Tumor suppressive effect of dehydroepiandrosterone (DHEA) on the experimentally induced hepatocellular carcinoma was investigated, especially focusing on glutatione transferase and transglutaminase with aptosis in the carcinogenesis. The chemical hepatocarcinogenic procedure of Solt-Farber method was used on Sprague-Dawley rats. Experimental groups were divided into AA group treated by the standard Solt-Farber regimen of diethylnitrosamine (DEN) and 2-acetamidofluorene (AAF) and AD group treated with DHEA simultaneously with AAF and the AAD group treated by DHEA after treatment with AAF. Each group was divided by time sequence further into four subgroups, GI (8wk), G2 (16wk), G3 (28wk), and G4 (36wk). For neoplastic lesion, the immuno histochemical study with anti GSTP antibody was carried out, while the activity and expression of TGase was compared at the same time. The results were summarized as follows; GST-P positive foci detected in AD groups were significantly more suppressed by DHEA treatment than AA groups (P<0.05). AD groups. AD group showed higher activities of TGase than AA groups (P<0.05), which was confirmed by Western and Northern blot analysis. But the number of apoptotic bodies was not correlated with activity and expression of TGase in the nodule. These results suggest that the suppressive effect of DHEA on the murine hepatocellular carcinogenesis might be operating on the promotion process of carcinogenesis rather than regression process of transformed hyperplastic nodules.
Carcinoma, Hepatocellular

Necleolar organizer regions(NORs) ARE LOOPS OF DNA which transcribe to ribosomal RNA by RNA polymerase I. Since NOR-associated proteins are argyrophilic, silver staining method has been used for demonstration of AgNORs. The numbers and/or configurations of NORs may reflect the activities of cells in hyperplastic and neoplastic conditions. To evaluated the applicability of AgNORs in the diagnosis of hepatocellular carcinoma, the author had performed silver staining on the routinely processed, formalin-fixed, paraffin-embedded sections of 14 cases of normal liver(control), 23 cirrhotic liver, and 21 hepatocellular carcinoma. The results are summarized as follows: 1) The mean number of AgNORs per nucleus(mAgNOR) of normal liver, cirrhotic liver and hepatocellular carcinoma was 1.45+/-0.07, 2.53+/-0.38 and 5.52+/-1.63, respectively. The difference of mAgNOR between normal and cirrhotic liver, and between cirrhotic liver and hepatocellular carcinoma was statistically significant, respectively(p<0.01). 2) The percentage of nuclei showing five or more AgNORs per nucleus(pAgNOR) was 0.07% in normal liver, 7.59% in cirrhotic liver, and 60.49% in hepatocellular carcinoma. 3) AgNORs in hepatocellular carcinoma were large, pleomorphic and irregularly clumped, in addition to increase of mAgNOR and high pAgNOR. In conclusion, the increase of mAgNOR, high pAgNOR and large, irregular AgNORs are regarded as an additional helpful finding for the histopathological diagnosis of hepatocellular carcinoma.
Carcinoma, Hepatocellular

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

To pursue a desirable format for the pathological diagnosis of liver cirrhosis, the authors attempted to classify 369 biopsy-proven cirrhosis on the basis of etiology and made effort to find out the morphological characteristics of each category. About 735 of total cases were HBsAg seropositive postnecrotic cirrhosis. Alcholic cirrhosis ws the second most frequent type, although accounted only 6.8%. In about 15%, the etiology was not known. Excluding the congenital biliary atresia, chronic biliary obstruction appeared to be a rare cause of cirrhosis among these biopsied cases. Of the HBsAg positive postnecrotic cirrhosis, the eAg seropositive cases tended to be micronodular and to show a higher necroinflammatory activity, in contrast to eAg seronegative cases and those complicated by hepatocellular carcinoma (HCC), suggesting that the loss of eAg is followed by a decrease of the destructive activity, active regeneration of hepatocytes and finally the development of HCC. alcoholic cirrhosis was micronodular in 64% and revealed histologic evidences of alcoholic liver disease in most cases. The results indicate that etiological diagnosis can be made in most cases of cirrhosis by the morphological characteristics and the precise clinical informations, including those on the NANB virus and the inborn error of metabolism, and that the pathological diagnosis should be more comprehensive, implicating the etiology, the nodular size and the necroinflammatory activity.
Carcinoma, Hepatocellular

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

No abstract availalbe.
Carcinoma, Hepatocellular*

Sclerosing hepatic carcinoma (SHC) is composed of slender cords or small nests of tumor cells with peripheral palisading, and abundant intervening sclerosis. The tumor seems to have the histologic features of both hepatocellular carcinoma (HCC) and cholangiocarcinoma. To evaluate the phenotypic expression of SHC and to investigate its cellular origin, immunohistochemical studies on three cases of SHC were performed. In all cases, the tumor cells showed positive staining for cytokeratins AE1, AE3 and 19, carcinoembryonic antigen (CEA) and epithelial membrane antigen (EMA). The expressions of cytokeratins AE1 and 19 were stronger in the palisading cells than the interior of the cords and nests. Conversely, CEA and EMA were expressed mainly in the inner portion. Alpha-fetoprotein was expressed in only one case, mainly in the palisading cells. In summary, SHC has the histological as well as the immunohistochemical profiles intermediate between HCC and cholangiocarcinoma, and the immunohistochemical profile suggests that SHC arises from primitive hepatoblast with a tendency of differentiation to the bile duct epithelium.
Carcinoma, Hepatocellular