Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Examination of nucleolar RNA from cultured Novikoff hepatoma cells treated for 3 hr with 5 x 10-4 M 5-azacytidine shows that significant amounts of analog-substituted 45S RNA are processed to the 32S RNA species, but 28S RNA formation is completely inhibited. Under these conditions of analog treatment 37% of the cytidine residues in the 45S RNA is replaced by 5-azacytidine. During coelectrophoresis of nucleolar RNA from 5-azacytidine-treated and control cells, the analog-substituted 45S RNA and 32S RNA display reduced mobilities compared to the control 45S RNA and 32S RNA. Coelectrophoresis of analog-substituted and control RNA after formaldehyde denaturation shows no differences in electrophoretic mobility between the two RNA samples, suggesting that 5-azacytidine incorporation may alter the secondary structure of the 45S RNA and the 32S RNA. 5-Azacytidine at 5 x 10-4 M severely inhibits protein synthesis in Novikoff cells by 3 hr. After this length of treatment, however, CsCl buoyant density analysis reveals no difference in density of either the 80S or 55S preribosomal ribonucleoprotein particles when compared to normal particles. Also 5-azacytidine treatment does not appear to cause major changes in the polyacrylamide gel electrophoresis patterns of the proteins in the 80S and 55S preribosomal particles. These results together with previous findings suggest that 5-azacytidine's inhibition of rRNA processing is possibly related to its alteration of the structure of the ribosomal precursor RNAs and is not a consequence of a general inhibition of ribosomal protein formation.
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PMID:Effects of 5-azacytidine on nucleolar RNA and the preribosomal particles in Novikoff hepatoma cells. 4 43

Formalin-fixed paraffin-embedded autopsy tissue of liver and tumor from 50 male black mineworkers with hepatocellular carcinoma were examined by orcein stain for the presence of cytoplasmic hepatitis B surface antigen. The results were correlated with the serum hepatitis B antigen (HBAg). In 72% serum HBAg was positive. Orcein staining of nontumor liver cell cytoplasm was present in 18 (36%). Sixteen (89%) of these orcein-positive cases were serum HBAg positive. The two false negative serum HBAg results were obtained by immunodiffusion, immunoelectrophoresis and complement fixation. Serum HBAg, measured by radio-immunoassay and hemagglutination, was positive in 14 orcein-negative cases. Six other negative orcein results appeared to be due to sampling error. Orcein staining was noted in tumor cells of three serum HBAg positive patients. Provided the limitations of the technique are realized, orcein staining of liver tissue from hepatocellular carcinoma patients may prove useful for retrospective screening surveys to assess the prevalence of HBAg positivity in these patients.
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PMID:Hepatitis B antigen in black patients with hepatocellular carcinoma: correlation between orcein stained liver sections and serology. 7 53

Tissue localization of a subcomponent of the first component of complement (CLq) was examined in one postmortem case of HBs antigen (HBs Ag) positive hepatocellular carcinoma and in six cases of chronic hepatitis from liver biopsy specimens. The direct immunofluorescent method was used after fixation with 2% para-formaldehyde in concentrated ammonium sulfate. CLq localization was found in collagen fibers and the cytoplasm of fibroblasts in the connective tissues of specimens examined. The localization was particularly marked in the region of the fundal glands of the gastric wall. Apart from collagen fibers, other sites of localization included the surface membrane of lymphocytes, especially those cells of the mesenteric lymph nodes. In HBs Ag positive specimens, immune deposit-like substances appeared localized intra-hepatically and in the renal glomeruli. Since C3 and C4 were identified concomitantly, it indicates that these substances were indeed immune diposits. Despite the finding that C3 and C4 were identified together in the hepatic cell cytoplasm, C1q itself was not demonstrated in all hepatic cell cytoplasms.
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PMID:Tissue localization of C1q in HBs antigen positive liver disease patients by direct immunofluorescent technique. 19 61

The authors studied histochemically the morphologic features of proliferating hepatocytes positive for proliferating cell nuclear antigen (PCNA/cyclin) to analyze the process of liver regeneration in embedded tissues fixed with formaldehyde using an anti-PCNA/cyclin monoclonal antibody. In liver specimens from patients with acute viral hepatitis (AVH) and confluent necrosis, many small basophilic hepatocytes surrounding large clear hepatocytes were positively stained in the areas next to the confluent necrosis. Therefore these small hepatocytes may be daughter cells derived from large clear hepatocytes that probably enter the mitotic cell cycle repeatedly to repair a large necrotic area. In the case of AVH with spotty necrosis, the positively stained hepatocytes were scattered around the necrotic foci. In the liver specimens from patients with chronic active hepatitis, most of the positively stained hepatocytes were located next to the necrotic area. As for cirrhosis of the liver, the number of hepatocytes positive for PCNA/cyclin varied greatly in different pseudolobules, and in the specimens of hepatocellular carcinoma (HCC), the HCC cells positive for PCNA/cyclin were detected throughout the cancer nests.
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PMID:Analysis of proliferating hepatocytes using a monoclonal antibody against proliferating cell nuclear antigen/cyclin in embedded tissues from various liver diseases fixed in formaldehyde. 134 35

Phenotypic expression of sialylated Lewis(x) antigen by means of the monoclonal antiserum SNH3 was studied in 87 livers, which included normal and steatotic livers and livers with chronic persistent and chronic active hepatitis, alcoholic hepatitis, allograft rejection, focal nodular hyperplasia, hepatocellular carcinoma, cholangiocarcinoma, metastatic carcinoma, cirrhosis of various causes (autoimmune, alcoholic, viral, drug induced, Wilson's disease, and primary biliary cirrhosis). The biotin-streptavidin-peroxidase method was used on formaldehyde-fixed, paraffin-embedded sections. Sialylated Lewis(x) antigen was not demonstrated in normal livers. Hepatocellular expression in a diffuse or perinodular honeycomb pattern was seen in cirrhosis, irrespective of cause. Sialylated Lewis(x) antigen was also observed in hepatocytes around metastatic carcinoma in the absence of inflammation, cirrhosis, or regeneration. Some bile ductules, most likely ductular hepatocytes, but not bile ducts, expressed sialylated Lewis(x) antigen. Sialylated Lewis(x) antigen was seen diffusely in fibrolamellar hepatocellular carcinoma, focally in other hepatocellular carcinomas, and either focally or diffusely in cholangiocarcinomas.
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PMID:Expression of sialylated Lewis(x) antigen in chronic and neoplastic liver diseases. 135 99

The authors investigated whether immunocytochemical staining with a monoclonal antibody to proliferating cell nuclear antigen (PCNA/cyclin) could be used to identify proliferative hepatocytes in frozen sections fixed in a mixture of periodate, lysine, and 2% paraformaldehyde. Paraffin sections also were used, which were fixed in 10% formaldehyde. Specimens of liver tissue were obtained from 27 patients with various hepatic diseases. Hepatocytes that were positive for PCNA/cyclin were observed in both types of substrate specimens. In acute hepatitis and chronic active hepatitis, most hepatocytes that were labeled for PCNA/cyclin were located near necrotic foci. However, in cirrhosis, they were detected most often near fibrotic septa; the number of immunoreactive cells varied greatly in different areas of tissue sections in such cases. In hepatocellular carcinoma, many PCNA/cyclin-positive tumor cells were seen throughout the neoplasms. Hepatocytes that were positive for DNA polymerase-alpha showed a similar distribution pattern in serial sections of study cases.
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PMID:Immunocytochemical identification of proliferative hepatocytes using monoclonal antibody to proliferating cell nuclear antigen (PCNA/cyclin). Comparison with immunocytochemical staining for DNA polymerase-alpha. 137 17

The glucocorticoid receptor (GR) is often described to be localized in the cytoplasm in the absence of hormone and to translocate to the nucleus upon binding of the hormone. This apparently different behavior of the GR compared to that of other members of the steroid receptor superfamily is unexpected because similarities in the molecular structures of steroid hormone receptors would predict similarities in their working mechanisms. The absence of the unliganded GR from the nuclear compartment may be due to an artefactual redistribution, occurring during the immunocytochemical procedure. We systematically studied the effects of various fixation and permeabilization procedures on the distribution of the GR in hepatoma cells that were incubated in steroid-free or steroid-containing medium. Immunofluorescent labeling of the GR in formaldehyde-fixed and detergent-permeabilized cells resulted in the almost complete absence of immunoreactivity of cells when the receptor was in its unliganded form, whereas the liganded receptor was detected mainly in the nucleus. On the other hand, labeling of cryosectioned glutaraldehyde/formaldehyde-fixed cells demonstrated that receptor antigenicity is present in the nucleus in the absence as well as the presence of steroid. We conclude that the results obtained with the cryosectioning procedure reflect the receptor distribution in the living cell, since glutaraldehyde fixation of the cells prevented the washout of loosely bound receptor. The predominantly nuclear location of the unliganded GR in hepatoma cells and the absence of changes in distribution after steroid stimulation imply that the nuclear translocation model is not true for the GR.
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PMID:The unliganded glucocorticoid receptor is localized in the nucleus, not in the cytoplasm. 159 54

Formalin-fixed, paraffin-embedded specimens from 110 cases of primary hepatocellular carcinoma were stained for hepatitis B x antigen (HBxAg), hepatitis B surface antigen (HBsAg), and hepatitis B core antigen (HBcAg). Eighty-four % of these patients were HBxAg positive in their tumor cells. Among the 110 cases studied, 80 had adjacent nontumorous tissue in the same block, and 65 of these nontumorous liver tissues stained positive for HBxAg (81%). HBsAg was positive in 19% of cases within tumor tissue and 61% in surrounding nontumorous tissue. HBcAg was positive in 11% of cases within tumor tissue and 26% in surrounding nontumorous tissue. These findings show that HBxAg is a common marker in the liver of patients with hepatitis B virus (HBV)-associated primary hepatocellular carcinoma and that it is closely associated with tumor cells in these individuals. In addition, the finding of HBxAg in the absence of detectable HBsAg and HBcAg in the liver tissues of many HBsAg carriers suggests that HBxAg could be expressed independent of HBV replication and implies that the synthesis of this antigen may be directed from integrated HBV DNA templates. The finding of HBxAg in the nucleus of hepatocytes from primary hepatocellular carcinoma patients with dysplasia, combined with the known trans-activating properties of HBxAg, implies that HBxAg plays one or more important roles in hepatocarcinogenesis. The finding of HBxAg in bile duct epithelium and cholangiocarcinoma tissues is compatible with the hypothesis that HBV may contribute to this other primary tumor type in the liver. Together, these results further implicate HBxAg in the pathogenesis of primary liver cancers.
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PMID:Hepatitis B x antigen in hepatitis B virus carrier patients with liver cancer. 165 8

An in situ hybridization technique with biotinylated hepatitis B virus (HBV)-DNA probes was used to localize HBV-related DNA sequences in cells of human hepatocellular carcinoma (HCC). Formalin fixed, paraffin-embedded liver biopsies of 11 patients with HCC studied; nuclear HBV-DNA hybridization was observed in 7 of the patients. Sensitivity and specificity of the method were determined by examining appropriate controls. The number of cells exhibiting nuclear fluorescence and intensity of fluorescence varied from tumor to tumor. In two instances liver tissue adjacent to HCC exhibited nuclear staining. HBV-DNA nuclear staining did not correlate with tumor localization of HBsAg or HBcAg, nor with type or with differentiation of the tumor. The use of biotinylated HBV-DNA probes offers a powerful and reproducible technique to localize HBV-related DNA sequences even in formalin-fixed, paraffin-embedded tumor tissue, and also to compare the presence of HBV-DNA with that of viral antigens stained in parallel sections. The frequent localization of HBV-DNA in nuclei of HCC cells fortifies the important epidemiologic association between infection and HCC. The random cellular localization of HBV-DNA sequences in HCC suggests that HBV-DNA may be incorporated, or perhaps replicated, unequally in tumor cells.
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PMID:Varying nuclear staining intensity of hepatitis B virus DNA in human hepatocellular carcinoma. 242 67

A panel of antibodies to intermediate filaments, oncofetal antigens, and hepatocellular markers was tested on a prospective series of liver fine-needle aspirates to determine its utility in distinguishing hepatocellular carcinoma (HCC) from metastatic carcinomas. All fine-needle aspirations were assisted to ensure adequate cellularity, and were examined by a multimodal approach that included the preparation of B-5-formaldehyde-fixed cell blocks by the plasmathrombin technique. alpha-Fetoprotein was positive in four of eight HCCs, including the one example of combined hepatocellular-cholangiocarcinoma, but negative in the one case of pure cholangiocarcinoma and all cases of metastatic carcinoma. Carcinoembryonic antigen positivity was noted in four HCCs, a high proportion of metastatic adenocarcinomas, and occasional metastatic squamous cell carcinomas, but not in the one example of cholangiocarcinoma. Hepatitis B surface antigen was positive in only two cases of HCCs, but not in any metastatic tumors. Keratin and vimentin were positive, respectively, in four and three HCCs, and a variable proportion of metastatic carcinomas often coexpressed both antigens. Epithelial membrane antigen was positive in five of the eight HCCs. Our findings are consistent with the view that alpha-fetoprotein and hepatitis B surface antigen are reliable markers for HCC. However, none of the immunocytochemical markers reliably distinguished the primary site of metastatic carcinoma. The intensity of the immunostains in the fine-needle aspirations was comparable with that observed in tissues, but fragmentation of cell groups interfered with interpretation. Multiple passes and verification of the cellularity of the aspirates are crucial factors for the success of this approach to diagnosis.
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PMID:Immunocytochemical evaluation of liver fine-needle aspirations. 247 56


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