Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A synthetic HDAg 27 peptide which was selected and designed by the authors and synthesised by Shanghai Institute of Biochemistry, Chinese Academy of Science was used with ELISA method to detect serum anti HD in HBV infected subjects in Chongqing. Anti HD was positive in one of 300 blood donors and was negative in all of 113 cases of hepatitis A and 58 cases of hepatitis non-B. Anti HD was positive in 106 out of 882 cases with positive HBV marker (12.02%), among which anti HD was positive in 3.17% (13/410) of HBsAg carrier, 14.4% (11/76) of acute hepatitis, 7.6% (1/13) of chronic persistent hepatitis, 17.68% (22/121) of chronic active hepatitis, 19.77% (17/86) of severe hepatitis, 29.49% (23/78) of liver cancer and 19.39% (19/98) of primary hepatic cancer. These results coincided with those of previous reports. The coincidence rate was 94.9% (74/78) when compared with Abbott EIA kit. When the natural HDAg was used to compete anti HD in four anti HD positive and two anti HD negative serum specimens, anti HD was negative in all specimens. It is shown that the HDAg 27 peptide has natural HDAg activity capable of being recognized by natural anti HD and is a new diagnostic agent being more simple, save, stable and reliable.
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PMID:[Application of synthetic 27 oligopeptide of HDV antigen for detecting serum anti-HD in HBV infected subjects in Chongqing]. 795 61

We studied the presence of Hepatitis C Virus (HCV) antibodies in a defined Malaysian population and examined the association, if any, between HCV and the Hepatitis B Virus (HBV), using sensitive recombinant DNA second generation Enzyme Immunoassay (EIA) test kits. This sero-prevalence study comprised 1,434 sera from eleven distinct groups comprising intravenous drug users (IVDU), haemophiliacs, male homosexuals, female prostitutes, healthy blood donors, staff of dialysis unit and laboratory personnel, chronic renal failure patients undergoing dialysis (CRFD), patients with liver cirrhosis, chronic active hepatitis, chronic persistent hepatitis and primary liver cancer. Except in laboratory personnel and dialysis staff, HCV antibodies were detected in each group of patients ranging from 3% in blood donors to 85% in IVDU. The main modes of HCV transmission identified were parenteral drug use, transfusion and/or dialysis related. The HBV was found to be the major viral etiological agent in 75% of chronic liver disease (CLD); while in 10% of cases both HCV and HBV were detected. HCV was implicated as the sole viral agent in only a small proportion (1.5%) of patients with chronic liver disease.
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PMID:Hepatitis C--the Malaysian story. 826 52

A review of the histopathology and demonstration of alpha-interferon with a monoclonal anti-alpha-interferon antibody reagent were carried out in 71 consecutive cases of acute and chronic hepatitis, and also in some cases of cirrhosis and HCC. The main cells expressing alpha-interferon were lymphocytes, plasma cells, fibroblasts and polymorphonuclears. There was no evidence for local alpha-interferon production near the site of virus replication in hepatitis B infection. Eleven cases of hepatitis were positive for alpha-interferon. The carrier state showed the highest positive rate in the different types of hepatitis. The positive rate in acute and chronic persistent hepatitis was lower than that in carrier state but higher than that in cirrhosis and HCC. The alpha-interferon positive cells were mainly located in the portal area and in the fibrotissue band around the necrotic and/or carcinomatous cells. These suggest that the function of the interferon system was related mainly to the pathological changes of liver tissue. Early use of interferon might be of therapeutic value to protect liver tissue from injury and to improve the interferon response of the host.
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PMID:[Detection of alpha-interferon positive cells in liver tissue from patients with hepatitis]. 839 41

Soluble HLA-class I and CD8 molecules were determined by sandwich ELISA in patients with viral-induced hepatic disorders. As a whole, the patients with hepatic disorders (acute hepatitis: AH; chronic hepatitis: CH; liver cirrhosis: LC; hepatocellular carcinoma: HCC) showed higher sHLA-class I and sCD8 levels than normal controls (P < 0.001). AH patients had the highest sHLA-class I levels (mean, 3513 +/- 2112 ng/ml), followed by CH (2896 +/- 1290 ng/ml), LC (2293 +/- 1266 ng/ml), and HCC (2221 +/- 1212 ng/ml) sCD8 levels wer highest in AH, followed by HCC, LC, and CH, in that order. Among histologically defined C virus-positive patients, sHLA-I levels were higher in those with chronic active hepatitis (CAH) 2A (3802 +/- 1124 ng/ml) than in those with chronic persistent hepatitis (CPH; 2200 +/- 711 ng/ml; P < 0.01), the levels then decreased as the disease progressed (CAH2B, 3564 +/- 1783 ng/ml, LC, 2376 +/- 1265 ng/ml). In contrast, sCD8 values showed little difference among the disorders. sHLA-class I levels showed a positive correlation with sCD8 values both in whole patients and in patients with AH (P < 0.01), but no correlation was shown, in any patients, with biochemical parameters such as GPT and GOT. These findings, taken together, suggest that hepatic destruction is not the only cause of sHLA-class I production, but that sHLA-class I levels, together with sCD8 levels, may reflect immunological activity in hepatic disorders.
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PMID:Serum concentrations of soluble HLA-class I and CD8 forms in patients with viral hepatic disorders. 921 47

We present here a comprehensive review of the current literature plus our own findings about in vivo and in vitro analysis of hepatitis C virus (HCV) infection, viral pathogenesis, mechanisms of interferon action, interferon resistance, and development of new therapeutics. Chronic HCV infection is a major risk factor for the development of human hepatocellular carcinoma. Standard therapy for chronic HCV infection is the combination of interferon alpha and ribavirin. A significant number of chronic HCV patients who cannot get rid of the virus infection by interferon therapy experience long-term inflammation of the liver and scarring of liver tissue. Patients who develop cirrhosis usually have increased risk of developing liver cancer. The molecular details of why some patients do not respond to standard interferon therapy are not known. Availability of HCV cell culture model has increased our understanding on the antiviral action of interferon alpha and mechanisms of interferon resistance. Interferons alpha, beta, and gamma each inhibit replication of HCV, and the antiviral action of interferon is targeted to the highly conserved 5'UTR used by the virus to translate protein by internal ribosome entry site mechanism. Studies from different laboratories including ours suggest that HCV replication in selected clones of cells can escape interferon action. Both viral and host factors appear to be involved in the mechanisms of interferon resistance against HCV. Since interferon therapy is not effective in all chronic hepatitis C patients, alternative therapeutic strategies are needed to treat chronic hepatitis C patients not responding to interferon therapy. We also reviewed the recent development of new alternative therapeutic strategies for chronic hepatitis C, which may be available in clinical use within the next decade. There is hope that these new agents along with interferon will prevent the occurrence of hepatocellular carcinoma due to chronic persistent hepatitis C virus infection. This review is not inclusive of all important scientific publications due to space limitation.
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PMID:HCV-hepatocellular carcinoma: new findings and hope for effective treatment. 1627 14


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