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[Cancer Research 31, 348-365, March 1, 1971]
© 1971 American Association for Cancer Research

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Ultrastructural Analysis of Renal Mesenchymal Tumor Induced in the Rat by Dimethylnitrosamine

G. C. Hard and W. H. Butler

Toxicology Research Unit, Medical Research Council Laboratories, Woodmansterne Road, Carshalton, England

With a method of large-area sectioning to reduce the randomness of tissue sampling, 17 renal mesenchymal tumors induced by dimethylnitrosamine were examined with the electron microscope. Despite the broad histological spectrum displayed by the tumors, they were ultrastructurally very uniform. The predominant cell type was fibroblast-like, constituting the highly cellular areas and grading into a less active stellate cell type of fibrocytic or primitive mesenchymal nature in the highly stromal areas. Tumor cells also differentiated into types identical with pericytes, endothelial cells, vascular smooth muscle fibers, and rhabdomyoblasts. An outstanding feature was the tendency for tumor cells to form small groups enclosing a cleft-like lumen simulating capillary formation. The tumor areas were richly supplied with vascular channels lined by endothelial cells associated with pericytes, which were indistinguishable from adjacent free tumor cells. The nature of these structures and their frequency indicated that they were an integral part of the tumor. Epithelial structures consisted of sequestered, preexisting tubules and glomeruli and nests of transitional epithelium arising from engulfed pelvic lining. Some tubules were stimulated to hyperplastic proliferation. Cystic structures represented dilated tubules and Bowman's capsules. There was no evidence suggesting that any epithelial elements arose from bipotential differentiation of mesenchymal tumor cells. It was concluded that the dimethylnitrosamine-induced renal mesenchymal tumor cannot be classified as a nephroblastoma or embryonal nephroma but is a vascular neoplasm originating from mesenchymal cells within the renal cortical interstitial space, which retain the ability to function as vasoform reserve elements.

Received 7/23/70. Accepted 11/ 2/70.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1971 by the American Association for Cancer Research.