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. 2012 Jun;460(6):629-36.
doi: 10.1007/s00428-012-1236-9. Epub 2012 May 4.

Intratumoral hemorrhage, vessel density, and the inflammatory reaction contribute to volume increase of sporadic vestibular schwannomas

Affiliations

Intratumoral hemorrhage, vessel density, and the inflammatory reaction contribute to volume increase of sporadic vestibular schwannomas

Maurits de Vries et al. Virchows Arch. 2012 Jun.

Abstract

Vestibular schwannomas show a large variation in growth rate, making prediction and anticipation of tumor growth difficult. More accurate prediction of clinical behavior requires better understanding of tumor biological factors influencing tumor progression. Biological processes like intratumoral hemorrhage, cell proliferation, microvessel density, and inflammation were analyzed in order to determine their role in vestibular schwannoma development. Tumor specimens of 67 patients surgically treated for a histologically proven unilateral vestibular schwannoma were studied. Preoperative magnetic resonance imaging (MRI) scans were used to determine tumor size and to classify tumors as homogeneous, inhomogeneous, and cystic. Immunohistochemical studies evaluated cell proliferation (histone H3 and Ki-67), microvessel density (CD31), and inflammation (CD45 and CD68). Intratumoral hemorrhage was assessed by hemosiderin deposition. The expression patterns of these markers were compared with tumor size, tumor growth index, MRI appearance, patients' age, and duration of symptoms. No relation between cell proliferation and clinical signs of tumor volume increase or MRI appearance was found. Intratumoral hemosiderin, microvessel density, and inflammation were significantly positively correlated with tumor size and the tumor growth index. Cystic and inhomogeneous tumors showed significantly more hemosiderin deposition than homogeneous tumors. The microvessel density was significantly higher in tumors with a high number of CD68-positive cells. The volume increase of vestibular schwannomas is not based on cell proliferation alone. Factors like intratumoral bleeding, (neo)vascularization, and intensity of the inflammatory reaction also influence tumor volume.

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Figures

Fig. 1
Fig. 1
Examples of Chalkley counts in vascular hotspots, specimen a and b score 10 and 6, respectively (original magnification × 200)
Fig. 2
Fig. 2
a Proliferating cells (Ki-67/histone H3), b intratumoral bleeding (hemosiderin), c high microvessel density (CD31), and d intratumoral inflammation (CD45/CD68) (original magnification × 400)
Fig. 3
Fig. 3
Relation between CD68 expression and microvessel density. The mean Chalkley count is significantly higher in tumors with strong CD68 expression. Asterisk denotes statistical differences calculated with the Scheffe test

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