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Vasculature in nontumorous hypophyses, pituitary adenomas, and carcinomas: A quantitative morphologic study

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Abstract

Vascular supply is essential for tumor proliferation and metastasis formation. Correlation was noted between vascular density and tumor size as well as metastases in several tumor types. The aim of the present study was to assess vascular density in nontumorous hypophyses, pituitary adenomas, primary pituitary carcinomas, and carcinomas metastatic to the pituitary.

Twenty nontumorous hypophyses, 87 endocrinologically active or inactive pituitary adenomas, 8 primary pituitary carcinomas, 8 metastatic carcinomas, and 10 randomly selected noninvasive and 6 invasive adenomas were included in the study. Tissues were fixed in formalin, embedded in paraffin, cut, stained with hematoxylin and eosin, PAS, and immunostained for adenohypophysial hormones as well as Factor VIII-related antigen using the streptavidin-biotin-peroxidase complex method Four counts were performed: percentage of capillary area, number of vessels per field, percentage of endothelial cells, and number of endothelial cells per field. The results show that pituitary adenomas have significantly lower vascular densities as compared to nontumorous adenohypophyses. Prolactin-producing adenomas removed from untreated patients have the highest counts and growth hormone-producing adenomas the lowest counts. However, the observed differences among adenoma types are not of statistical significance. No differences are noted between noninvasive and invasive tumors. Primary pituitary carcinomas show no significant increase in vascular densities. Some metastatic tumors exhibit high vascularity. It can be concluded that pituitary adenomas have a limited capacity to induce angiogenesis. Lack of significant angiogenesis may play a role in the slow pace of pituitary tumor growth and rarity of metastases.

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Jugenburg, M., Kovacs, K., Stefaneanu, L. et al. Vasculature in nontumorous hypophyses, pituitary adenomas, and carcinomas: A quantitative morphologic study. Endocr Pathol 6, 115–124 (1995). https://doi.org/10.1007/BF02739874

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