Expressions of VEGF, Vasohibin-1, and Vasohibin-2 in Benign Parotid Gland Tumor

Abstract

The vasohibin (VASH) family includes vasohibin-1 (VASH1), whose expression is induced in vascular endothelial cells by angiogenic factors such as vascular endothelial growth factor (VEGF) to inhibit angiogenesis via a negative feedback loop, and vasohibin-2 (VASH2), a homolog of VASH1, which is mainly expressed in cancer cells and promotes angiogenesis. VASH proteins have been associated with tumor angiogenesis and prognosis in various tumor types, drawing attention to their role in tumor biology. To date, no studies have reported on the expression of VEGF, VASH1, and VASH2 in benign parotid gland tumors. Therefore, in this study, we aimed to investigate their expression in these tumors. Our cohort consisted of 28 patients with benign parotid gland tumors, aged 31-79 (mean age 60.0 ± 13.8) years. Tumors were histologically diagnosed as pleomorphic adenoma in 15 patients (15 specimens) and Warthin’s tumor in 13 patients (15 specimens). Immunohistochemical staining for VEGF, VASH1, and VASH2 was assessed based on the percentage of stained cells per slide (0-100%) and staining intensity, quantified using the H score. Immunostaining for VEGF, VASH1, and VASH2 demonstrated that Warthin’s tumors had statistically significantly higher H-scores compared to pleomorphic adenomas. In addition, CD31 immunostaining showed a higher mean microvessel density (MVD) in the tumor stroma in Warthin’s tumors than in pleomorphic adenomas. Similarly, CD34 immunostaining showed a higher number of spindle cells in the tumor stroma in Warthin’s tumors than in pleomorphic adenomas. These findings suggest that the overexpression of VEGF, VASH1, and VASH2 is likely involved in the pathogenesis of benign parotid gland tumors.