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Access of tumor‐derived macromolecules and cells to the blood: An electron microscopical study of structural barriers in microvessel clusters in highly malignant primary prostate carcinomas
Author(s) -
Wieser Elisabeth,
Strohmeyer Dagmar,
Rogatsch Hermann,
Horninger Wolfgang,
Bartsch Georg,
Debbage Paul
Publication year - 2004
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20129
Subject(s) - microvessel , pathology , osmium tetroxide , stromal cell , bone canaliculus , prostate , ultrastructure , chemistry , biology , medicine , electron microscope , cancer , immunohistochemistry , optics , physics
BACKGROUND The neo‐angiogenetic microvessels forming a major reactive stromal element in highly malignant prostate neoplasms may exhibit fine‐structural features relevant to our understanding of the passage of macromolecules from tumor to blood, on the one hand, and of events facilitating the metastatic cascade, on the other hand. METHODS Ensuring rapid, optimal fixation in buffered glutaraldehyde was a foremost concern. Thin parings from radical prostatectomy specimens of Gleason scores (GS) 5–9 were taken from the tumor and from the contralateral side of the gland, glutaraldehyde‐fixed, diced to smaller than 1 mm 3 , postfixed in osmium tetroxide, embedded in Epon, ultrathin‐sectioned, contrasted with lead and uranyl salts, and viewed in a transmission electron microscope. RESULTS In dysplastic tissue areas, intraductal microvessels located in gland ducts were occasionally observed, and found to be aggressively invasive and highly active in producing neo‐angiogenetic sprouts. Closely spaced microvessel clusters contained almost exclusively neo‐angiogenetic microvessels, which were in cell–cell contact with numerous ameboid migratory cells, some of which were likely to be tumor cells. In these microvessel clusters, all structural barriers hindering passage of tumor‐derived molecules or cells to the blood were eliminated. CONCLUSION In microvessel clusters, the ultrastructural equivalent of microvascular hotspots, tumor invasion of microvessels is facilitated, but equally microvessels are observed invading the gland duct epithelial walls. This reciprocal invasivity of tumor cells and microvascular endothelial cells generates ideal conditions for tumor products and metastatic cells to enter the blood. © 2004 Wiley‐Liss, Inc.