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)

To this day, viral hepatitis remains a major public health problem in Thailand. Chronic infection with hepatitis B and C viruses are the leading causes of chronic liver diseases, including cirrhosis and hepatocellular carcinoma (HCC). Outbreaks of hepatitis A virus continue to occur in Thailand, even after several years of consistently declining prevalence rates. Also, the reduction in prevalence of hepatitis D virus infection has been observed among intravenous drug users over the past decade. Hepatitis E virus constitutes a rather unusual cause of sporadic acute hepatitis in Thailand. Highly effective vaccines are currently available for prevention of hepatitis A and B, however, as yet no effective vaccine for hepatitis C is imminent. Following rapid progress in the development of molecular techniques, several new hepatitis viruses have been identified. Among these, Hepatitis G, TT and SEN viruses have recently been described but their significance as to causation of human liver disease has yet to be established. This article reviews the current epidemiology, molecular biology, and strategies aimed at prevention and control of hepatitis virus infection in Thailand emphasizing new developments and recent data obtained from our research studies.
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PMID:Problems and prevention of viral hepatitis in Thailand. 1152 32

Chronic infection with the hepatitis B virus (HBV) affects 350 million people worldwide, or approximately 5% of the global population, and commonly results in cirrhosis and hepatocellular carcinoma. Until recently, the only available treatment was injectable interferon alpha and response rates were suboptimal. Moreover, this expensive and toxic therapy had little applicability in the endemic regions of the world, i.e., Asia and Africa. The realisation that orally available nucleoside and nucleotide agents may effectively control this infection opened a new era in the management of chronic hepatitis B. Oral lamivudine recently became approved for treatment of hepatitis B worldwide. It is free of significant toxicity, improves liver histology and rapidly diminishes HBV DNA levels; lamivudine is expected to become the first-line therapy of choice. Nevertheless, the consistent emergence of lamivudine-resistant variants mandates the need to develop additional therapeutic agents. Adefovir dipivoxil, a nucleotide, and entecavir, a nucleoside agent, are promising new drugs that might eventually be used in combination with lamivudine and therefore reduce the incidence of drug resistance. There is a critical need to advance the research of hepatitis B antiviral agents so that effective combination therapies can become widely available.
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PMID:Current pharmacotherapy for hepatitis B infection. 1158 97

Chronic infection with the hepatitis B virus infection remains a major problem worldwide despite some decrease in its incidence after improvement in public health policies and the utilization of hepatitis B vaccine. The clinical spectrum of the disease ranges from the asymptomatic carrier and individuals with mild liver injury to cirrhosis and hepatocellular carcinoma. During the past two decades there has been important progress in the field of viral hepatitis, and several drugs for the treatment of chronic hepatitis B have been developed and analyzed in clinical trials. Currently, two forms of therapy have been approved and are available for clinical practice: alpha interferon and lamivudine. Neither therapy is entirely satisfactory because of side effects and lack of universal responses. There is also controversy over which patients should be treated and what agent and regimen should be used. In this review we discuss the advantages and disadvantages of utilizing either drug, the response rates to therapy and what regimen should be used.
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PMID:What is the optimal therapy for chronic hepatitis B? 1174 Apr 31

Chronic infection with hepatitis B virus (HBV) is associated with an increased risk for the development of cirrhosis and hepatocellular carcinoma (HCC). Although clonal HBV DNA integrations are detected in nearly all HCCs the role of these integrations in hepatocarcinogenesis is poorly understood. We have used a cloning protocol that allows studying the frequency and the natural history of HBV DNA integrations in cell culture. Southern blot analysis of the genomic DNA of HepG2 2.2.15 subclones, which replicate HBV, enabled us to detect new HBV DNA integrations in approximately 10% of the HepG 2.2.15 subclones over 4 rounds of sequential subcloning, whereas no loss of any preexisting HBV DNA integrations was observed. Treatments of HepG2 cells with H(2)O(2), designed to increase DNA damage, increased the frequency of HBV integrations to approximately 50% of the subclones and treatments designed to inhibit DNA repair, by inhibiting Poly(ADP-ribosyl)ation, also increased the frequency of HBV integration to 50%. These findings suggest that DNA strand breaks induced by oxidative stress during persistent HBV infection in humans may increase HBV DNA integration events, whereas PARP-1 activity may function to limit the occurrence of de novo HBV DNA integrations.
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PMID:Increase in de novo HBV DNA integrations in response to oxidative DNA damage or inhibition of poly(ADP-ribosyl)ation. 1178 79

Chronic infection with the hepatitis B virus (HBV) is a known risk factor in the development of human hepatocellular carcinoma (HCC). The HBV-encoded X protein, HBx, has been investigated for properties that may explain its cancer cofactor role in transgenic mouse lines. We discuss here recent data showing that HBx is able to induce hepatocellular proliferation in vitro and in vivo. This property of HBx is predicted to sensitize hepatocytes to other HCC cofactors, including exposure to carcinogens and to other hepatitis viruses. Cellular proliferation is intimately linked to the mechanism(s) by which most tumor-associated viruses transform virus-infected cells. The HBx alteration of the cell cycle provides an additional mechanism by which chronic HBV infection may contribute to HCC.
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PMID:Stimulation of cellular proliferation by hepatitis B virus X protein. 1179 Aug 80

Chronic infection with hepatitis C virus (HCV) is a major risk factor for development of hepatocellular carcinoma (HCC). In general, HCC develops only after 2 or more decades of HCV infection and the increased risk is restricted largely to patients with cirrhosis or advanced fibrosis. Factors that predispose to HCC among HCV-infected persons include male sex, older age, hepatitis B virus (HBV) coinfection, heavy alcohol intake, and possibly diabetes and a transfusion-related source of HCV infection. Viral factors play a minor role. The likelihood of development of HCC among HCV-infected persons is difficult to determine because of the paucity of adequate long-term cohort studies; the best estimate is 1% to 3% after 30 years. Once cirrhosis is established, however, HCC develops at an annual rate of 1% to 4%. Successful antiviral therapy of patients with HCV-related cirrhosis may reduce the future risk for HCC. The incidence of and mortality caused by all HCC has doubled in the United States over the past 25 years, an increase that has affected all ethnic groups, both sexes, and younger age groups. Given the current prevalence of HCV infection among persons 30 to 50 years of age, the incidence and mortality rates of HCC are likely to double in the United States over the next 10 to 20 years. Future research should focus on improving understanding of the incidence and risk factors for HCC, causes of HCV-related carcinogenesis, means of early detection, and better treatment for HCC.
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PMID:Hepatocellular carcinoma and hepatitis C in the United States. 1240 79

The incidence of hepatocarcinoma (HCC) has increased in industralized countries. Its relation with hepatitis C virus (HCV) has already been established. The mechanisms by which HCV promotes HCC development are poorly understood. The continuous necrotic and inflammatory effect with subsequent liberation of various cytoquines and modifications in hepatocyte genome have been proposed. Chronic infection with HCV leads to chronic liver disease and cirrhosis which is described as the main precursory lesion to HCC. The assessment methods for patients with chronic liver diseases allow those patients with high risk for HCC to be identified and the process to identify this tumor at an early stage to be initiated.
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PMID:[Relation between hepatocarcinoma and hepatitis C virus infection]. 1271 51

Many of the emerging technologies for the global evaluation of gene expression, at both the RNA and protein level, are being applied to the problem of finding biomarkers for human disease progression. These analyses can be made difficult, however, by variation between samples that arises from both technical and nondisease related physiological or genetic causes. In an effort to identify serum polypeptides whose presence or absence correlates with the clinical status of patients at high risk for hepatocellular carcinoma (HCC), we have developed a strategy that helps to focus the analysis on meaningful changes in protein levels above the background of variation. For the current study we divided the patient population into four clinically defined diagnostic groups that represent a generally increasing risk for HCC. Chronic infection with hepatitis B virus (HBV) is a major risk factor for HCC and our groups included patients with no indication of liver disease (healthy), those with inactive chronic HBV, those with active chronic HBV, and patients with a diagnosis of HCC and history of chronic HBV infection. Serum polypeptides from these patients were first analyzed in two-dimensional gels by combining the serum from patients in each of the four groups to generate composite gel profiles. Analysis of these composite gels allowed us to identify two relatively abundant features that were reduced in the HCC group as compared to the healthy group. Tryptic fragment mass fingerprinting identified the features as a carboxy terminal fragment of complement C3 and an isoform of apolipoprotein A1. These two features were examined by two-dimensional gel electrophoresis of serum from each individual in the four groups in order to verify that the inter-group differences seen in composite gels reported changes in abundance for most members of the group, rather than extreme changes for a small fraction of the group. These preliminary studies suggest that a proteomic methodology can be used for the identification of serum biomarkers for HCC and other liver disease.
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PMID:A strategy for the comparative analysis of serum proteomes for the discovery of biomarkers for hepatocellular carcinoma. 1274 40

Chronic infection with Hepatitis C virus (HCV) often results in cirrhosis and enhances the probability of developing hepatocellular carcinoma (HCC). The underlying mechanisms that lead to malignant transformation of infected cells, however, remain unclear. Observations made with isolated HCV antigens and/or with HCV subgenomic replicon systems demonstrated that the products encoded in the HCV genome interfere with and disturb intracellular signal transduction, often by phosphorylation of cellular proteins. Moreover, some of the HCV-encoded proteins seem to serve as substrates for host cell protein kinases. These phosphorylations affect the biological functions of the antigens. In many cases it could be demonstrated that only short stretches of the linear sequence of the viral or cellular proteins are involved and play a crucial role for these phosphorylation events. The identification of these small polypeptide elements and the subsequent development of strategies to inhibit protein-protein interactions involving them may be the first step towards reducing the chronicity and/or of the carcinogenicity of the virus. This review summarizes current knowledge of intracellular phosphorylation processes that are affected by HCV.
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PMID:The proteins of the Hepatitis C virus: their features and interactions with intracellular protein phosphorylation. 1282 59

Hepatitis C virus is an RNA virus in the Flavivirus family that was identified in 1989. Since then, blood donor screening has reduced the incidence of acute infections; however, because this virus frequently leads to asymptomatic chronic infection, the prevalence of infection remains high. Chronic infection leads to increased risks of cirrhosis and hepatocellular carcinoma, as well as extrahepatic manifestations. Guidelines for widespread screening continue to evolve, and early diagnosis is likely to become more important with the development of more effective treatments. Current recommendations regarding screening are reviewed.
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PMID:Hepatitis C: a review. 1290 Jun 22


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