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Original Articles
- Immunohistochemical Investigation on Expression of Hepatitis B Surface Antigen, Transforming Growth Factor-alpha, and Proliferating Cell Nuclear Antigen in Hepatocellular Carcinoma.
- Bang Hur, Man Ha Hur
- Korean J Pathol. 1995;29(4):478-491.
- 1,686 View
- 15 Download
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Abstract
PDF - In an attempt to evaluate the expression of hepatitis B surface antigen(HBs Ag), transforming growth factor-ct(TGF-alpha), and proliferating cell nuclear antigen(PCNA) in hepatocellular carcinoma(HCC), an immunohistochemical investigation(ABC method) was performed using 31 surgically resected HCCS. The authors examined the expression rate and patterns, histopathologic correlation, and inter-relationships among these expressions. The results were summarized as follows. 1) Among 25 seropositive HCCS, 15 cases showed tissue expression of HBs Ag(60.0%), being expressed as a predominantly cytoplasmic pattern. Its expression rate in low grade HCC was significantly high(76.9%), in contrast to a low rate in high grade HCC(41.7%)(P<0.05). Adjacent nonenoplatic tissue showed a higher expression rate(82.6%). 2) TGF-alpha was expressed in 23 of 31 cases of HCC(74.3%). The intensity and extent of its expression did not correlate tyros with histopathologic features. Bile duct epithelium, juxtaposed and/or entrapped liver cells, and cirrhotic nodules were variably expressed, of which intense peripheral reaction within the nodules was frequently noted. 3) PCNA was expressed throughout the neoplastic tissue of HCC. Its index was significantly high(34.4 13.6), being compared to low index index(3.5 2. 1) in the nonneoplastic tissue(P<0.005). High grade tumors revealed a higher index than the low grade tumors(P<0.05). Conclusively, this data confirms that PCNA index offers useful information about cell proliferation associated with histologic degrees of malignancy of HCC, albeit TGF-alpha is also involved in cellular proliferation of both liver cell and bile duct epithelium. Changes in incidence and cellular localization of HBs Ag expression between the neoplastic and nonneoplastic tissues suggest that an integrated viral genome could be functionally altered during hepatocarcinogenesis. A significant inter-relationship among these expressions was not observed.
- Effects of Active Hexose Correlated Compounds on Drug Induced Liver Injury in Mice.
- Ki Ouk Min, Hi Jeong Kwon, Eun Joo Seo, Jeana Kim, Seok Jin Kang, Byung Kee Kim
- Korean J Pathol. 2000;34(7):509-515.
- 1,747 View
- 22 Download
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Abstract
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- AHCC (Active Hexose Correlated Compounds), which was at first extracted from cultured broth of Basidiomycotina, is known to be one of the Biological Response Modifiers (BRM). We examined the protective effects of AHCC on carbon tetrachloride (CCl4) and thioacetamide (TAA)-induced liver injury in mice. The AHCC pretreatment prevented the suppression of several physiological and biochemical parameters in the mice injected with CCl4 or TAA for 5 days. The liver weights and serum ALT and AST levels were increased by CCl4 or TAA, the degree of which was significantly reduced with the AHCC pretreatment. The AHCC pretreatment induced increasing activity of GST (glutathione s-transferase) and showed an increasing tendency of P450 and EROD (ethoxyresorufin o-dealkylation). The AHCC pretreatment also showed negative effects against the suppression of drug metabolizing enzymes, such as P450, EROD, and GST induced by CCl4 or TAA. AHCC pretreatment showed protective effects with significant inhibition of fatty change, inflammation, and necrosis in CCl4 and TAA intoxicated mice liver. The present study suggests that the protective effect of AHCC pretreatment might be related to the protection of liver from the drug induced liver injury in mice model.
- Inactivation of TPEF Gene by Aberrant Methylation in Hepatocellular Carcinoma.
- Woon Bok Chung, Soon Young Kim, So Young Chun, Ku Seong Kang, Hae Ahm Lee, Joung Ok Kim, Ji Young Park, Yoon Kyung Sohn, Jung Wan Kim
- Korean J Pathol. 2008;42(1):9-15.
- 1,877 View
- 19 Download
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Abstract
PDF
- BACKGROUND
Abnormalities of genomic methylation patterns have been shown to play a role in the development of carcinoma, and the silencing of tumor suppressor genes is related to local de novo methylation.
METHODS
Using methylation specific arbitrarily primed-Polymerase Chain Reaction (Ms AP-PCR), we identified a 322 bp sequence that contained a 5' un-translated and exon1 regions of the TPEF gene. To evaluate the inactivation of the TPEF gene through hypermethylation in hepatocellular carcinoma (HCC), we investigated the correlation between methylation patterns and TPEF expression in tumor tissues of human HCC and cell lines via a Combined Bisulfite Restriction Assay (CoBRA) and RT-PCR.
RESULTS
A dense methylation pattern of the TPEF was detected in most cell lines, as well as in 10 of the 14 (71.4%) HCC tissues. In addition, loss of heterozygosity (LOH) from the TPEF gene was observed in 5 of the 14 (36%) HCC tissues. Furthermore, RT-PCR analysis revealed TPEF expression in 5 of 8 (62.5%) cell lines. Finally, treatment with a demethylating agent, 5-Aza- 2'-deoxycitidine (5-AzaC), increased the expression of TPEF mRNA.
CONCLUSION
These results indicate that inactivation of the TPEF gene through hypermethylation may be a mechanism by which tumorigenesis occurs in HCC.
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