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)

The hepatitis B virus (HBV), the causal agent of serum hepatitis, has a diameter of 42 nm and is comprised of an outer surface coat and a 27 nm core. A unique DNA-dependent DNA polymerase is associated with the core of the virus. The core also houses a circular DNA that contains both double-stranded and single-stranded regions. In the endogenous reaction, the DNA polymerase repairs the single-stranded gaps of the viral DNA. The surface protein of the virus, called hepatitis B surface antigen, contains both lipid and carbohydrate, and is often present in particulate form in the blood of infected patients. In Asia and Africa HBV infection is associated with subsequent development of primary hepatocellular carcinoma. Although most patients recover completely from acute illness, the hepatitis B virus may cause chronic infection. Recently, a virus similar to human HBV was discovered in woodchucks. HBV has not yet been propagated in a cell culture system and the mode of replication of this unusual virus in hepatocytes is still moot. Although reliable therapy has not yet been provided, the problem of this world-wide infection has led to many interesting approaches to both vaccine production and anti-viral chemotherapy.
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PMID:The hepatitis B virus and its DNA polymerase: the prototype three-D virus. 9 Oct 92

The PLC/PRF/5 cell line derived from a human hepatoma produces hepatitis B surface antigen (HBsAg) in 22-nm particles of the same buoyant density as those found in the serum of infected patients. The HBsAg particles from this cell line were labeled with [35S]methionine and purified, and the polypeptides were compared by sodium dodecyl sulfate-polyacrylamide gel electrophoresis with those of serum-derived particles. The two major polypeptides of serum-derived HBsAg particles (p20 and p23) were found in the same relative amounts in the particles from the cell line. The three smallest of the five minor components observed in HBsAg particles from serum were present in particles from the cell line. These polypeptides (p31, p36, and p43), as well as p20 and p23, were precipitated with anti-HBs-containing serum. The two largest polypeptides of serum particles (p49 and p66) were not detected in particles from these cells. When the PLC/PRF/5 HBsAg particles were radiolabeled with tritiated sugars, p23, and not p20, was found to contain radioactivity, indicating that the pattern of polypeptide glycosylation is similar to that of serum HBsAg. None of the other possible gene products of hepatitis B virus was detected in the PLC/PRF/5-derived HBsAg particles, in the cells, or in the cell supernatants.
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PMID:Polypeptides of hepatitis B virus surface antigen produced by a hepatoma cell line. 9 75

The presence of hepatitis B virus (HBV) antigens was examined in specimens of liver tissue obtained at necropsy from black Senegalese patients suffering from primary hepatocellular carcinoma (PHC). The results were correlated with markers of hepatitis B infection in serum. Hepatitis B surface antigen (HBsAg) and core antigen (HBcAg) were sought for in 15 liver extracts. HBsAg was found in the liver in 10 of 12 cases with HBsAg-positive serum. HBcAg was detected in three livers. The HBsAg was detected in seven of eight livers by immunofluorescence and orcein staining. HBsAg-positive cells were mainly located in the peri-tumoral cirrhotic tissue, although positive hepatocytes were also found in tumour nodules in liver from one of the patients. HBcAg was found in five of seven cases by immunofluorescence in hepatocytes of the cirrhotic areas. HBcAg fluorescence was primarily nuclear but, in some lobules, a patchy cytoplasmic fluorescence was observed. This suggests a cytoplasm-nucleus pathway in the synthesis of the HBV core antigen. Electron microscopy was performed on two HBsAg- and HBcAg-positive cases. Fibrillar and crystalline cytoplasmic inclusions were observed in tumour cells. In the same cells, 20-25 nm virus-like particles were present in swollen cisternae of the endoplasmic reticulum.
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PMID:Hepatitis B virus antigens in human primary hepatocellular carcinoma tissues. 9 79

Two antigenic systems of the woodchuck hepatitis virus have been identified. The relationship between viral antigens of the woodchuck hepatitis virus and the human hepatitis B virus was determined by using immunoprecipitation, hemagglutination, and immune electron microscopy techniques. Antigens found on the cores of the two viruses were cross-reactive. Lack of cross-reactivity between the surface antigens of the two viruses in immunodiffusion experiments suggested that the major antigenic determinants of the viral surfaces are different; however, results of passive hemagglutination tests indicated that there are common minor determinants. Nucleic acid homology, as measured by liquid hybridization, was found to be 3 to 5% of the viral genomes. The results of this study provide further evidence that woodchuck hepatitis virus is the second member of a new class of viruses represented by human hepatitis B virus. Since virus-infected woodchucks may acquire chronic hepatitis and hepatocellular carcinoma, these antigens and their respective antibodies will be useful markers for following the course of virus infection in investigations of the oncogenic potential of this class of viruses. The nucleocapsid antigen described may be a class-specific antigen of these viruses and, thus, may be useful in discovering new members of the group.
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PMID:Serological relationship of woodchuck hepatitis virus to human hepatitis B virus. 9 59

Soluble part of hepatocellular carcinoma (HCC) tissue extracts with or without hepatitis B surface antigen (HBsAg) was tested against leukocytes of 13 histologically confirmed HCC patients. Inhibition of leukocyte migration was observed in 9 out of 13 cases when tested by soluble HCC extract containing HBsAg, while inhibition of lukocyte migration was observed in 8 out of 13 cases when tested by solublp greater than 0.05, by Fisher's exact test). In the meantime, soluble HCC extract with or without HBsAg did not significantly cause inhibition of leukocyte migration in 12 non-HCC patients. Therefore, it is concluded that inhibition of leukocyte migration in HCC patients is caused by the tumor-associated antigen, not caused by HBsAg.
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PMID:Lack of leukocyte migration inhibition by hepatitis B surface antigen in hepatocellular carcinoma patients. 9 50

The frequency of Hepatitis Bs antigen and antibody was determined in healthy subjects and patients with acute and chronic liver disease. The frequency of HBs Ag in healthy subjects was 2.9% and HBs Ab 35%. The high prevalence of antibody in normal individuals suggests a constant non-parenteral sub-clinical exposure to hepatitis virus. Thirty-three per cent patients with acute viral hepatitis, 20% with cirrhosis and 10% with hepatocellular carcinoma were HBs Ag positive, while HBs Ab was detected in 22% cases of acute viral hepatitis and 37% with other liver disorders. This pattern of prevalence of HBs Ab suggests that hepatitis B virus may be an important etiological agent in acute and chronic liver disease in Pakistan.
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PMID:Prevalence of hepatitis B surface antigen and antibody in healthy subjects and patients with liver disease. 9 84

A patient with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease), treated with ethinyl estradiol, multiple blood transfusions, and iron-dextran, developed hepatocellular carcinoma and acquired hepatocerebral degeneration. In addition to the carcinoma, the liver contained extensive arteriovenous maliformations, telangiectasis, and changes of Osler atypical cirrhosis. The carcinoma possibly had its genesis in the presence of an ocongenic serum hepatitis virus, or the cirrhosis, or both.
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PMID:Hereditary hemorrhagic telangiectasia. A case with hepatocellular carcinoma and acquired hepatocerebral degeneration. 16 31

Most of the knowledge of post-hepatitic cirrhosis comes from studies performed in the last five years on the hepatitis B antigen-related variety. The position of other types of hepatitis (particularly type A) as an aetiological factor in cirrhosis remains conjectural. In general, the post-hepatitic cirrhosis develops insidiously after a mild or unrecognised acute episode of hepatitis. General progress is slow. Early deaths are due to liver failure. Later, primary hepatocellular carcinoma assumes increasing importance. Needle biopsy of the liver is usually necessary to confirm the diagnosis of cirrhosis and to estimate the degree of activity. Sampling errors when such a small specimen of liver is obtained must be taken into account, when formulating a diagnosis and prognosis. Prednisolone therapy is usually given if the patient is symptomatic, biochemical tests are abnormal and the liver biopsy confirms active chronic hepatitis with or without cirrhosis. The evidence of benefit is not so strong as for other forms of active hepatitis and cirrhosis such as the lupoid type. The management of the cirrhosis is otherwise along orthodox lines.
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PMID:Viral hepatitis and cirrhosis. 16 21

The hypothesis that hepatitis B infection is etiologically related to hepatoma has been investigated by studying the interrelationships between hepatitis B surface antigen (HBsAg, Australia antigen) and the fast-moving 5'-nucleotide phosphodiesterase Band V isoenzyme (5'-NPDase-V). Sera from 58 patients with viral hepatitis were tested for 5'-NPDase-V and HBsAg. The isoenzyme was found in 34 of 37 patients who were also positive for HBsAg but in only 4 of 21 hepatitis patients who were HBsAg negative. Five patients convalescing from hepatitis were negative for both HBsAg and the isoenzyme. Preparative gel electrophoresis showed that these 2 markers were different proteins. Of 34 hepatoma patients, 29 were positive for 5'-NPDase-V. Only 1 isoenzyme-positive patient was positive for HBsAg by counterimmunoelectrophoresis. However, of 16 isoenzyme-positive hepatoma patients available for radioimmunoassay, 8 were NBsAg positive (50%). None of 21 hepatoma samples tested for antibody to NBsAg was positive. Of 21 "normal" carriers of HBsAg and 10 carriers with Down's syndrome, 4 persons were detected with the isoenzyme. The results suggest that HBsAg and 5'-NPDase-V in the presence of liver damage are associated and thus provide a new marker enzyme between hepatitis B infection and hepatoma.
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PMID:5'-nucleotide phosphodiesterase isoenzyme in patients with hepatitis B infection. 16 56

The frequency of occurrence of hepatitis B antigen (HBAg) and certain tissue autoantibodies [antinuclear antibody (ANA), smooth muscle antibody (SMA) and mitochondrial antibody (MIA)] were studied with the microtiter complement fixation and immunofluorescence techniques respectively in a group of patients suffering from chronic liver diseases. These were chronic hepatitis (30), cirrhosis of the liver (66) and hepatocellular carcinoma, mostly with underlying cirrhosis (100). A group of closely matched hospital in-patients served as controls. HBAg was found in high frequency in the patients with liver disease (60% in chronic hepatitis, 36.4% in cirrhosis and 49% in hepatocellular carcinoma) whereas tissue auto-antibodies were found in lower frequencies (16.7%, 10.6% and 13% in the three groups respectively). However, in both the frequency was significantly higher than that in the controls (9.2% for HBAg and 0.8% for auto-antibodies). There was a negative correlation between HBAg and tissue auto-antibodies in the group of patients with liver disease when taken as a whole (x2=14.3, P less than 0.001). These results suggest a possible aetiological role played by hepatitis virus B in hepatocellular carcinoma through chronic hepatitis and cirrhosis in Hong Kong while the mutual exclusion between HBAg and auto-antibodies supports the hypothesis of heterogeneity in the aetiology of chronic liver diseases. The patients with auto-antibodies may belong to the auto-immune category but no definate conclusion can be reached until the role played by hepatitis virus A in chronic liver diseases is clarified when more reliable techniques for its identification are available.
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PMID:Hepatitis B antigen and auto-antibodies in chronic liver diseases in Hong Kong. 16 80


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