OBJECTIVES: Acoustic neurinoma (AN) can grow to a large size, but the growth-promoting molecular pathways remain unknown. As angiogenesis has been described as being activated in many cancers, we undertook this study in order to examine the microvascular network of AN and the expression of angiogenic growth factors and their cognate receptors in AN. The aim was to draw conclusions regarding the underlying mechanisms and potential benefit of a pathway-specific anticancer therapy. MATERIAL AND METHODS: Surgical specimens from 34 patients with AN were analysed immunohistochemically for the expression of vascular endothelial growth factor (VEGF), VEGF-receptor 1 (VEGF-R1), VEGF-receptor 2 (VEGF-R2) and transforming growth factor-beta1 (TGF-beta1). The microvessel density (MVD) was defined using CD31 staining and macrophage infiltration using CD68 staining. MVD was correlated to tumour size, patient age and duration of symptoms. RESULTS: With 1 exception each for VEGF and VEGF-R1, none of the 34 tumours expressed either VEGF, TGF-beta1, VEGF-R1 or -R2. No tumour-infiltrating macrophages were detected. The MVDs determined were low and did not correlate with tumour size, duration of symptoms or patient age. CONCLUSION: These findings indicate that ANs either do not express or express very low levels of the analysed proangiogenic growth factors. We conclude that tumour angiogenesis is not likely to be a relevant mechanism of AN growth and might therefore not be a suitable anticancer therapy target.
OBJECTIVES:Acoustic neurinoma (AN) can grow to a large size, but the growth-promoting molecular pathways remain unknown. As angiogenesis has been described as being activated in many cancers, we undertook this study in order to examine the microvascular network of AN and the expression of angiogenic growth factors and their cognate receptors in AN. The aim was to draw conclusions regarding the underlying mechanisms and potential benefit of a pathway-specific anticancer therapy. MATERIAL AND METHODS: Surgical specimens from 34 patients with AN were analysed immunohistochemically for the expression of vascular endothelial growth factor (VEGF), VEGF-receptor 1 (VEGF-R1), VEGF-receptor 2 (VEGF-R2) and transforming growth factor-beta1 (TGF-beta1). The microvessel density (MVD) was defined using CD31 staining and macrophage infiltration using CD68 staining. MVD was correlated to tumour size, patient age and duration of symptoms. RESULTS: With 1 exception each for VEGF and VEGF-R1, none of the 34 tumours expressed either VEGF, TGF-beta1, VEGF-R1 or -R2. No tumour-infiltrating macrophages were detected. The MVDs determined were low and did not correlate with tumour size, duration of symptoms or patient age. CONCLUSION: These findings indicate that ANs either do not express or express very low levels of the analysed proangiogenic growth factors. We conclude that tumour angiogenesis is not likely to be a relevant mechanism of AN growth and might therefore not be a suitable anticancer therapy target.
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Authors: Maurits de Vries; Pancras C W Hogendoorn; Inge Briaire-de Bruyn; Martijn J A Malessy; Andel G L van der Mey Journal: Virchows Arch Date: 2012-05-04 Impact factor: 4.064