Hepatitis-B surface antigen in tumour tissue and non-tumorous liver in black patients with hepatocellular carcinoma

Kew, M. C.; Ray, Mukunda B.; Desmet, Valeer; Desmyter, Jan

doi:10.1038/bjc.1980.63

Cited by 40 publications

(20 citation statements)

References 16 publications

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“…It was never found without DNA polymerase nor in carcinoma tissue, where reaction in man is sometimes encountered (23,24). The orcein reaction in the Shikata stain deserves further exploration.…”

Section: Resultsmentioning

confidence: 99%

Woodchuck hepatitis and hepatocellular carcinoma: Correlation of histologic with virologic observations

et al. 1981

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The livers of 33 captive woodchucks were examined histologically in 30 biopsy and 10 autopsy specimens and the findings were correlated with serum determinations for woodchuck hepatitis virus (WHV), surface antigen (WHsAg) and antibody (anti-WHs), and WHV DNA and DNA polymerase. The liver appeared normal in all 3 serum-negative animals, 7 of 16 with indeterminate WHV status, and 1 of 4 with anti-WHs, but not in 10 animals with WHsAg, WHV DNA, and DNA polymerase. Mild hepatic inflammation was found in 7 woodchucks with indeterminate status, 4 with anti-WHs, and 2 with each marker of WHV infection. Significant inflammation was found in 2 of indeterminate status and 4 with every marker, whereas more severe lesions (2 of chronic active type) occurred, almost always in autopsy specimens, in 8 animals with every marker. Eight of 10 animals with all markers had orcein-positive inclusions (Shikata's technique) and 6 had hepatocellular carcinoma associated with acute and chronic hepatic inflammation and, usually, neoplastic nodules in the noncarcinomatous parenchyma. Features distinguishing the woodchuck lesion from human hepatitis B disease were: association of carcinoma with acute hepatic inflammation (but not with cirrhosis) and DNA polymerase in the serum; transition to carcinoma from neoplastic nodules; conspicuous plasma-cellular reaction of hepatic inflammation, and hematopoietic cells in the tumor. Significant hepatic lesions in the woodchucks were regularly associated with serum WHsAg, WHV DNA, and DNA polymerase. In contrast to man, hepatocellular carcinoma in woodchucks was regularly associated with these markers of active viral replication. The nature of the orcein-positive inclusions requires elucidation, although they may assist in screening for similar viruses in other species. The woodchuck may help in the study of the relation between hepatocellular carcinoma and hepatitis B, including the possibility of cocarcinogenic factors.

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Section: Resultsmentioning

confidence: 99%

Woodchuck hepatitis and hepatocellular carcinoma: Correlation of histologic with virologic observations

et al. 1981

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“…These results seemed contradictory, as the reduction of PKR was observed in HCC tumor tissues but an elevation of PKR level was associated with an increase in the serum levels of HBV. It has been observed that HBV replication usually persists in HCC cells at a lower level than non-HCC cells in liver [Kew et al, 1980;Tanaka et al, 1988], though HBV is a causative agent in the development of HCC. The integration of HBV DNA is thought to occur in heterogenous sites of cellular DNA before hepatocarcinogenesis, and thereafter HBV replication in HCC cells may not be as active as in those non-HCC cells.…”

Section: Discussionmentioning

confidence: 99%

Reduction of double‐stranded RNA‐activated protein kinase in hepatocellular carcinoma associated with hepatitis B virus

Chen

Lai

et al. 2004

Journal of Medical Virology

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Chronic hepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC) in Asia. Double-stranded RNA (dsRNA)-activated protein kinase (PKR) is an interferon-induced, serine/threonine protein kinase. Recent studies have suggested that PKR is involved in the pathogenesis of HCC with hepatitis virus C infection by inhibiting viral and cellular proteins related to cell growth and proliferation. In the present study, PKR was examined in both tumor and non-tumor tissues from HCC livers infected with HBV. The expression of PKR was determined by TaqMan real-time PCR and immunohistochemical methods. The level of PKR was also analyzed in relation to pathological changes observed in HCC. The result showed that PKR was reduced in tumor tissues of HCC from HBV carriers with low serum viral load (<0.7 x 10(6) copies/ml) compared to those with higher serum viral load. However, the overall PKR level was much lower in tumor tissues than that in non-tumor tissues, irrespective of HBV carrier status or serum viral load. PKR level tended to be lower in HCC samples with alpha-fetoprotein (AFP) more than 500 ng/ml (mean: 4024.2 ng/ml) than those with AFP less than 500 ng/ml (mean: 50.6 ng/ml). There was no significant difference in the expression of PKR between tumor tissues with well differentiation and those with poor or moderate differentiation. In conclusion, the level of PKR was reduced in HCC tumor tissues, suggesting a possible role of PKR in promoting the growth of tumor. HBV may participate in altering the level of PKR, but factors other than HBV should play a more determining role in the regulation of PKR in HCC. The association between PKR and AFP levels may offer an alternative tumor marker for HCC.

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“…This agreement among separate among studies. 23,[26][27][28][29][30] One recent report has proposed that studies using different methodologies and patient popula-LCC represents a response to prolonged cholestasis. 31 tions strongly suggests that the two lesions are linked in To help untangle this controversy, we assessed the prog-some underlying pathogenetic fashion and argues against nostic value of LCC for HCC through a matched case-control LCC representing merely a degenerative or regenerative alterstudy that compared the occurrence of LCC between cir-ation.…”

Section: Discussionmentioning

confidence: 99%

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case-control study, pathological analysis, and pathogenetic hypothesis

1997

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Liver cell dysplasia is the term originally applied by AnLarge cell change (LCC), characterized by cellular enthony et al. 1 in 1973 to cytologically atypical hepatocytes largement, nuclear pleomorphism and hyperchromasia, showing cellular enlargement, nuclear pleomorphism with and multinucleation of hepatocytes, is a common lesion hyperchromasia, and multinucleation. In their study, this in cirrhotic livers, but its nature, significance, and pathoalteration was uncommon in normal livers and occasionally genesis remain uncertain. Therefore, we assessed the noted in cirrhotic livers, particularly with chronic hepatitis prognostic value of LCC as a marker of subsequent hepato-B infection, but was most prevalent in cirrhotic livers bearing cellular carcinoma (HCC) through a case-control study hepatocellular carcinoma (HCC). Because of this relationthat compared pretransplant liver biopsy specimens from ship, liver cell dysplasia, later termed large cell dysplasia, 37 cirrhotic liver transplant recipients with HCC to speciwas proposed to represent a premalignant change.1 mens from a control group of recipients without HCC, Over the succeeding 25 years, however, this proposal has matched for sex, age ({5 years), and cause of cirrhosis.been contested, and other workers have concluded that large LCC was identified in 16 (43%) of the study and 7 (19%) cell dysplasia instead represents a regenerative or degeneraof the control group biopsy specimens. By matched-pair tive phenomenon. Evidence has been marshalled to support analysis, LCC conveyed a moderately increased risk of both sides of this controversy, but much of the data are later HCC with an estimated odds ratio of 3.3 (95% CI, conflicting or circumstantial in nature, and no consensus has 1.2-15; P Å .038). However, a pathology review of 45 been reached as to the nature or significance of the alteration. HCCs showed adjoining LCC in only 12 (27%) and didBecause of this lingering uncertainty, the pathogenetically not suggest a morphological transition or a histogenetic noncommittal term large cell change (LCC) is now recomassociation between the two lesions. LCC hepatocytes dismended as an alternative designation.2 played a low proliferative rate by Ki-67 or proliferating The controversy over LCC poses a practical conundrum: cell nuclear antigen immunostaining (labeling indices of Should it receive special notice as a potential precursor of 0.27 and 0.73) but showed a greater degree of apoptosis malignancy, or should it be dismissed as an inconsequential than normal hepatocytes (labeling indices of 1.9 and 0.23; marker of chronic liver injury? To address this issue, we P Å .03) To reconcile these findings, we propose that LCC evaluated three different aspects of LCC. First, we performed derives from derangements in the hepatocyte's normal a case-control study to evaluate whether the presence of LCC process of polyploidization. Such derangements, possibly presaged any increased risk for the subsequent presence of caused by chronic inflammation-induced DNA damage, HCC...

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Hepatitis-B surface antigen in tumour tissue and non-tumorous liver in black patients with hepatocellular carcinoma

Cited by 40 publications

References 16 publications

Woodchuck hepatitis and hepatocellular carcinoma: Correlation of histologic with virologic observations

Woodchuck hepatitis and hepatocellular carcinoma: Correlation of histologic with virologic observations

Reduction of double‐stranded RNA‐activated protein kinase in hepatocellular carcinoma associated with hepatitis B virus

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case-control study, pathological analysis, and pathogenetic hypothesis

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