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)

Infection of Novikoff rat hepatoma cells (subline NlSL-67) with mengovirus resulted in a two- to threefold increase in the rate of choline incorporation into membrane phosphatidylcholine at about 3 hr after infection, without affecting the rate of transport of choline into the cell or its phosphorylation. The time course of virus-stimulated phosphatidylcholine synthesis was compared with the time courses of other virus-induced processes during a single cycle of replication. The formation of viral ribonucleic acid (RNA) polymerase and of viral RNA commenced about 1 hr earlier than the virus-stimulated choline incorporation. Further, isopycnic centrifugation of cytoplasmic extracts indicated that the excess of phosphatidylcholine synthesized by infected cells is not located in the membrane structures associated with the viral RNA replication complex, but with structures of a lower density (1.08 to 1.14 g/cc). These membrane structures probably represent the smooth vesicles which accumulate in the cytoplasm of infected cells during the period of increased phosphatidylcholine synthesis between 3 and 5 hr after infection. They are formed with both newly synthesized phosphatidylcholine and phosphatidylcholine present prior to infection. However, concomitant protein synthesis is not required for the stimulated synthesis of membranes; the effect was not inhibited by treating the cells with inhibitors of protein synthesis at 3 hr after infection, although virus production was inhibited about 90% and virus-induced cell degeneration was markedly reduced and delayed. Production of mature virus began normally at about the same time as the stimulation of phosphatidylcholine synthesis. Treatment of infected cells with puromycin at 2 hr, on the other hand, completely inhibited the stimulation of phosphatidylcholine synthesis.
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PMID:Effect of mengovirus replication on choline metabolism and membrane formation in novikoff hepatoma cells. 432 83

The prevalence of hepatitis B virus infection was markedly different in two neighbouring Gambian villages. 62% of children in Manduar aged 2-4 years were infected whereas in Keneba, the other village, only 27% of this age-group were infected. However, in both villages few infants were infected--none under 6 months of age and only 2 of 58 between the ages of 6 and 12 months. Carriage of hepatitis B surface antigen (HBsAg) was high, reaching a peak of 36% in the 5-9 age-group in Manduar and 17.6% in the 2-4 age-group in Keneba. 86% of all the children under the age of five who were HBsAg-positive also carried hepatitis B e antigen (HBeAg). This proportion fell to 17.6% for children aged 10-14 years and to 12.9% for mothers. Infection clustered in families, transmission from sib to sib being of major importance. The chances of a child being an HBsAg carrier were approximately 42% if an elder sib carried the antigen, 27% if either mother or father was a carrier, and 15% if neither mother or father was a carrier. There were 4 HBeAg-positive mothers who were highly infectious, since 10 of 11 of their children became HBsAg carriers. Carriage of surface antigen lasted many years; 63% of those carrying the antigen in 1972 were still positive in late 1980. 4 cases of primary hepatocellular carcinoma out of 672 adults have been diagnosed in the past five years. All 4 were in HBsAg carriers.
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PMID:Hepatitis B virus infection in two Gambian villages. 613 99

Hepatitis B virus (HBV) infections occur world-wide and more than 200 million people have been estimated to be chronic carriers of HB surface antigen (HBsAg). Long-term chronic carriage of HBsAg has been associated with an increased risk of chronic active hepatitis (CAH), cirrhosis and hepatocellular carcinoma (HCC). In Western countries, the prevalence of HBV infection is low in the general population. Only particular subgroups, for the most part adults, are at risk of such infections: health care workers, haemodialysis patients, transfusion patients, drug abusers and homosexuals. In Asia and tropical Africa, however, the prevalence of HBV infection is relatively high. Transmission occurs mainly during the perinatal period and infancy. Infection at a young age often results in the chronic carrier state. A hepatitis B vaccine has been developed in France and has been demonstrated to be safe, immunogenic, and effective in preventing HBV infection. Extensive experience from clinical trials now makes it possible to recommend vaccination strategies in terms of target populations and of optimal schedules. This paper reports the results of hepatitis B vaccination and, in particular, presents an overview of the vaccination experience in newborns and children.
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PMID:Hepatitis B vaccine: clinical experience. 624 47

Of 209 patients with liver disease attending the Al Qassimi Hospital, Sharjah, 172 were suffering from acute hepatitis. The proportion harbouring the hepatitis B surface antigen was unknown. Of the remainder, 10 were suffering from chronic active hepatitis, five from primary hepatoma and six from cirrhosis. Infection with hepatitis virus B was regarded as of aetiological significance in three cases of chronic active hepatitis, four of primary hepatoma and two of cirrhosis.
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PMID:The spectrum of liver disease in the United Arab Emirates. 627 80

We studied the basis of rejection of retrovirus-infected tumor cells in guinea pigs by evaluating host response to injection of mixtures containing retrovirus-infected tumor cells and, antigenically and biologically distinct, uninfected tumor cells (line 10). After intradermal injection, line 10 grew progressively, metastasized to regional lymph nodes, and led to death of animals; line 107C3 4070A, a murine leukemia virus-infected fibrosarcoma cell line, grew for approximately 1 week and then regressed. Growth of the line 10 hepatoma was suppressed when the hepatoma cells were mixed with viable 107C3 4070A cells before injection into strain 2 guinea pigs. Viable virus-infected 107C3 cells were more effective than irradiated virus-infected cells in suppressing line 10 growth; mixture of line 10 with murine leukemia virus 4070A alone did not inhibit line 10 growth. Suppression of growth of line 10 cells by admixed murine leukemia virus 4070A-infected cells was less effective in animals with established viral immunity. Cyclophosphamide inhibited suppression of line 10 at sites of injection of virus-infected cells. Infection of line 10 with murine leukemia virus in vitro required cocultivation of line 10 cells with murine leukemia virus-infected fibrosarcoma cells; virus alone did not lead to acquisition of murine leukemia virus antigens by line 10 cells.
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PMID:Rejection of retrovirus-infected tumor cells in guinea pigs: effect on bystander tumor cells. 631 16

To target gene expression to malignant hepatic cells, we have constructed recombinant retroviral vectors containing a reporter gene encoding nuclear beta-galactosidase (nls-LacZ) under transcriptional control of regulatory sequences from the rat alpha-fetoprotein (AFP) or human insulinlike growth factor II (IGFII) genes. The AFP and IGFII P3 promoters activate transcription during fetal development and are often reactivated in hepatocellular carcinoma (HCC). Infection of several cultured cell types with the retroviral vector containing the IGFII P3 sequence resulted in expression of the reporter gene in all cell lines tested, including those that do not produce IGFII. In contrast, selective expression was achieved by vectors containing the AFP transcriptional regulatory sequence. Nuclear beta-galactosidase activity was detectable in cells from lines that produce AFP, and not in cells that do not express the AFP gene. In most infected cell lines, retroviral RNA synthesis from the 5' LTR was inhibited, and deletion of the retroviral LTR enhancer did not change expression from either the IGFII P3-nls-LacZ or the AFP-nls-LacZ cassettes. After treatment of cells with 12-O-tetradecanoylphorbol-13-acetate and epidermal growth factor (EGF), the decrease in concentrations of endogenous AFP messenger RNA (mRNA) and nls-LacZ mRNA transcribed from the transferred AFP regulatory sequence were similar. In the context of an integrated provirus, the AFP transcriptional regulatory sequence is therefore subject to similar regulatory control as that of the endogenous gene. These data show that the AFP sequence, and not the IGFII P3 promoter we used, is suitable for targeting gene expression to malignant hepatic cells.
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PMID:Hepatoma cell-specific expression of a retrovirally transferred gene is achieved by alpha-fetoprotein but not insulinlike growth factor II regulatory sequences. 748 90

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.
Infection
PMID:Anti-envelope antibodies in anti-hepatitis C virus (HCV) positive patients with and without liver disease. 753 99

Infections in immunocompromised hosts have been an important clinical problem. Patients with liver cirrhosis and/or hepatocellular carcinoma are at a high risk of infection due to multiple factors. Five hundred and two patients admitted with liver cirrhosis and/or hepatocellular carcinoma were evaluated for infection. The infection rate was not influenced by the etiology of hepatic diseases or the presence of hepatocellular carcinoma, however, it increased with the advance of clinical stages of liver cirrhosis and hepatoma. The respiratory tract and urinary tract were the most common sites of infection, being involved in 50% and 28% of cases, respectively. The major pathogens of respiratory tract infection were S. aureus, H. influenzae, and P. aeruginosa. Gram-negative bacteria was the common isolate from sputum and urine, and S. aureus was also common in gram-positive bacteria. The infection rate was high in patients who died although infections could rarely be implicated as the direct cause of death. These findings should be a guide for the clinicians in treating patients with liver cirrhosis and/or hepatocellular carcinoma who exhibit signs of infection.
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PMID:Infections in patients with liver cirrhosis and hepatocellular carcinoma. 754 30

Infections by the hepatitis B or C virus are extremely common causes of acute and chronic liver disease, and coexistence of the two viruses in the same patient is not rare. Evidence has been found that such interaction may play an important role in fulminant hepatitis and in the development of hepatocellular carcinoma in cirrhotic patients. Liver disease activity and prognosis have been reported to be generally more serious in the presence of double infection, although an inverse relationship in the replicative levels of the two agents has been noted, suggesting viral interference, particularly in cases of chronic hepatitis. Thus, the two viruses seem to inhibit each other at the molecular level, while cytopathic effects appear to be enhanced. Further studies are needed to explain the mechanisms of these apparently contrasting effects.
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PMID:The interaction between hepatitis B virus and hepatitis C virus in acute and chronic liver disease. 760 74

Hepatitis B virus (HBV) infections occur worldwide, with the endemicity of infection varying among geographical areas. Infections acquired by perinatal via commonly become persistent and can progress to chronic liver diseases, including cirrhosis and hepatocellular carcinoma. The possibility of vertical transmission of the VHB infection depend of the serological condition of the mother, women with AgsHB positive can infect 10 to 20% of her fetus while women with AgsHB more AgeHB positive can infect 80-90% of her products. Newborns of women with acute or chronic HBV infection must be immunized with vaccine and hepatitis B immune globulin at birth with the objective to reduce the risk of infection.
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PMID:[Hepatitis B in pregnancy: clinical and prophylactic implications]. 769 81


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