Journal of Pathology and Translational Medicine

Original Articles

DNA Ploidy and S-Phase Fraction in Proliferative Hepatic Lesions of Rat Liver Induced by Dietylnitrosamine and Partial Hepatectomy.: Chan Choi, Sung Hee Cho, Hyung Bae Moon, Ki Jung Yun, Hun Taeg Chung, Sang Woo Juhng; Korean J Pathol. 1991;25(4):346-356.

Abstract PDF: We have investigated the changes of DNA ploidy and S-phase fraction in proliferative lesions of rat liver. Proliferative lesions were induced by diethylnitrosamine and partial hepatectomy. DNA ploidy was measured by flow cytometer, and S-phase fraction was measured by in situ bromodeoxyuridine(BRdU)-anti BRdU monoclonal antibody techniques. Normal liver and initiated lesion revealed DNA diploidy or DNA tetraploidy. Hepatocyte nodule (NODULE) and hepatocelular carcinoma (HCC) revealed DNA diploidy, tetraploidy or aneuploidy. S-phase fraction was 1.0+/-0.9, 1.0+/-0.9m 3.7+/-2.3, 5.5+/-4.9, and 13.8+/-11.6 in normal liver, initiated lesion, NODULE not associated with HCC, NODULE associated with HCC, and HCC, respectively. In NODULE associated with HCC, it was widely distributed, ranging from 0.8 to 15.5%. In conclusion, S-phase fraction appeared to be increased as the hepatocarcinogenesis proceeded, but DNA ploidy did not. There was a heterogeneity of DNA ploidy and S-phase fraction in the proliferative hepatic lesions.

A Study on the Cell Kinetics of the Dysplastic Epithelium in the Stomach.: Jong Hee Nahm, Kyu Hyuk Cho; Korean J Pathol. 1989;23(1):29-35.

Abstract PDF: This study was designed to evaluate the biological behavior of the dysplastic lesion of the stomach by applying immunohistochemical method for bromodeoxyuridine (BrdUrd). The results obtained were as follows. 1) In most hyperplastic and dysplastic lesions, the proliferative cell zones, loci of BrdUrd-labelled cells, were found in the upper later of the mucosa, whereas they were confined to the neck zone in the normal gastric mucosa. 2) The labelling indices (LIs), percentages of BrdUrd-labelled cells, were 11.0% to 13.6% in the normal gastric mucosa, and were 14.3% to 17.9%, 16.4% to 19.2% and 17.4% to 20.7% in the simple hyperplasia, in the atypical hyperplasia and in the dysplasia, respectively. These findings suggested that proliferative potential in hyperplasia and dysplasia were greater than that in normal gastric mucosa, the higher the grade of dysplasia being, the greater the proliferative potentials.

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