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Premalignant Changes Identified by Enzyme-Histochemistry with Methacrylate Sections

Published online by Cambridge University Press:  02 July 2020

Theresa P. Pretlow  and
Thomas G. Pretlow
Theresa P. Pretlow
Affiliation:
Institute of Pathology, Case Western Reserve University Medical Center, 2085 Adelbert Road, Cleveland, OH, 44106
Thomas G. Pretlow
Affiliation:
Institute of Pathology, Case Western Reserve University Medical Center, 2085 Adelbert Road, Cleveland, OH, 44106
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Extract

The development of cancer is characterized by a long latency between the initial exposure to a carcinogenic substance and the final appearance of a macroscopic tumor. Histochemistry has provided the means to identify specific cells involved in this process and many of the changes that take place during the transformation of normal cells to malignant ones. Putative premalignant lesions have been studied extensively in liver carcinogenesis. Histological sections of grossly normal appearing liver a few weeks after treating animals with carcinogen contain discrete areas or “islands” of aberrant enzyme activity that can be detected with enzyme histochemistry and are commonly called “enzyme-altered foci.” These foci display altered activity of one or more enzymes; one of the most common is increased γ-glutamyl transpeptidase (GGT) activity. Since the activities of most enzymes are destroyed by the heat and solvents used for paraffin-embedding, most of this work was done with frozen sections that are often 10 μm in thickness

Type
Neoplasia: Abnormal Cell Growth or Death/Apoptosis? Insights from Microscopy
Information
Microscopy and Microanalysis , Volume 3 , Issue S2: Proceedings: Microscopy & Microanalysis '97, Microscopy Society of America 55th Annual Meeting, Microbeam Analysis Society 31st Annual Meeting, Histochemical Society 48th Annual Meeting, Cleveland, Ohio, August 10-14, 1997 , August 1997 , pp. 1 - 2
Copyright
Copyright © Microscopy Society of America 1997

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References

1.Peraino, C.et al., in Slaga, TJ, ed Mechanisms of Tumor Promotion Vol 1, Boca Raton, FL: CRC Press, (1983)1Google Scholar
2.Pretlow, T.P.et al., Lab Invest 56(1987)96.Google Scholar
3.Barrow, B.J.et al., Cancer Res 50(1990)1911.Google Scholar
4.Bird, R.P.Cancer Lett 37(1987)147.10.1016/0304-3835(87)90157-1CrossRefGoogle Scholar
5.Pretlow, T.P.et al., Cancer Res 51(1991)1564.Google Scholar
6.Pretlow, T.P.et al., Am J Pathol 142(1993)1695.Google Scholar
7.Pretlow, T.P.et al., Int J Cancer 56(1994)599.10.1002/ijc.2910560422CrossRefGoogle Scholar
8.Stopera, S.A.et al., Carcinogenesis 13(1992)2081.10.1093/carcin/13.11.2081CrossRefGoogle Scholar
9.Zaidi, N.H.et al., Carcinogenesis 16(1995)451.10.1093/carcin/16.3.451CrossRefGoogle Scholar
10.Pretlow, T.P.et al., J Cell Biochem Suppl 16G(1992)55.10.1002/jcb.240501111CrossRefGoogle Scholar
11.Pretlow, T.P.et al., J Natl Cancer bist 85(1993)2004.10.1093/jnci/85.24.2004CrossRefGoogle Scholar
12.Augenlicht, L.H.et al., Oncogene 12(1996)1767.Google Scholar
13.Pretlow, T.P.et al., Gastroenterology 107(1994)1719.10.1016/0016-5085(94)90812-5CrossRefGoogle Scholar
14.Siu, I.-M.et al., Am J Pathol 1997)in press.Google Scholar
15.Monger, L.E. Jr., et al., Am J Pathol 145(1994)54.Google Scholar
16.Pretlow, T.G.et al., J Cell Biochem Suppl 19(1994)224.Google Scholar
17.Pretlow, T.G.et al., Pathol Res Pract 191(1995)842.10.1016/S0344-0338(11)80966-0CrossRefGoogle Scholar
18.Supported in part by grants CA66725, CA54031, CA43703, and DK51347.Google Scholar