Epithelial versus endothelial CEACAM1 expression and angiogenesis in epididymal adenomatoid tumor.

BACKGROUND/AIM: To study the expression of the pro-angiogenic factor carcinoembryonic antigen-related cell adhesion molecule-1 (CEACAM1) in epididymal adeno-matoid tumor tissue, a very rare benign neoplasia, in relation to its vascularization. MATERIALS AND METHODS: Immunohistochemistry for CEACAM1 and for both endothelial markers CD31 and CD34 was performed in normal human epididymal and epididymal adenomatoid tumor tissue. The vessel density was calculated in four tumor regions with different degrees of vascularization in comparison to the vascularization of the normal epididymal tissue. RESULTS: CEACAM1 was found in normal epididymal epithelium, while the epithelium of tumor glands was mostly negative. Only few blood vessels and lymphatics in adenomatoid tumor tissue expressed CEACAM1. The assessment of vascularization revealed either equal or a significantly lower vessel density in some adenomatoid tumor regions in comparison to normal epididymal tissue. DISCUSSION: These data demonstrate that despite its epithelial down-regulation, CEACAM1 is not present in the majority of adenomatoid tumor blood vessels, which might be related to the lower angiogenic activity and benign behaviour of this tumor.

Infarcted adenomatoid tumor: a report of five cases of a facet of a benign neoplasm that may cause diagnostic difficulty.

We describe five cases in which adenomatoid tumors showed extensive necrosis, presumably due to infarction, and posed diagnostic difficulty. The tumors occurred in four males (three with epididymal tumors and one with an intratesticular tumor) and one female (with a parafallopian tube tumor) 35 to 44 years of age. Two of the men presented with acute scrotal pain simulating epididymitis, and two with a palpable mass. The parafallopian tube tumor was an incidental finding. The tumors were solitary, grossly well-circumscribed, uniformly solid masses that ranged in size from 1.1 to 3.5 cm. Microscopically, they were all characterized by central necrosis with pale mummified adenomatoid tumor identified at least focally but often overshadowed by nondescript necrotic tissue. Viable adenomatoid tumor was identified in all cases but was minor in amount in two of them. The necrosis was surrounded by a florid reactive process of fibroblasts and myofibroblasts that had plump nuclei often with prominent nucleoli, and occasional mitoses. Two of the epididymal cases had adjacent rete testis showing epithelial hyperplasia with hyaline globule formation. The microscopic appearance often suggested the possibility of a malignant neoplasm because of: 1) blurring of the normal relatively easily identifiable junction between adenomatoid tumor and adjacent tissue; 2) irregular pseudo-infiltration of fat by reactive tissue and adenomatoid tumor; 3) paucity of typical adenomatoid tumor due to the infarction and the fact that viable tumor usually showed a solid pattern; and 4) atypia of the associated reactive cells. This unemphasized feature of adenomatoid tumors may potentially lead to more aggressive therapy than warranted if it is not correctly interpreted.