Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of 10151 organ allograft recipients who developed 10813 de novo malignancies after transplantation, 755 involved the hepato-biliary-pancreatico-duodenal (HBPD) area. If nonmelanoma skin cancers and in situ carcinomas of the uterine cervix were excluded (as they are from most cancer statistics), then the HBPD area was affected by 10% of neoplasms. Many of the tumors encountered were uncommon in the general population. The largest group of neoplasms was 474 lymphomas, which comprised 63% of the total. Other major malignancies were hepatocellular carcinomas (HCC; 15%), pancreatic carcinomas (11%), cholangiocarcinomas (3%), Kaposi's sarcomas (3%), and other sarcomas (1%). Lymphomas occurred at a younger age than other tumors (average, 39 versus 50 years), appeared earlier after transplantation (average, 24 versus 77 months), and were more frequently associated with immunosuppressive therapy with the antilymphocytic agents (ALG/ATG) and/or (OKT3) (59% versus 28%). Lymphomas were localized to the HBPD area in only 18% of patients, whereas in 82% there was involvement of other organs or sites. The liver was involved in 95% of lymphomas. Lymphomas frequently involved allografts, the liver in 84%, and the pancreas in 59%. Of 292 patients treated for lymphomas 67 (23%) had complete remissions lasting 6 months or more. HCC was frequently associated with hepatitis B or C infection. Kaposi's sarcomas were rarely confined to the HBPD area, and in 25% of cases there were no associated skin lesions. An unusual subset of tumors were leiomyosarcomas involving hepatic allografts of pediatric patients. The poor prognosis of most tumors in this series may be related to delays or problems in making the diagnosis in these immunosuppressed patients and, perhaps, it may also be related to the unusually aggressive behavior of some tumors.
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PMID:Primary malignancies of the hepato-biliary-pancreatic system in organ allograft recipients. 974 82

TP53 gene mutations occur in 30 to 55% hepatocellular carcinomas. Both the frequency and the type of p53 mutations in HCC vary according to geographical location of tumors. A specific mutation at codon 249 (AGG-->AGT) was found at high frequency in tumors from high aflatoxin-areas. TP53 mutations in other geographic locations are less frequent and scattered on the exons encoding the central region of the protein. TP53 mutations observed in hepatocellular carcinoma are accompanied by a loss of wild-type p53 function. Moreover, the p53-249ser mutant appears to display a gain of function at some degree. In addition to p53 inactivation by gene mutation, there is growing evidence that the wild-type p53 functions can be inactivated by the HBx protein of Hepatitis B Virus. The hepatocellular functions of wild-type p53 protein are not entirely known. The present data suggest that the DNA damaging agents induce p53-dependent cell cycle arrest or apoptosis in cell lines derived from normal liver or hepatocellular carcinoma. In contrast, the exposure of mice to genotoxic agents does not induce p53-dependent changes in normal adult liver. This could be due to the fact that the hepatocytes of the adult liver are quiescent cells.
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PMID:TP53 and hepatocellular carcinoma. 976 50

The aims of this study were twofold: (1) to determine the prevalence and clinical features of hepatitis delta virus (HDV) infection among subjects positive for hepatitis B surface antigen (HBsAg) living in the Miyako Islands, Okinawa Prefecture, Japan, and (2) to clarify the relationship between HDV-RNA level and severity of HDV-related liver disease. One hundred and ninety-nine HBsAg-positive subjects (123 asymptomatic carriers [ASCs], 3 patients with acute hepatitis [AH], 50 patients with chronic hepatitis [CH], 15 patients with liver cirrhosis [LC], and 8 patients with hepatocellular carcinoma [HCC], were tested for antibody to HDV (anti-HDV) by radioimmunoassay. Anti-HDV-positive individuals were examined to determine semi-quantified HDV-RNA level by polymerase chain reaction (PCR). The overall prevalence of anti-HDV among the 199 subjects was 21.1%. The positivity rate tended to increase with age or the severity of the underlying liver disease: anti-HDV-positive rates were 10.6% (13/123) in ASCs, 32.0% (16/50) in patients with CH, 40.0% (6/15) in patients with LC, and 87.5% (7/8) in patients with HCC. None of the patients with AH were positive for anti-HDV. There was no correlation between semi-quantified serum HDV-RNA levels and the severity of chronic liver disease in patients positive for anti-HDV. The present study showed the local spread of HDV infection in the Miyako Islands, Okinawa, Japan. Although the anti-HDV positivity rate tended to increase with the severity of the underlying liver disease, the severity of HDV-related liver disease did not correlate with the semi-quantified serum HDV-RNA level.
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PMID:Prevalence and clinical features of hepatitis delta virus infection in the Miyako Islands, Okinawa, Japan. 985 58

In two cases of childhood hepatocellular carcinoma in Thailand, we established vertical transmission of hepatitis B virus infection as the underlying cause. With the first patient, the family history of HBV carriage became evident and a pedigree could be devised which demonstrated the high prevalence among the family members and hence evidence of vertical transmission. In the case of the second patient, we performed PCR and subsequent direct sequencing of HBV DNA isolated from his HBsAg-positive mother's, as well as from his serum, comparing the nucleotide sequences with those of a pregnant woman diagnosed as an asymptomatic HBV carrier, of another asymptomatic HBV carrier and of a reference strain, respectively, all belonging to the same genotype and subtype as the samples tested. Our results clearly indicate the necessity for nation-wide hepatitis B vaccination starting at birth, at least in hyperendemic areas like the Far East, in order to forestall HBV carriage and ensuing cirrhosis and/or HCC by preventing vertical transmission.
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PMID:Hepatocellular carcinoma: significance of HBV vertical transmission. 987 47

We report construction and characterization of tetracycline-controlled hepatitis B virus pX-expressing hepatocyte (AML12) cell lines. These cell lines were constructed in AML12 clonal isolates (clones 3 and 4), which express constitutively the tetracycline-controlled transactivator. Since pX is implicated in HCC, this immortalized hepatocyte model system was used to investigate the mechanism of pX in transformation. Clonal isolates of 3pX and 4pX lineages display conditional synthesis of pX mRNA and protein and a 2-fold increase in growth saturation density following tetracycline removal, implicating pX in monolayer overgrowth. Interestingly, only 3pX clones display pX-dependent anchorage independence. Clone 3 lineages express hepatocyte nuclear factor-1alpha and hepatocyte-specific marker genes; clone 4 lineages express hepatocyte nuclear factor-1beta and reduced levels of hepatocyte-specific marker genes, suggesting the importance of the differentiated hepatocyte in pX-mediated oncogenic transformation. Importantly, 3pX and 4pX lineages display differential expression of immediate early genes c-fos and ATF3. The pX-transforming 3pX lineage displays early, pX-dependent induction of ATF3 and prolonged induction of c-fos. The nontransforming 4pX cells display an absence of pX-dependent ATF3 induction and transient induction of c-fos. Our results support the direct link of pX expression to oncogenic transformation in 3pX lineage clones and underscore the advantage of this conditional cellular model system for studying mechanisms of pX-mediated oncogenesis.
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PMID:Differential immediate early gene expression in conditional hepatitis B virus pX-transforming versus nontransforming hepatocyte cell lines. 989 Sep 99

TT virus(TTV) was recently reported as candidate for a new hepatitis virus from post transfusion hepatitis of unknown etiology. In the present study, influence of TTV superinfection on acute hepatitis B was analyzed. TTV DNA was detected in sera from 10 of 44(23%) patients with acute hepatitis B, but prevalence was comparable with normal blood donor. It was unlikely that TTV superinfection affected clinical course of acute hepatitis B. In cases of TTV superinfection on hepatitis B, T. Bil and ALT values were higher than in cases of non-superinfected patients. Furthermore, HCC was appearanced in a patient of recover from acute hepatitis B.
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PMID:[TTV superinfection on acute hepatitis B]. 1039 Sep 92

Tumor metastasis to a cirrhotic liver is rare. It has been suggested that colorectal cancer does not metastasize to the cirrhotic liver. We reported a 65 year-old man, a known carrier of hepatitis B surface antigen, diagnosed to have hepatocellular carcinoma with routine screening. A partial hepatectomy with resection of segments VI and VII was performed. The hepatectomy specimen revealed a 4.5 cm diameter HCC in a cirrhotic liver. Incidentally, 0.8 cm diameter ulcer at the descending colon. Histological examination of the left hemicolectomy specimen showed a moderately differentiated adenocarcinoma.
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PMID:Carcinoma of the colon with synchronous hepatic metastasis in a cirrhotic liver harboring a hepatocellular carcinoma. 1052 97

Recent data suggest that Bin1, a novel C-MYC interacting protein, is a suppressor gene whose loss of expression is a frequent aberration associated with several malignancies. The mechanism responsible for loss of BIN1 expression is not understood. The purpose of this study is to investigate DNA profile of the BIN1 gene in human hepatoma Hep G2 cells, previously documented with lack of BIN1 expression. Chromosome and molecular analyses of Hep G2 cells were initiated to exclude the possibility of genetic alterations as a factor affecting BIN1 gene expression in these cells. We used Hep G2 cell line and its hepatitis B virus (HBV) transfected variants--Hep G2T14.1 and Hep G2215 cell lines. The cytogenetic localization of BIN1 was identified in the 2q14 region. Fluorescence in situ hybridization (FISH) with the chromosome 2 whole chromosome painting probe (WCP) demonstrated three or four intact copies of chromosome 2 in all three hepatoma cell lines studied. FISH analyses with the BIN1-specific probe of the Hep G2, Hep G2T14.1, and Hep G2215 metaphase chromosomes document no rearrangement of the BIN1 gene on any of the multiple copies of chromosome 2. FISH with the specific HBV probe did not identify the HBV integration site in Hep G2T14.1 and Hep G2215 cells within the BIN1 locus. Southern blot analyses revealed no genetic rearrangements in the BIN1 gene in any of the cell lines studied. Our RNA analyses (northern blot and RT-PCR) document lack of BIN1 message in Hep G2 cells in contrast to the presence of BIN1 in Hep G2T14.1 and Hep G2215 cells. No difference was identified in other transcripts analyzed, including c-myc. Analyses of BIN1 expression of Hep G2 cells at different passages were initiated and document low levels of BIN1 transcript in Hep G2 cells of passage < 85. Furthermore, BIN1 transcript was identified in additional seven HCC cell lines analyzed. Our data indicate that lack of Bin1 expression in HepG2 cells previously documented is a characteristic of cells of passage > 85 and is not due to genetic loss, or rearrangement within the BIN1 DNA sequence. Loss of the BIN1 transcript is not a characteristic of HCCs analyzed.
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PMID:Investigation of the expression of Bin1, a putative suppressor, in human hepatoma cells. 1061 29

The serum AFP concentration in man falls rapidly after birth and its synthesis in adult life is normally repressed. However, AFP is synthesized in large amounts by human hepatocellular carcinoma in greater than 70% of patients. Elevation of serum AFP in benign hepatic diseases such as acute and chronic viral hepatitis as well as toxic liver injury is associated with small transient increases in serum AFP. Therefore, quantification of serum alpha-fetoprotein (AFP) has been widely used as a diagnostic marker for hepatocellular carcinoma. Measurement of serum AFP levels have also been used in screening populations at high risk of human hepatocellular carcinoma such as those with cirrhosis or carriers of hepatitis B virus. However the specificity of the screening test in patients with only modestly raised AFP (below 400 ng/ml) is low, and false-positive results are frequent. A wide range of overlap in the distribution of serum AFP levels between hepatocellular carcinoma and chronic liver disease patients were observed mainly among HBsAg (+) patients. Therefore the specificity and predictive value of AFP are lower in HBsAg(+) than in HBsAg(-) patients, especially when AFP is between 25 and 200 ng/ml. In patients with chronic hepatitis B, the analysis of lectin reactivity of AFP has the advantages over quantification of serum AFP to detect HCC-specific variants in serum samples with only moderate raised AFP levels. Measurement of AFP serves as an important tool in the care and management of patients with benign and malignant hepatic disorders.
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PMID:[Alpha-fetoprotein: diagnostic value in hepatic disorders]. 1096 24

Animal models of hepatitis B virus infection have been valuable for determining the mechanisms of hepadnavirus replication, for studies of pathogenesis, and for investigations of viral hepatocarcinogenesis. The woodchuck model also seems to be useful in the discovery and development of antiviral drugs to treat HBV infection and for testing new forms of immunotherapy. In particular, the woodchuck seems to be ideal for studying the effect of antiviral treatment and immunotherapy on the outcome of hepadnavirus infection and on survival. The median life expectancy of experimentally infected, chronic WHV carriers is approximately 29 months, and almost all develop HCC. New types of prophylaxis or therapy can be evaluated under controlled experimental conditions, in a relevant animal model, and within a reasonable time frame.
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PMID:Animal models of hepadnavirus-associated hepatocellular carcinoma. 1121 19


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