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)

Analysis of the serum of duck hepatitis B virus (DHBV)-infected ducks has revealed the presence of C-terminally truncated viral core proteins (e antigens). These proteins are glycosylated and therefore were not released from infected cells by lysis but rather by active secretion, indicating that the DHBV core protein can be synthesized alternatively as a cytoplasmic or a secretory protein. Transient expression of cloned wild-type DHBV DNA and of a specifically designed viral mutant in a human hepatoma cell line (Hep-G2) showed that the DHBV core gene promoter is active in differentiated human liver cells and that synthesis and secretion of the processed core proteins are dependent on the expression of the pre-C region, a small open reading frame which precedes the core gene. In addition, these experiments showed that the mechanism of core protein processing and secretion is conserved between DHBV and the human hepatitis B virus and therefore might be important for the hepatitis B virus life cycle in general. In spite of this, intrahepatic injection of the pre-C mutant into uninfected ducks resulted in viremia without concomitant e-antigen synthesis, indicating that virus formation is independent of pre-C expression.
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PMID:The duck hepatitis B virus pre-C region encodes a signal sequence which is essential for synthesis and secretion of processed core proteins but not for virus formation. 368 59

Series of experiments were carried out with chickens (line 15-I and Canadian white leghorn) for establishing the oncogenic properties of Mc-29 virus strain after its multiple replication in cells transformed by it (hepatoma cells). It was established that: 1. After s. c. and i. m. inoculation of intact hepatoma cells local hepatomas of varying size developed after 8--15 days accompanied with general viremia; after i. p. or i. v. injection multiple hepatoma growths occurred in the visceral organs and bone marrow. 2. The i. v. or i. p. inoculation of cell-free material of hepatoma or blood plasma of hepatoma bearing chicken lead after 48--80 days to the formation of hemocytoblastic and myelocytoma growths in the visceral organs and in the bone marrow and exclusively rare--of primary liver and kidney carcinomas. After s. c. injection of cell-free material the result is negative. A conclusion could be drawn that strain Mc-29 virus though replicated in the transformed hepatoma cells preserved its basic leukemogenic potentialities to induce myelocytomatosis and hemocytoblastosis and very rarely--liver and kidney carcinomas.
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PMID:Neoplastic growths in chickens treated with cell and cell-free material from transplantable hepatoma induced by virus strain MC-29. 624 1

The liver disease associated with duck hepatitis B viremia was investigated in naturally infected ducks from Chi-tung county in China and in both naturally and experimentally infected ducks from the United States. Liver and serum specimens of adult Chinese ducks were examined for duck hepatitis B virus (DHBV) DNA by dot and gel blot hybridization. DHBV was found in serum and (in episomal form only) in livers of 6 of 11 birds exhibiting various degrees of chronic hepatitis. In 1 bird with hepatocellular carcinoma, DHBV DNA was detected at the limit of assay sensitivity and in another not at all, contrasting with findings in humans and woodchucks. In work with California Pekin and Khaki Campbell ducks, known amounts of DHBV were injected into the egg 10 days before, or into ducklings 1 day after, hatching and the livers were examined 6 weeks later. The majority of the injected ducklings had viremia detectable by hybridization 1 or 2 weeks after injection. The presence but not the amount of viremia correlated with incidence and degree of hepatitis, determined under code. The most severe instances of hepatitis, all in Pekin ducks, resembled the hepatitis in adult Chinese ducks of Chi-tung county. Severe and moderate hepatitis were found only in indoor-caged injected animals with viremia and in some uninjected birds without viremia that had been kept in outdoor flocks. The latter hepatitis, as some hepatitis in adult Chinese ducks, may not be related to DHBV. Mild and insignificant hepatitis were also found in injected and noninjected ducklings, some of which had the vertically transmitted spontaneous viremia previously described. The good correlation of experimentally induced viremia with incidence and severity of hepatitis in the Pekin duckling provides a simple, rapid, and relatively inexpensive model to study the relation of lesions to hepatitis B family infection in nonprimates.
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PMID:Liver disease associated with duck hepatitis B virus infection of domestic ducks. 658 86

Five Swedish patients with chronic hepatitis C were prospectively followed until hepatocellular carcinoma (HCC) developed. Hepatitis C virus (HCV) antibodies were analysed by a second generation anti-HCV ELISA and a recombinant immunoblot assay (RIBA-2) and viraemia by detection of serum HCV RNA by polymerase chain reaction. Four patients had post transfusion hepatitis and in one patient the source of infection was unknown. HCC developed after 8 to 23 years of mostly asymptomatic disease and all patients died. Four of them were repeatedly biopsied during follow-up and all had chronic active hepatitis. When HCC was diagnosed, cirrhosis was present in all 5. In 4 patients with available sera, anti-HCV was positive and confirmed with RIBA-2, whereof 2 were reactive only to the c-22 and c-33c epitopes. HCV-RNA was present in all sera when HCC was diagnosed. Thus, after prolonged disease duration these patients were still viraemic.
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PMID:Hepatitis C virus infection with progression to hepatocellular carcinoma: a report of five prospectively followed patients in Sweden. 750 21

In testing for antibodies to the hepatitis C virus (anti-HCV) in 112 patients with primary hepatocellular carcinoma, 10 of 33 white patients (30%) and 15 of 79 Asian patients (19%) had a positive response to the antibody. The antibody profile to individual hepatitis C viral antigens and the presence of circulating hepatitis C viral RNA were determined in the 25 patients. The anti-HCV antibodies most frequently detected were toward the antigens from the core (C22) and NS3 regions. Serum hepatitis C viral RNA was present in 17 of the 25 patients (68%), and these patients tended to have serum levels of alanine and aspartate aminotransferases higher than those patients without viremia (136 +/- 22 U per liter versus 64 +/- 11 U per liter and 161 +/- 26 U per liter versus 79 +/- 14 U per liter, respectively, both P < .05). Of the 15 Asian patients with hepatocellular carcinoma and anti-HCV, 4 (27%) had coexisting hepatitis B surface antigen (HBsAg) and 13 (87%) had antibodies to either hepatitis B core or surface antigen. Of the 10 white patients with anti-HCV, however, only 1 (10%) had hepatitis B virus antibodies (P < .01). Among 4 Asian patients with coexisting anti-HCV and HBsAg, 1 was found to have serum hepatitis B viral DNA and the other 3 had hepatitis C viral RNA. A history of blood transfusion was obtained from 12 of the 25 patients with anti-HCV (48%); 20 (80%) had coexisting cirrhosis. Our findings support the hypothesis that hepatitis C virus is an important etiologic agent in the development of primary hepatocellular carcinoma in both white and Asian patients in the United States.
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PMID:Evidence for hepatitis C viral infection in patients with primary hepatocellular carcinoma. 751 78

Our aim was to verify whether the presence of antibodies to HCV envelope protein might mark the occurrence of liver damage, as recently suggested in the literature. Sera from 104 patients (62 male, 42 female) were tested: 84 were positive and 20 were negative to a second generation enzyme immunoassay for anti-HCV antibodies; 51 patients had mild chronic liver disease (44 chronic hepatitis, seven steatosis), 43 had liver cirrhosis (superimposed by hepatocellular carcinoma in 18) and ten were asymptomatic anti-HCV positive subjects with normal liver function tests. Besides, all sera were tested by means of an enzyme immunoassay for the presence of serum antibodies to the synthetic peptide S24A (SIYPGHVSGH RMAWDMMMNW SPTA) derived from amino acids 307-330 of HCV polyprotein. Anti-S24A antibodies were detected in 40/84 sera positive and 1/20 negative at anti-HCV testing (Pearson chi 2 12.29; p = 0.005). Among anti-HCV positive sera, no significant difference existed in anti-S24A status with regard to clinical evidence of liver disease, ALT concentration or HCV RNA positivity. Thus, anti-S24A antibodies are detectable in approximately half of HCV-positive sera, but they do not seem to add significant clinical information to existing tests or to be useful as putative markers of viraemia.
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PMID:Anti-envelope antibodies in anti-hepatitis C virus (HCV) positive patients with and without liver disease. 753 99

We tested for infection with hepatitis C virus (HCV) in 58 patients affected by humoral immunodeficiencies: 43 common variable immunodeficiency (CVI), two hyper IgM syndrome (HIM), two IgG subclass deficiency, four ataxia-telangiectasia (AT), and seven X-linked agammaglobulinaemia (XLA). While the assessment of serum specific HCV antibodies in some of these patients was not informative because of the impairment in specific antibody production, the reverse transcriptase polymerase chain reaction (RT-PCR) assay used to detect serum HCV RNA was a useful method for diagnosing infection. We found that 38% of late onset hypogammaglobulinaemic patients (CVI, HIM or IgG subclass deficiency) had evidence of HCV infection. HCV infection was not detectable in patients with XLA or AT. The majority of our patients had persistent viraemia, and those who underwent liver biopsy showed histological findings of chronic hepatitis. Moreover, we could demonstrate in vitro that eight of 18 HCV-infected patients were actively producing anti-HCV antibodies, despite their impaired antibody production. The high rate of HCV infection in hypogammaglobulinaemic patients could be related to several nosocomial routes of transmission, including intravenous immune globulin administration. Despite the persistent viremia only two patients had cirrhosis and none had hepatocarcinoma.
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PMID:HCV infection in patients with primary defects of immunoglobulin production. 755 76

Serum HCV-RNA levels were determined by newly developed branched DNA probe (bDNA) assay in 87 patients with hepatocellular carcinoma (HCC), compared with 73 patients with chronic hepatitis active and 30 patients with liver cirrhosis. Patients with decompensated liver cirrhosis (LC-d) had a significant lower viremia (mean 3.2Meg.eq./ml, bDNA positive rate; 40%) than chronic hepatitis active (18.0; 64%) and compensated LC (LC-c, 17.9; 80%) (p < 0.05). Those data indicates that HCV replication may decrease as progression of LC. In contrast, there was no difference between the levels of HCC with LC-c (8.2; 85%) and LC-d (6.1; 89%), and their positive rate of bDNA assay were significantly higher than LC-d without HCC (p < 0.01). Therefore, patients undergoing LC in whom serum HCV-RNA sustained high level may correspond to the high risk group of HCC. In HCC of heavy drinker, serum HCV-RNA levels (11.3; 91%) were significantly higher than the levels (4.6; 79%) of HCC without heavy drink (p < 0.05). The result indicates that heavy drink may induced an increase in HCV replication.
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PMID:[Study of hepatocellular carcinoma type C by quantitation of serum HCV-RNA using branched DNA probe assay]. 760 18

To compare the levels of hepatitis C virus (HCV) viraemia in carriers of the same genotype in various stages of chronic HCV infection, we quantified the amount of HCV RNA by competitive polymerase chain reaction and determined HCV genotype using type-specific primers. The study population included 255 patients with chronic HCV infection (asymptomatic 33, chronic hepatitis 141, liver cirrhosis 50, hepatocellular carcinoma 31). Of these 255, the prevalence of HCV RNA genotype II was 67.8%, genotype III, 17.3% and genotype IV, 14.9%; no genotype I was found. The level of HCV RNA (logarithmic transformed copy numbers per 50 microliters of serum) was significantly higher in subjects of genotype II than in those of genotypes III or IV (mean titre 5.8 +/- 1.0 vs. 5.1 +/- 1.2 and 4.8 +/- 1.1, P < 0.05, respectively). There was no significant difference in the level of HCV RNA between genotypes III and IV. Of 173 patients of genotype II, there were no significant differences between the level of HCV RNA and the stage of liver disease or in the level of HCV RNA by age. Of the 129 with genotype II with a history of blood transfusion, there was no significant difference between the level of HCV RNA of patients with and without a history of transfusion or between that of patients with a history of blood transfusion and the time elapsed since blood transfusion. The level of HCV viraemia depended on the genotype of HCV RNA and did not correlate to age or to the stage of liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of genotype to level of hepatitis C viraemia determined by competitive polymerase chain reaction. 767 48

Hepatitis B virus (HBV) infection in children is worldwide in distribution, but the features of HBV-associated liver disease differ depending on the route of transmission and the time of acquisition of the infection. The degree of liver injury varies from a mild disease to the development of cirrhosis and hepatocellular carcinoma, and depends on the replicative status of the viral genome. It is believed that the immune function plays a key role in the severity of HBV disease, and the impact of HBV mutants needs to be assessed. The goals of antiviral therapy in children are therefore, the clearance of viremia and HBV sequences from infected tissues, together with an improvement in the liver disease. Administration of 10 MU/m2 b.s. 3 times weekly over 6 months resulted in a significantly higher clearance of viremia, with normalization of ALT values and greater improvement in liver histology in treated than in untreated patients. Long-term follow-up of these cases reveals the presence of the viral genome in serum and liver by PCR without clearance of HBsAg. Complete eradication of HBV might need more years of evolution as for adult patients. The combination of more than one antiviral agent, as well as the potentiation of the immune system, needs to be assessed to improve the actual response rate obtained with interferon-alpha.
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PMID:Chronic hepatitis B in children. Natural history and treatment. 768 64


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