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)

During an 11-yr period (1979-1989), we have experienced five patients with idiopathic Budd-Chiari syndrome (BCS), four (80%) of whom had associated hepatocellular carcinoma (HCC). In contrast, the incidence of BCS complicated by HCC was 0.7% of a total of 556 patients who underwent surgery for HCC or were autopsied. Hepatitis B virus-related antigen or antibody was positive in one patient each. Four of our five patients were asymptomatic and were initially diagnosed by ultrasonography (n = 3) or computed tomography (n = 1). The hepatic parenchyma histopathological findings were cirrhosis and fibrosis in one each. Infection of hepatitis B virus rather than BCS was speculated as a causative factor for HCC in two patients. Membranous obstruction with spotty calcification, intrahepatic bizarre communicating vessels, and the dilated anterior longitudinal veins in spinal canal were recognized in three patients. Three patients had two HCCs which were similar in size and arose from the right and left hepatic lobe, separately, suggesting multicentricity of HCC. Both percutaneous transluminal angioplasty with Gruntzig balloon catheters for the obstruction of the inferior vena cava and hepatic arterial embolization for HCC(s) were performed in three patients. These patients survived 29.3 months on average after the diagnosis of BCS complicated by HCC(s). The opened IVC was confirmed to be patent on an average of 26.3 months after the first angioplasty.
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PMID:Radiological study of idiopathic Budd-Chiari syndrome complicated by hepatocellular carcinoma. A report of four cases. 830 12

A case of portal vein thrombosis due to Candida albicans in a patient with alcoholic hepatic cirrhosis in the absence of hepatocarcinoma is described. Infection is a known cause of portal vein thrombosis but thrombosis by Candida albicans has not to our knowledge been previously reported.
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PMID:Portal vein thrombosis due to Candida albicans associated with hepatic cirrhosis. 849 42

Infection by hepatitis C virus (HCV) generally induces an asymptomatic acute hepatitis. HCV infection becomes chronic in about 80% of cases. Chronic HCV infection is asymptomatic with persistent viremia and normal liver tests in a minority of the subjects. Chronic HCV infection is associated with chronic hepatitis with increased serum transaminases levels in the majority of the subjects. Among the patients with chronic hepatitis, the majority have minimal lesions; about 20% have a more severe disease and will develop after 5 to 20 years cirrhosis. In patients with cirrhosis, the incidence of hepatocellular carcinoma is high (around 5% per year). The factors influencing the evolution of HCV infection are not know. Alcohol is certainly an important factor. Virus related factors, such as genotype and level of replication, might also be important factors.
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PMID:[Natural history of hepatitis C virus infection]. 874 88

Hepatitis B remains one of the most important infectious diseases in China. In 1980, an overall hepatitis B virus (HBV) infection rate of 42.6% was reported and a hepatitis B surface antigen (HBsAg) carrier rate of 10.3%. HBsAg positivity among children under 1 year of age ranged from 5.1% in Beijing to 7% in Guangdong. A peak in carrier rate was observed in 7 to 14 year olds, reaching 24% in Guangdong. During the past decade, there has been no significant change in overall HBV carrier rates. However, in areas where hepatitis B vaccination for all neonates has been introduced, a decline in HBsAg positivity in lower age groups has been observed. Perinatal transmission is believed to account for 35-50% of carriers although horizontal transmission is also important, particularly within families. Infants born to HBeAg positive carrier mothers are at even greater risk of infection. HBV infection during childhood leads to an increased risk of serious longterm sequelae, including hepatocellular carcinoma (HCC). It is hoped that universal childhood immunisation will allow control of HBV infections in China within a few generations.
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PMID:Perinatal transmission of hepatitis B virus infection and vaccination in China. 878 51

Infection with the hepatitis C virus (HCV) commonly causes persistent disease, which may lead to cirrhosis and hepatocellular carcinoma. The pathogenesis of HCV infection is not well understood. It is most likely that both viral and host factors contribute to HCV persistence. This review focuses on the host's immune response to HCV in an attempt to present the current knowledge and concepts of the interactions between the virus and the host during HCV infection. Expansion of B lymphocytes and antibody production to virtually any HCV protein can be detected in most infected patients. However, observations in HCV-infected humans as well as experimental infections in chimpanzees suggest that natural HCV infection does not induce protective immunity, and reinfection can readily be demonstrated after inoculation with homologous or independent strains in HCV-seroconverted animals. Nevertheless, the immune system may gain partial control over HCV even in patients with chronic infection, as HCV infection in severely immunocompromised patients runs a particular cholestatic course which may rapidly lead to death from liver failure. Cytotoxic CD8+ T lymphocyte responses to HCV proteins have been characterized in peripheral blood and liver tissue and were found to be remarkably polyclonal and multispecific. Epitopes were identified on all of the putative HCV proteins, although only few major histocompatibility complex molecules were considered restriction elements. Immunoregulation may be particularly important in HCV infection. The HCV core and NS4 proteins appear to be most immunogenic for peripheral blood lymphocytes, and NS4 specific CD4+ lymphocytes are preferentially compartmentalized to the liver. However, there is an inverse relationship between CD4+ lymphocyte responses and antibody levels in infected patients. Furthermore, a strong cellular response to the HCV core protein apparently favors a benign course of infection. This unusual T-B cell relationship may be the consequence of an altered cytokine release during HCV infection. Alternatively, this virus may have found devices that can disturb immunoregulation in infected patients. A better understanding of these immunological mechanisms induced by HCV infection should make it possible to develop more effective strategies for the prevention and treatment of this insidious disease.
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PMID:Immune responses in hepatitis C virus infection. 883 85

A great deal of information on the molecular heterogeneity of hepatitis C virus (HCV) has been achieved since its discovery in 1989. However, little is known about the clinical significance of these variations. Based on the degree of sequence variation, HCV has been classified into six major groups or types, differing by 31-34% at the nucleotide level over the entire virus genome. Each type is divided into several subtypes that differ by 20-23% in nucleotide sequence. Viruses within the same subtype are up to 10% divergent and, within infected individuals, vary by up to 1.5%. Genotype distributions are not homogeneous around the world and may reflect both historical and recent parenteral routes of transmission. The clinical implication of these genomic variations are not yet fully elucidated: genotype 1b has been associated with end-stage liver disease, including liver cirrhosis and hepatocellular carcinoma, but this finding might rather reflect its earlier introduction to the populations studied. Consistent evidence exists that types 2 and 3 have a higher response rate to interferon treatment than type 1, although the interplay between genotype and viral load in determining the response is still unclear. Immunohistochemical studies indicate a stronger activation of the endogenous interferon system in the liver of patients infected with type 1 compared to those infected with types 2 and 3, explaining, at least in part, its low responsiveness to exogenous interferon treatment. Biological, sequence-dependent variations of genotypes have been poorly investigated to date, but differential efficiency of translation activity of the 5' non-coding region has been reported. The availability of "in vitro" systems for evaluating pathogenetic aspects and neutralization mechanisms will improve the present knowledge on this world-wide infectious disease and on the clinical usefulness of distinguishing between genotypes.
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PMID:Heterogeneity of hepatitis C virus. 886 32

Rare benzo[a]pyrene-resistant clones were previously isolated from the mouse hepatoma cell line, Hepa-1 (Hepa1c1c7), and shown to be deficient in induction of CYP1A1 mRNA by ligands for the aryl hydrocarbon receptor (AHR). Clones belonging to complementation group B were shown to have reduced levels of ligand binding to AHR. It is shown here that all 15 independently derived B clones analyzed had much reduced levels of AHR mRNA, but in each case, the mRNA was normal in size. Infection of B clones with a retroviral expression vector for AHR restores CYP1A1 inducibility (although viral AHR expression is progressively silenced and CYP1A1 expression progressively diminishes as the cells are maintained in culture). Treatment of the B clones with the histone deacetylase inhibitors sodium butyrate or trichostatin A restores AHR expression and also restores CYP1A1 inducibility to nearly 100% of the cells in the treated cultures. Fusion of a representative B clone with a rat hepatoma cell line restores expression to the mouse AHR gene encoded by the B clone's genome. These results demonstrate that the loss of CYP1A1 inducibility in B clones is probably totally ascribable to their reduced levels of AHR and that the clones are most probably not mutated in the AHR gene but are deficient in its expression. The evidence suggests that the reduction in expression of mRNA encoded by the endogenous AHR gene in the B clones is not due to an epigenetic alteration in chromatin structure but that the clones are probably defective either in a transcription factor for the AHR gene or in a protein required for generating an open chromatin configuration over the gene.
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PMID:Basis for the loss of aryl hydrocarbon receptor gene expression in clones of a mouse hepatoma cell line. 896 65

The influence of the hepatitis C virus (HCV)-genotype on liver disease severity was evaluated in 429 consecutive patients with chronic hepatitis C, including 109 with cirrhosis who were followed up prospectively, allowing for the assessment of the role of the HCV-genotype on disease outcome and on the development of hepatocellular carcinoma (HCC). HCV-1 was detected in 147 (46%) patients without cirrhosis and in 47 (43%) with cirrhosis (P: not significant), being mainly HCV-1b. HCV-2 was found in 103 (32%) cases without cirrhosis and in 30 (27.5) with cirrhosis (P: not significant), being mainly HCV-2a. HCV-3 was detected in 32 (10%) patients without cirrhosis and in 2 (2%) with cirrhosis (P < 0.005). Infection with more than one genotype (HCV-1/HCV-2 and HCV-1/HCV-3) was observed only in cirrhotic patients (6 of 109; 5.5%). During a mean follow-up of 67 +/- 22 months, 21 (19%) patients with cirrhosis showed worsening in Child's stage, 5 (4.5%) underwent liver transplantation, 23 (21%) developed HCC, and 24 (22%) died of complication of liver disease; the overall incidence of at least one of these events was 38.5%. By the Kaplan-Meier method and log-rank test, the cumulative probability of developing each or at least one of the above events did not differ in relation to the genotype of infecting HCV, apart from patients with mixed genotype infection who showed a significantly higher incidence of death (P < .05). These data indicate that HCV-genotypes do not have a significant effect on the severity and outcome of liver disease in patients with chronic HCV-infection. Patients with cirrhosis who are also infected by HCV-1 and HCV-2 had a similar prognosis and progression to HCC, while patients infected by more than one genotype showed the most unfavorable course of disease.
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PMID:Lack of correlation between hepatitis C virus genotypes and clinical course of hepatitis C virus-related cirrhosis. 898 92

Hepatitis C is becoming the main cause of cirrhosis and primary liver carcinoma. Infection by hepatitis C virus (HCV) generally induces an asymptomatic acute hepatitis. HCV infection becomes chronic in about 80% of cases. In a minority of the subjects, chronic HCV infection is asymptomatic with persistent viremia and normal liver tests. These asymptomatic subjects have minimal liver histologic lesions and a good prognosis. In a majority of the subjects, chronic HCV infection is associated with chronic hepatitis with increased serum transaminases levels. Among the patients with chronic hepatitis, the majority have a mild liver disease with a moderate increase in serum transaminases levels and, at liver histology, minimal lesions; a minority (about 20%) have a more severe liver disease and will develop cirrhosis after 5 to 20 years. In patients with HCV related cirrhosis, the incidence of hepatocellular carcinoma is high (around 5% per year). The factors influencing the evolution of HCV infection are not known. Alcohol is certainly an important factor which increases the risk of development of fibrosis then cirrhosis. Virus related factors, such as genotype and level of replication, might also be important. Autoimmune diseases have been reported in association with hepatitis C. HCV infection is a major cause of mixed cryoglobulinemia associated with vasculitis or glomerulonephritis. A relationship between HCV and auto-immune diseases such as thyroiditis or Gougerot syndrome has been suggested but not demonstrated. HCV infection is frequent in patients with porphyria cutanea tarda; in these patients, HCV related liver disease might trigger the expression of the metabolic disease.
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PMID:[Clinical picture and evolution of hepatitis C]. 899 8

Infection with hepadnaviruses and exposure to aflatoxin B1 (AFB1) are considered major risk factors in the development of hepatocellular carcinoma (HCC) in humans and in animals. A high rate of mutations in the p53 tumor suppressor gene in hepatocellular carcinomas of predominantly hepatitis B virus (HBV) carrier patients has been recently related to dietary aflatoxin. Another member of the hepadnavirus family, the woodchuck hepatitis virus (WHV), infects woodchucks in a manner similar to that of HBV in humans. Therefore, it was of particular interest to determine whether the p53 gene in woodchuck HCCs associated with hepadnavirus infection and with exposure to AFB1 is affected in the same manner as in human HCCs. By direct PCR-sequencing, we analyzed exons 4-9 of the p53 gene in 13 HCCs from 12 woodchucks (two uninfected, ten WHV carriers). Six WHV carrier and two uninfected woodchucks were treated with AFB1. None of the analyzed HCC samples exhibited mutations, either in p53 gene exons 4-9, or in splicing donor-acceptor sites. The present data are consistent with our previous study that indicated a low rate of p53 mutations in HCCs of AFB1-treated ground squirrels, either infected or not infected with ground squirrel hepatitis virus, and in WHV carrier woodchucks not exposed to AFB1. Overall, our findings indicate that in woodchucks and in ground squirrels exposure to aflatoxin may affect the development of p53 mutations less than in humans.
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PMID:Absence of mutations in the p53 tumor suppressor gene in woodchuck hepatocellular carcinomas associated with hepadnavirus infection and intake of aflatoxin B1. 900 7


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