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STEM Cells and Liver Carcinogenesis: Contributions of Light, Confocal and Electron Microscopy

Published online by Cambridge University Press:  02 July 2020

P. M. Novikoff
Affiliation:
Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, 10461
A. Yam
Affiliation:
Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, 10461
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Extract

Three cell types not previously described were revealed by the application of several microscopic procedures in combination with cytochemistry and irnmunocytochemistry in the livers of rats treated according to the Solt et al carcinogenesis protocol. This protocol consists of the administration of an initiating carcinogen (diethynitrosamine), a mitoinhibitory carcinogen, (acethylaminofluorene) and a growth stimulus (partial hepatectomy) (1). Two of the cell types were found in intrahepatic bile ductules and one within the connective tissue stroma surrounding the ductules. These findings have implications for understanding the cell lineage pathways that operate in an experimental rodent hepatocarcinogenesis system in which hepatocyte regeneration is inhibited and in which preneoplastic nodules and hepatomas develop. Our previous studies have determined some of the enzymatic, antigenic and structural properties of these cell types and their interrelations to each other, to parenchymal hepatocytes and to preneoplastic nodules (2).

Proliferation of bile ductule cells occurs early (24-48 hrs) after the partial hepatectomy step of the protocol with extensive branching of the ductules into the hepatic parenchyma.

Type
Neoplasia: Abnormal Cell Growth or Death/Apoptosis? Insights from Microscopy
Copyright
Copyright © Microscopy Society of America 1997

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References

1.Solt, D. B.et al., Am J Path 88(1977) 595.Google Scholar
2.Novikoff, P. M.et al., Am J Path, 148 (1996)1473Google Scholar
3.Thorgeirsson, S. S. In: Liver Regeneration and Carcinogenesis: Cellular and Molecular Mechanisms Academic Press, NY (1995) 99.10.1016/B978-012385355-4/50006-0CrossRefGoogle Scholar
4.Fausto, N. In: The Liver:Biology and Pathobiology, Raven Press, NY (1994)1501.Google Scholar
5.Hixson, et al., In: The Role of Cell Types in Hepatocarcinogenesis CRC Press FL (1992)151Google Scholar
6.Sell, S. and Pierce, G. B.,Lab Invest 70(1994) 6Google Scholar
7.Farber, E., In: The Role of Cell Types in Hepatocarcinogenesis CRC Press FL (1992) 1Google Scholar
8.Gerling, P.et al., Carcinogenesis, 15 (1994), 5310.1093/carcin/15.1.53CrossRefGoogle Scholar
9.Wilson, J. W. and Leduc, E. H., J Pathol Bacteriol 76 (1958) 44110.1002/path.1700760213CrossRefGoogle Scholar
10.Novikoff, P. M. and Yam, A.Proceedings: Am Assoc Ca Res 38 (1997)Google Scholar
11.Novikoff, et al., Am J Path 139(1991) 1351Google Scholar
12. This work was supported by NIH NCI CA06576Google Scholar