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Query: UMLS:C0345904 (liver cancer)
15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with the hepatitis C virus (HCV) has become a leading cause of scarring of the liver (i.e., fibrosis) and cirrhosis in the United States. HCV-related cirrhosis (with its associated complications, such as liver cancer) is a major cause of death, although it develops slowly and occurs only in approximately one-third of HCV-infected patients. Alcohol can exacerbate HCV infection and the associated liver damage by causing oxidative stress and promoting fibrosis, thereby accelerating disease progression to cirrhosis. Furthermore, alcohol may exacerbate the side-effects associated with current antiviral treatment of HCV infection and impair the body's immune defense against the virus. Of the HCV-infected people who do not consume alcohol, only a minority progresses to severe liver disease and requires antiviral treatment. Because alcohol potentiates the fibrosis- and cancer-inducing actions of HCV, alcoholics are particularly vulnerable to HCV infection and most in need of treatment.
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PMID:Alcohol and hepatitis C. 1191 Jul 1

BACKGROUND: Hepatitis B virus is the cause of acute disease and several chronic conditions, such as chronic hepatitis, cirrhosis and liver cancer.In 1982, hepatitis B vaccine was developed. Since 1984, many immunization programs against hepatitis B were implemented in several countries and 15 years later we can visualize some epidemiological changes in those countries.OBJECTIVE: To review the papers published about the results of hepatitis B immunization programs in several countries from Asia, Africa, Europe (Italy) and Peru, since 1984.METHODS: Pertinent literature was identified in MEDLINE (1980-2000) and references quoted in published papers. RESULTS: The impact of vaccination against hepatitis B over the incidence of acute disease, chronic carriers, hepatitis B virus prevalence and hepatocarcinoma incidence, was anayzed.The following results were obtained: In Afragola (Italy), a reduction of acute disease incidence from 63 cases/100,000 population before the vaccination (1983), to 3 cases/100,000 population after the vaccination (1997), was obtained HBsAg carriers rate decreased: From 13.4% to 3.7% in the general population and from 6.8% to 0.7% in infant population.Infection prevalence: From 66.9% to 34.2% in general population. In Taiwan:HBsAg carriers rate decreased: From 10.0% to <1.0% in children from 1 to 10 years old.Infection prevalence: From 38.0% to 16.0% in children under 13 years old. In Peru:Infection prevalence: From 24.4-30.4% to 2.3-5.1% in children of 3 and 4 years old. In Senegal:HBsAg carriers rate decreased: From 18.7% to 2.2% in children. In Gambia:HBsAg carriers rate decreased: From 10.0% to 0.6% in children.Finally, the hepatocarcinoma incidence in children from 6 to 14 years old, decreased from 0.70/100,000 children to 0.36/100,000 (p<0.01) in Taiwan.CONCLUSION: The results of these studies support the hypothesis that the vaccination against the hepatitis B virus infection reduce the incidence of acute disease, carriers rate, prevalence of the infection and hepatocarcinoma incidence.
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PMID:[HEPATITIS B.VACCINATION IMPACT ON ACUTE DISEASE,CHRONIC CARRIERS AND HEPATOCARCINOMA INCIDENCE] 1214 May 76

Liver cancer is one of the most common cancers worldwide. Infection with hepatitis B virus and exposure to aflatoxins in the diet act synergistically to amplify risk. From a public health perspective, hepatitis virus vaccination programs and efforts to both reduce aflatoxin exposures and to attenuate the toxicological consequences of unavoidable exposures should have major impacts on the incidence of this disease. Experimentally, aflatoxin-induced hepatocarcinogenesis can be inhibited by over a score of different chemopreventive agents with multiple mechanisms of action. One agent, oltipraz, is a potent inducer of phase 2 enzymes involved in the detoxication of carcinogens including aflatoxin. A second agent, chlorophyllin, impedes the bioavailability of carcinogens by forming molecular complexes and enhances their elimination in the fecal stream. This review highlights the findings of recent randomized clinical trials with oltipraz and chlorophyllin conducted in individuals exposed to dietary aflatoxins and at high risk for development of liver cancer. Both chemopreventive agents modulated levels of aflatoxin biomarkers in the study participants in manners consonant with protection.
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PMID:Strategies for chemoprevention of liver cancer. 1257 Mar 36

Unlike many other types of human cancer, the aetiology of liver cancer is well understood. Infection with hepatitis viruses, coupled with dietary exposure to the fungal toxin aflatoxin, increases the risk of the disease. Although primary prevention, based on vaccination and avoiding exposure to these agents, is an appealing option, such strategies will require considerable investment of time and resources to be successful. In the developing world--where the burden of liver cancer is highest--immediate, practical and economical approaches are essential. So, targeted chemoprevention might be most appropriate for the present generation of individuals at risk.
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PMID:Translational strategies for cancer prevention in liver. 1272 30

Hepatocellular carcinoma is one of the most common cancers worldwide. Infection with hepatitis B virus and exposure to aflatoxins in the diet act synergistically to amplify risk. From a public health perspective, hepatitis virus vaccination programs and efforts to both reduce aflatoxin exposures and to attenuate the toxicological consequences of unavoidable exposures should have major impacts on the global incidence of this disease. Experimentally, aflatoxin-induced hepatocarcinogenesis can be inhibited by over a score of different chemopreventive agents with multiple mechanisms of action. One agent, oltipraz, is a potent inducer of phase 2 enzymes involved in the detoxication of carcinogens including aflatoxin. A second agent, chlorophyllin, impedes the bioavailability of carcinogens by forming molecular complexes and enhances their elimination in the fecal stream. This review highlights the findings of recent randomized clinical trials with oltipraz and chlorophyllin conducted in individuals exposed to dietary aflatoxins and at high risk for development of liver cancer. Both chemopreventive agents modulated levels of aflatoxin biomarkers in the study participants in manners consonant with protection. Although pharmacological approaches establish proof of principle and help identify key molecular targets for interventions, food-based approaches that also use these molecular targets may be the most practical for widespread application in high-risk populations.
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PMID:Chemoprevention of hepatocellular carcinoma in aflatoxin endemic areas. 1550 99

Hepatocellular carcinoma (HCC) is a highly malignant, generally fatal neoplasm arising from hepatocytes. HCC accounts for over 80% of all primary liver cancers which ranks fourth among the organ-specific causes of cancer-related deaths worldwide. HCC is particularly prevalent in Korea where the age standardized incidence rate is 46.5 per 100,000 population. Infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) or presence of liver cirrhosis are important risk factors for HCC development globally. Infection with HBV is the most important risk for HCC in Asia except Japan. The high incidence rate of HCC in Korea is thought to be related to the high carrier rate (5-6%) of HBV, which is currently being fought via a nationwide vaccination program. Although progress has been made in the management of HCC including chemoembolization and local ablation therapy, there has been little overall reduction in HCC mortality during the past 20 years. Recently, five year survival rate of primary liver cancer is 9.6% in Korea. Such poor prognosis of HCC results from the late detection of cancer, an aggressive tumor biology and underlying chronic liver diseases. Only a limited proportion of patients are candidates for potentially curative forms of treatment. Therefore efforts should be directed toward an effective surveillance program. The early detection of HCC is the important approach in reducing HCC mortality in the short term. Because almost eighty percent of HCC is diagnosed in late stage, we launched a nationwide surveillance program to screen high risk groups (HBV or HCV carriers or liver cirrhosis, over 40 years old) and formulated the Korean practice guideline for the diagnosis and treatment of HCC with special emphasis on advanced stage of HCC.
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PMID:[Hepatocellular carcinoma in Korea: introduction and overview]. 1584 47

Infection with the hepatitis B virus has been identified as one of the major causes of liver cancer. A large body of experimental work points to a central role for the virally encoded protein HBx in this form of carcinogenesis. HBx is expressed in HBV-infected liver cells and interacts with a wide range of cellular proteins, thereby interfering in cellular processes including cell signaling, cycle regulation and apoptosis. In order to identify possible new targets of the HBx protein, we performed a yeast two-hybrid screen using a truncated protein mini-HBx(18-142) as the bait. In addition to known interacting partners, such as RXR and UVDDB1, we identified several new candidates including the human transcriptional regulatory protein p120E4F, which has been implicated in the regulation of mitosis and the cell cycle. In vitro pull down experiments confirmed the interaction and transcription activation assays in the yeast demonstrated that HBx protein was able to repress GAL4AD-p120E4F-dependent activation of a reporter gene under the control of E4F binding sites found in the adenovirus E4 promoter and the HBV enhancer II region. We also showed that the cysteine residues in HBx are necessary for its interaction with UVDDB1 but not for the interaction with RXR or p120E4F. The possible functional relevance of the interaction between HBx and E4F proteins is discussed in the contexts of cellular transformation and host-virus co-evolution.
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PMID:Interaction of the hepatitis B virus protein HBx with the human transcription regulatory protein p120E4F in vitro. 1611 66

Infections with hepatitis C virus (HCV) are marked by frequent viral persistence, chronic liver disease, and extraordinary viral genetic diversity. Although much has been learned about HCV since its discovery, progress has been slowed by a lack of permissive cell culture systems supporting its replication. Productive infections have been achieved recently with genotype 2a virus, but cirrhosis and liver cancer are typically associated with genotype 1 HCV, which is more prevalent and relatively resistant to IFN therapy. We describe production of infectious genotype 1a HCV in cells transfected with synthetic RNA derived from a prototype virus (H77-S). Viral proteins accumulated more slowly in H77-S transfected cells than in cells transfected with genotype 2a (JFH-1) RNA, but substantially more H77-S RNA was secreted into supernatant fluids. Most secreted RNA was noninfectious, banding in isopycnic gradients at a density of 1.04-1.07 gm/cm(3), but infectivity was associated with H77-S particles possessing a density of 1.13-1.14 gm/cm(3). The specific infectivity of H77-S particles (5.4 x 10(4) RNA copies per focus-forming unit) was significantly lower than JFH-1 virus (1.4 x 10(2) RNA copies per focus-forming unit). Infection with either virus was blocked by CD81 antibody. Sera from genotype 1a-infected individuals neutralized H77-S virus, but had little activity against genotype 2a virus, suggesting that these genotypes represent different serotypes. The ability of this genotype 1a virus to infect cultured cells will substantially benefit antiviral and vaccine discovery programs.
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PMID:Production of infectious genotype 1a hepatitis C virus (Hutchinson strain) in cultured human hepatoma cells. 1646 99

Infection with hepatitis B causes between 500,000 and 1.2 million deaths per year worldwide, and is the leading cause of liver cancer. Over 12 years ago, WHO recommended that universal childhood hepatitis B vaccination be implemented globally. Despite this, Denmark, Finland, Iceland, Ireland, the Netherlands, Norway, Sweden, and the UK have yet to implement such a policy and instead currently adopt an "at-risk" strategy. Although all eight countries are classed as having low endemicity, factors such as increased travel and integration of immigrant communities are increasing the number of at-risk individuals in these countries. Considering the difficulty in identifying all at-risk individuals, and the lack of effectiveness of at-risk vaccination on reducing the overall incidence of hepatitis B, we recommend that these countries reassess their hepatitis B prevention strategies. Universal vaccination against hepatitis B is the only way to eliminate the major public-health impact of this disease.
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PMID:Should hepatitis B vaccination be introduced into childhood immunisation programmes in northern Europe? 1822 58

Hepatitis C virus (HCV) is a common RNA virus that causes hepatitis and liver cancer. Infection is treated with IFN-alpha and ribavirin, but this expensive and physically demanding therapy fails in half of patients. The genomic sequences of independent HCV isolates differ by approximately 10%, but the effects of this variation on the response to therapy are unknown. To address this question, we analyzed amino acid covariance within the full viral coding region of pretherapy HCV sequences from 94 participants in the Viral Resistance to Antiviral Therapy of Chronic Hepatitis C (Virahep-C) clinical study. Covarying positions were common and linked together into networks that differed by response to therapy. There were 3-fold more hydrophobic amino acid pairs in HCV from nonresponding patients, and these hydrophobic interactions were predicted to contribute to failure of therapy by stabilizing viral protein complexes. Using our analysis to detect patterns within the networks, we could predict the outcome of therapy with greater than 95% coverage and 100% accuracy, raising the possibility of a prognostic test to reduce therapeutic failures. Furthermore, the hub positions in the networks are attractive antiviral targets because of their genetic linkage with many other positions that we predict would suppress evolution of resistant variants. Finally, covariance network analysis could be applicable to any virus with sufficient genetic variation, including most human RNA viruses.
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PMID:Genome-wide hepatitis C virus amino acid covariance networks can predict response to antiviral therapy in humans. 1940 6


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