No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

No abstract available.
Carcinoma, Hepatocellular*

It has been well known that liver cirrhosis, regardless of its etiology, is an important predisposing factor in hepatocarcinogenesis. However, the type of cirrhosis in hepatocellular carcinoma(HCC)-bearing liver varies not only by geographic areas but also with the cirteria applied for morphological classification of cirrhosis. To elucidate the relationship between the nodule size of HCC-bearing cirrhotic liver and clinicopathologic features, we measured cirrhotic nodule areas of 49 surgically resected HCC cases using image analyzer. The morphological type of cirrhosis was predominantly macronodular(49%), and followed by mixed(37%) and micronodular(14%). Seventy percent of the cases showed seropositivity for HBsAg. The average area of cirrhotic nodules was significantly larger in HBsAg-positive cases(mean: 6.14 mm2) than that of HBsAg-negative cases(mean: 2.5 mm2)(p<0.05), and their size was bigger in cases with grossly expansile pattern of HCC than those cases with infiltrative ones(p<0.05). Based on the above findings, we assume that seropositivity of HBsAg may influence on the regenerative activity of cirrhotic nodules and also subsequent increase of risk for further development of HCC. The presence of cirrhohsis and nodule size seem to be the important contributing factors to determine the growing patterns of HCC.
Carcinoma, Hepatocellular

No abstract availalbe.
Carcinoma, Hepatocellular*

Since the discovery of hepatitis B virus as one of the causes of hepatitis, liver and hepatocellular carcinoma, many hepatitis B viral markers that appear in infected individuals have been discovered and many efforts to understand the relationship between the emergence of viral markers and the progression of hepatitis have been performed. Gudat (1975) compared the expression of HBcAg and HBsAg in various conditions and stages of hepatitis but the pattern of expression of viral markers and its significance have not been understood. Recently it was found by mierocytotoxicity assay that HBcAg might be the target of T lymphocytes. This study attempted to identify any correlation of the tissue expression rate and pattern of HBcAg and HBsAg with the histologic activity of 46 cases of liver cirrhosis using immunohistochemical staining. The expression rate and pattern of HBcAg and HBsAg in relation to the nodular size and positivity of serum HBeAg were also compared. The results were as follows; 1) The expression rate of HBcAg in the liver was 41.3% (19/46). and that of HBsAg was 67.4% (31/46). 2) The histologic activity of liver cirrhosis appeared to be correlated with the expression of HBcAg, especially cytoplasmic HBcAg. 3) The positivity of serum HBeAg was significantly higher in active liver cirrhosis. 4) There was no relationship between the tissue expression of HBsAg and the histologic activity of liver cirrhosis. relationship existed between the nodular size and expression rate and pattern of HBcAg and HBsAg. This study suggests that the tissue HBcAg, especially the cytoplasmic HBcAg is the most likely factor determining the histologic activity of liver cirrhosis, and that the cytoplasmic HBcAg may be the ultimate cause and target of most host immune response.
Carcinoma, Hepatocellular

No abstract available.
Carcinoma, Hepatocellular*

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