We have previously reported on vasohibin as a novel endothelium-derived
vascular endothelial growth factor (
VEGF)-inducible inhibitor of angiogenesis. The aim of our present study was to define the role of vasohibin in endometrioid endometrial
adenocarcinoma. We collected 78 sections of
endometrial carcinoma for assessment using immunohistochemistry. Twenty-seven were well differentiated (G1), 25 were moderately differentiated (G2), and 26 were poorly differentiated
endometrioid adenocarcinomas (G3). We also included 12 sections of normal cyclic endometria, six of which were in the proliferative phase and six were in the secretory phase. We investigated the expression of vasohibin, and compared it to
VEGF receptor-2 (VEGFR-2: KDR/flk-1), CD34, Ki-67,
VEGF-A, and D2-40 (as a lymphatic vessel marker). We assessed the ratio of vasohibin- and VEGFR-2-positive vessels in the stroma of
endometrial carcinoma. Immunohistochemical assessment was classified as negative or positive based on staining intensity. Vasohibin was selectively expressed on vascular endothelial cells in both cyclic endometria and
endometrial carcinomas. Vasohibin was highly expressed in the normal functional endmetrium of the secretory phase, especially in the spiral artery, and was highly expressed in all grades of
endometrioid adenocarcinomas. The stromal endothelial cells in G3 expressed vasohibin and
VEGFR-2 more frequently than these in G1. In
endometrioid adenocarcinomas, there was a significant correlation between the expression percentage of vasohibin and that of
VEGFR-2 (P < 0.0001, r(2) = 0.591). This is the first study to elucidate the correlation between expression of vasohibin in the stromal endothelial cells and that of
VEGFR-2 in human
carcinomas.