brain edema on computerized tomography scanning

Angiopoietin-1 reduces vascular endothelial growth factor-induced brain endothelial permeability via upregulation of ZO-2

Molecular Biology of Unreresectable Meningiomas: Implications for New Treatments and Review of the Literature

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