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 high frequency of hepatitis B antigen (HBsAg) in hepatocellular carcinoma (HCC) patients has led to the hypothesis that immunoresponsiveness to hepatitis B virus (HBV) may be deficient in some patients, and that the immune response deficiency may have a genetic basis. Radioelectrocomplexing (REC), a radioimmunoassay in gel based on the principle of counterimmunoelectrophoresis (CIE), has been used to identify four HBV immune status subgroups: 1) HBsAg +ve/HBsAb +ve; 2) HBsAg +ve/HBsAb -ve; 3) HBsAb -ve/HBsAb +ve; 4) HBsAg -ve/HBsAb -ve/HBsAb -ve. These subgroups comprise 2, 6, 70, and 22 percent, respectively, among blood donors, and 32, 19, 23, and 26 percent, respectively, among HCC patients. Although the HBV exposure rates in the two groups were similar, the immune complexemic rates and HBs antigenemic rates were significantly higher in HBB patients than in the blood donors. It is proposed that the failure of termination of HBV infection revealed by these high rates reflects an immunodeficiency state characterized by an inability to produce high-avidity HBsAb. The immunodeficiency might have a primary genetic basis, or it might be secondary to the immunodepressive effects of concurrent viral or parasitic infections.
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PMID:Immunodeficiency to hepatitis B virus infection and genetic susceptibility to development of hepatocellular carcinoma. 17 28

Replication of hepatitis A virus (HAV) in the human hepatoma-derived PLC/PRF/5 cell line was neither inhibited in the presence of various concentrations of guanidine or D-2-(alpha-hydroxybenzyl)benzimidazole (D-HBB), nor were the two chemicals effective in combination. Under identical conditions, however, replication of poliovirus type 1 was inhibited. Tracer experiments with radiolabelled guanidine and D-HBB also furnished no evidence that the two antiviral substances were metabolized gradually to inactive derivatives in PLC/PRF/5 cells. Therefore, it is concluded that resistance to the action of guanidine and D-HBB is an inherent characteristic of HAV. However, the insensitivity of HAV to these drugs does not exclude the virus from the family of picornaviruses.
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PMID:Failure of guanidine and 2-(alpha-hydroxybenzyl)benzimidazole to inhibit replication of hepatitis A virus in vitro. 628 46

Recent studies revealed that hemoglobin is expressed in some non-erythrocytes and it suppresses oxidative stress when overexpressed. Oxidative stress plays a critical role in the pathogenesis of non-alcoholic steatohepatitis (NASH). This study was designed to investigate whether hemoglobin is expressed in hepatocytes and how it is related to oxidative stress in NASH patients. Analysis of microarray gene expression data revealed a significant increase in the expression of hemoglobin alpha (HBA1) and beta (HBB) in liver biopsies from NASH patients. Increased hemoglobin expression in NASH was validated by quantitative real time PCR. However, the expression of hematopoietic transcriptional factors and erythrocyte specific marker genes were not increased, indicating that increased hemoglobin expression in NASH was not from erythropoiesis, but could result from increased expression in hepatocytes. Immunofluorescence staining demonstrated positive HBA1 and HBB expression in the hepatocytes of NASH livers. Hemoglobin expression was also observed in human hepatocellular carcinoma HepG2 cell line. Furthermore, treatment with hydrogen peroxide, a known oxidative stress inducer, increased HBA1 and HBB expression in HepG2 and HEK293 cells. Importantly, hemoglobin overexpression suppressed oxidative stress in HepG2 cells. We concluded that hemoglobin is expressed by hepatocytes and oxidative stress upregulates its expression. Suppression of oxidative stress by hemoglobin could be a mechanism to protect hepatocytes from oxidative damage in NASH.
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PMID:Upregulation of hemoglobin expression by oxidative stress in hepatocytes and its implication in nonalcoholic steatohepatitis. 2193 90