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)

Although Singapore is in an endemic region for hepatitis B infection, the hepatitis B carriage rate of 5-6% is relatively low. The highest positivity rates for hepatitis B surface antigen (HBsAg) are found in the paediatric age group, with another peak in 40-49 year olds. Studies suggest that, although perinatal transmission is an important route of infection, most children acquire the virus through horizontal transmission between family members. Viral replication continues at a high rate in young carriers and tends to slow down with increasing age. Up to 50% of hepatitis B carriers in Singapore have chronic hepatitis, shown by raised serum ALT values and liver histology, and about 10% are infected with the precore mutant virus. About 20% of carriers have cirrhosis. Among patients with HCC, up to 75% are HBsAg positive, of whom 45% are still viraemic. Mass vaccination against hepatitis B was introduced into Singapore on a voluntary basis in 1983, with compulsory vaccination of babies born to HBeAg positive mothers since 1985. The number of cases of acute hepatitis B has fallen by 60% between 1989 and 1995 although the problems of the longterm complications of chronic hepatitis B still need to be tackled.
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PMID:Hepatitis B virus infection in Singapore. 878 46

Some of the multiple factors involved in the molecular pathogenesis of hepatocellular carcinoma have been elucidated in recent years but no clear picture of how and in what sequence these factors interact at the molecular level has emerged yet. Transformation of hepatocytes to the malignant phenotype may occur irrespective of the aetiological agent through a pathway of chronic liver injury, regeneration and cirrhosis. The activation of cellular oncogenes, the inactivation of tumour suppressor genes and overexpression of certain growth factors contribute to the development of HCC. There is increasing evidence that the hepatitis B virus may play a direct role in the molecular pathogenesis of HCC. Aflatoxins have been shown to induce specific mutations of the p53 tumour suppressor gene thus providing a clue to how an environmental factor may contribute to tumour development at the molecular level.
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PMID:The molecular pathogenesis of hepatocellular carcinoma. 879 May 56

Truncated hepatitis B virus transcripts terminating downstream of a cryptic CAUAAA polyadenylation signal within the HBx open reading frame have previously been identified in tissue samples from two patients with hepatocellular carcinoma (Hilger et al., 1991, J. Virol. 65, 4284-4291). In this study an HBx expression plasmid was systematically deleted in order to elucidate the DNA sequence context which is required for the conversion of the usually inactive CAUAAA motif into a functional polyadenylation signal. Deletions were made progressively on a stretch of viral DNA which, seen on the transcript level, started downstream of the established UAUAAA polyadenylation signal and proceeded to the cryptic CAUAAA motif. The plasmid constructs obtained were used to transfect cells of the HepG2 line. The analysis of newly synthesized RNA via an RNase protection assay revealed termination downstream of the CAUAAA motif following the removal of GU-rich auxiliary sequences downstream of the poly(A) addition site of the UAUAAA signal. Similar results were obtained when an anchored oligo(dT) primer which recognizes selectively truncated RNA was used for the differential, RT/PCR-mediated amplification of 3'-ends. Thus it could be documented in two ways that inactivation or removal of the UAUAAA signal rendered the CAUAAA motif functional as a poly(A) signal. On the basis of the results obtained, we suggest that chromosomally integrated viral DNA on which the TATAAA motif is removed may constitute a template for truncated as well as for virus/cell hybrid transcripts. We also suggest the use of anchored oligo(dT) primers for the rapid identification of truncated transcripts in tissue samples of HCC patients.
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PMID:DNA sequence requirements for the activation of a CATAAA polyadenylation signal within the hepatitis B virus X reading frame: rapid detection of truncated transcripts. 880 79

Among the six species of hepatitis viruses, HBV (hepatitis B virus) and HCV (hepatitis C virus) can induce persistent infection. HBV and HCV are transmitted parenterally, of which maternal transmission and transfusion-associated infection is a major route respectively. We opened the special clinic for carriers detected through blood donation, and followed them at regular intervals for their health care. The prevalence rate of HBV carriers decreased from 3.0% to 1.2% in these 10 years, and that of HCV decreased from 0.9 to 0.4% in these 4 years. Prevalence rate of HBV peaks at 50s and that of HCV peaks at 60s. Due to nearly complete screening of donated blood, post-transfusion hepatitis almost disappeared. HBV vaccine for neonates born from infected mothers reduced the new incidence of HBV carriers. In HBV carriers seroconversion of HBeAg to HBeAb occurs at teens with transient hepatitis and appearance of mutant virus. Ninety percent of the carriers remains healthy for the lifetime but some of them aggravate into chronic hepatitis leading to HCC (hepatocellular carcinoma). In HCV acute infection at adult age succeeds to chronic infection and eventually to liver cirrhosis with sporadic appearance of HCC. On the other hand, less than 50% of HCV carriers seem to be asymptomatic and do not lead to grave disease. In HBV carriers tendency to reject the virus occurs and eventually HBV is cleared in some percentage of the population. In contrast HCV does not tend to be cleared. HBsAb is a defensive antibody. In contrast HCVAb is not a defensive antibody but an infective antibody like HBcAb. DNA polymerase is a good marker of disease state in HBV, and HCV RNA is a good marker of HCV proliferation. Treatment with IFN is sometimes effective for seroconversion in HBV, and for eradication of virus in HCV.
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PMID:[Basic and clinical aspects of hepatitis virus carriers]. 880 69

Persistent human immunodeficiency virus (HIV) infection induces an immuno-suppressive state and therefore malignant tumors are a very common complication. Hepatocellular carcinoma is very rare, however, because it is associated with chronic liver disease by the persistent infection of hepatitis B or C virus (HBV or HCV). We reported a case of HCC with HIV infection who had no evidence of HBV or HCV infection, and that had a rapid growth and active pulmonary metastases. Pathological findings of the resected liver showed moderately differentiated HCC and no chronic liver disease. Despite efforts to find potential HBV integration in tumor and non-tumor tissue, none was observed. To our knowledge, this is the first report of HCC in HIV-infected patient with no evidence of hepatitis virus infection.
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PMID:A case of hepatocellular carcinoma in HIV-infected patient. 888 41

The aim of this study was to determine whether MAGE-4 protein is detectable in sera of patients with hepatocellular carcinoma and other liver diseases. An enzyme-linked immunosorbent assay was employed for detection of MAGE-4 protein in sera of liver disease patients, healthy men and women (control I) and those undergoing prostatic cancer screening (control II). MAGE-4 protein levels in sera of patients with hepatitis C virus-associated HCC (HCC-C) (n = 45, mean = 2.160 ng/ml) and HCV-associated cirrhosis (LC-C) (n = 55, 1.072 ng/ml) were significantly higher (P < 0.0001) than those of control I (0.327 ng/ml) or control II (0.394 ng/ml). MAGE-4 protein was positive in 21/45 (46.7%) HCC-C patients and 18/55 (32.7%) LC-C patients (cut-off, mean plus 2 SD in healthy controls) but in 0/12 (0%) hepatitis B virus-associated HCC (HCC-B) patients, 3/49 (6.1%) hepatitis B virus-associated LC (LC-B) patients, 4/47 (8.5%) alcoholic liver disease patients, and 1/49 (2.0%) controls. Serum MAGE-4 protein level may be useful as a marker for identification of LC-C patients suffering from HCC that is undetectable by presently available methods.
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PMID:Detection of MAGE-4 protein in the sera of patients with hepatitis-C virus-associated hepatocellular carcinoma and liver cirrhosis. 936 41

Cancer is thought to arise from the accumulation of several genetic mutations in a single cell. These include integration of viral genomes, activation of protooncogenes and inactivation of tumor suppressor genes. HCC is one of the most common cancers in Asia and Africa. Various studies have revealed its association with hepatitis B or C viral infection. While activation of known protooncogenes, such as ras genes does not seem to play an important role, frequent allelic loss on specific chromosomal arms, 4q, 13q, 16q and 17p, indicates that dysfunction of diverse tumor suppressor genes located on these chromosome arms is involved in the development of HCC. An informative p53 mutational spectrum of frequent G to T transversions in codon 249 is found in HCCs from either Qidong, People's Republic of China, or southern Africa. This observation links exposure to aflatoxin B1, a known cancer risk factor in these geographic regions. Recently, we found that expression of syndecan-1, which is a transmembrane heparan sulfate proteoglycan involved in cell matrix interactions and growth factor bindings, was inversely associated with metastatic potential in human hepatocellular carcinoma as like nm23-H1 expression was. Transfection with syndecan-1 gene suppresses invasive activity of hepatoma cells. These data support our hypothesis that syndecan-1 is one of important metastasis suppressor factors in hepatoma cells. PR-39 is a proline-rich antimicrobial peptide which was isolated from a pig small intestine and has been reported to induced syndecan-1 on mouse mesenchymal cells. Transfection with PR-39 gene caused induction of syndecan-1 and altered invasive phenotype and actin structure on hepatoma cells. Syndecan-1 and PR-39 may serve as a basis for design of drug or gene therapy effective against metastasis of hepatocellular carcinomas.
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PMID:[Alteration of genomic structure and/or expression of cancer associated genes in hepatocellular carcinoma]. 949 32

Chronic Hepatitis B virus (HBV) infection in children is commonly associated with Hepatitis B e antigen (HBeAg) seropositivity and histologic features of minimal to moderate hepatitis. Remission of liver disease is the rule following HBeAg to antiHBe seroconversion and clearance of HBV DNA from serum. In intermediate and low endemicity areas chronic HBV infection is usually acquired postnatally, and more than 80% of children are likely to achieve stable remission during the pediatric age. Severe sequelae, namely cirrhosis and HCC, have been observed only in less than 4% of children followed over two decades. In all cases cirrhosis was an early complication. Chronic HCV infection is usually silent in children. The chronicity rate seems to be high (50-80%) in post-transfusion hepatitis C as well as in perinatally acquired infection. HCV-associated liver disease is characterized by fluctuations of ALT which remain below two times the normal in about half of the cases. Liver histology shows minimal to mild hepatitis in the large majority of patients and cirrhosis is rare. Few patients achieve spontaneous remission and progression to a more severe liver disease might occur in adult life.
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PMID:Natural history of chronic viral hepatitis in childhood. 965 8

Combined hepatocellular (HCC) and cholangiocellular carcinoma (CCC) (mixed carcinoma) is a rare subtype of primary hepatic carcinoma. We report a case of mixed carcinoma that developed in a non-cirrhotic liver, in a patient who was serologically negative for both hepatitis B and C viruses. A 65-year-old Japanese woman with a 25-year history of chronic rheumatoid arthritis had been treated with steroids and anti-inflammatory drugs, and was diagnosed by ultrasonography with an asymptomatic solitary tumor in the right lobe of the liver. On computed tomography scan and hepatic arteriography, the tumor was well enhanced by contrast medium in the early phase. Based on the findings of elevated serum alpha-feto protein (AFP, 245 ng/ml) and normal carcino-embryonic antigen (CEA, 2.6 ng/ml) levels, a preoperative diagnosis of hepatocellular carcinoma was made. Right lobectomy of the liver was performed on January 7, 1997. Histological examination showed that the resected tumor consisted of combined CCC cells and HCC cells in an intermingled form, with CCC being far more dominant than HCC. The tumor was therefore determined to be a combined carcinoma, subclassified as intermingled type. This case appears to indicate that mixed type carcinoma developed in a non-cirrhotic liver, with CCC being dominant; such a finding is extremely unusual, based on previously published reports.
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PMID:Combined hepatocellular and cholangiocellular carcinoma in a non-cirrhotic liver. 971 50

Combined hepatocellular-cholangiocarcinoma (HCC-CC) is an uncommon form of primary liver cancer having features of both hepatocellular and biliary epithelial differentiation. We reviewed 21 cases of this tumour diagnosed between 1972 and 1996 (patient age range 16-79 years; mean patient age 49.7 years; 18 male and three female patients). Histologically, the majority (n = 18) of tumours were 'mixed' tumours, in which areas of hepatocellular and biliary epithelial differentiation were intimately mixed within the same tumours. Two patients had separate tumours in which discrete nodules of HCC and CC occurred in the same livers. One patient had a 'fibrolamellar' tumour that histologically simulated the fibrolamellar variant of HCC, but some of the tumour cells were mucin-producing cells. Of the 21 cases, mucin was demonstrable in 16 and, in the few mucin-negative tumours, electron microscopic studies confirmed the presence of the dual differentiation. The tumours frequently exhibited an invasive character with frequent venous permeation, direct invasion into adjacent liver parenchyma and tumour microsatellite formation, similar to that of ordinary HCC. Histological evidence of cirrhosis or chronic hepatitis was present in 77.8% of patients and 75% of patients were hepatitis B surface antigen positive. Raised serum alpha-fetoprotein (AFP) levels (above 300 ng/mL) were present in 61.5% of patients and AFP was detected immunohistochemically in 55% of tumours. The overall survival times of patients with HCC-CC were short. In conclusion, HCC-CC showed clinical and pathological features more akin to those of ordinary HCC than to CC.
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PMID:Combined hepatocellular-cholangiocarcinoma: a clinicopathological study. 973 69


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