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)

HepCV is the major cause of NANB PT hepatitis and is also implicated as the cause in a large proportion of sporadic cases of NANBH. Chronic infection with HepCV has also been linked to the development of hepatocellular carcinoma. Chimpanzees and marmosets are the only animals found to be experimentally infectable and the virus has not been propagated in any cell culture system. HepCV is an enveloped virus with a diameter of 30-60 nm and a 10-kb positive-stranded RNA genome. Its genome organization resembles that of the flaviviruses and pestiviruses. A 5'-untranslated segment of 341 nucleotides precedes a continuous ORF of 9030/9033 nucleotides which is followed by a 54 nucleotides long 3'-non-coding segment. Further work is required to resolve the question of whether the genomic RNA possesses a 3'-poly(U) or poly(A) tail. The genome also carries an internal poly(A) segment towards the 5'-end of its ORF. Genomic RNA is probably translated into a single polyprotein of 3010/3011 amino acids which is processed into functional proteins. The viral proteins have not been identified, but on the basis of the predicted amino acid sequences, hydrophobicity plots, location of potential glycosylation sites and similarities of these properties to those of pesti- and flaviviruses, the following genome organization has been predicted. The predicted viral structural proteins, a nucleocapsid protein and two envelope glycoproteins are located at the amino-terminal end of the polyprotein. They are followed by a highly hydrophobic protein and proteins that exhibit proteinase, helicase and replicase domains and thus are probably involved in RNA replication and protein processing. The replicase domain is located close to the carboxy terminus of the polyprotein. Although the overall nucleotide and amino acid homologies between HepCV and pestiviruses are low, a number of similarities exist that point to a closer ancestral relationship to the latter than the flaviviruses. First, the 5'-untranslated segment of the HepCV genome resembles that of the pestivirus genomes in size and presence of several short ORFs and it contains several segments with high nucleotide homology. Second, the two putative envelope glycoproteins of HepCV resemble two of the three putative envelope glycoproteins of the pestiviruses. Because its genome organization and predicted virion structure closely resemble those of the flaviviruses and pestiviruses, HepCV has been proposed to be placed in the family Flaviviridae.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hepatitis C virus. 165 96

Chronic infection with hepatitis B virus (HBV), the delta agent (HDV) or hepatitis C virus (HCV) carries high risks of chronic liver disease which can result in cirrhosis and hepatocellular carcinoma. Many antiviral agents have been tried to inhibit viral replication and thereby limit infectivity and the risks of eventual serious liver disease. Interferon offers a 30-40% chance of viral clearance to the hepatitis B carrier, offers a good chance of clinical response in parenterally acquired chronic non-A non-B hepatitis and may be of benefit for some patients with chronic delta infection.
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PMID:Therapy of chronic viral hepatitis. 171 77

Chronic infection with hepatitis B viruses (hepadnaviruses) is a major cause of hepatocellular carcinoma (HCC), but the incubation time varies from 1 to 2 years to several decades in different host species infected with indigenous viruses. To discern the influence of viral and host factors on the kinetics of induction of HCC, we exploited the recent observation that ground squirrel hepatitis virus (GSHV) is infectious in woodchucks (C. Seeger, P. L. Marion, D. Ganem, and H. E. Varmus, J. Virol. 61:3241-3247, 1987) to compare the pathogenic potential of GSHV and woodchuck hepatitis virus (WHV) in chronically infected woodchucks. Chronic GSHV infection in woodchucks produces mild to moderate portal hepatitis, similar to that observed in woodchucks chronically infected with WHV. However, HCC developed in GSHV carriers about 18 months later than in WHV carriers. Thus, although both viruses are oncogenic in woodchucks, GSHV and WHV differ in oncogenic determinants that can affect the kinetics of appearance of HCC in chronically infected animals.
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PMID:Woodchuck hepatitis virus is a more efficient oncogenic agent than ground squirrel hepatitis virus in a common host. 200 38

Two major aetiological factors have been definitively incriminated in the pathogenesis of HCC: these are chronic hepatitis and hepatic cirrhosis. Chronic infection with hepatotropic viruses may account for the majority of cases of hepatocellular carcinoma in high incidence areas, and a varying prevalence of human hepatitis B and hepatitis C virus infection appears to determine the differing geographical prevalence of hepatocellular carcinoma in high and low incidence areas of the world. Patients with advanced hepatocellular carcinoma have a grave prognosis. However, at-risk groups have been characterized, and recent advances in hepatic imaging and tumour marker testing have made screening for asymptomatic primary liver cancer feasible. It it not clear, however, whether screening for small hepatocellular carcinoma improves the prognosis. Lipiodol has been shown to serve as a useful vehicle for diagnosis of small, centimetre sized nodules of tumour, and for delivery of cancer chemotherapeutic or radioactive agents to HCC. The combination of early diagnosis, and coupled medical and surgical treatments including targeted lipiodol or monoclonal antibody conjugates and hepatic resection or transplantation may lead to an improved outlook for viral-associated hepatocellular carcinoma.
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PMID:Hepatocellular carcinoma associated with chronic viral hepatitis. Aetiology, diagnosis and treatment. 216 44

Chronic infection with the hepatitis B virus can result in the development of serious liver disease such as chronic active hepatitis, cirrhosis, and hepatocellular carcinoma. Vertical transmission from infected mothers to infants is thought to be partially responsible for the high prevalence of infection in certain high-risk groups. Immunoprophylaxis using hepatitis B vaccine and hepatitis immune globulin has been highly effective in decreasing the probability of chronic hepatitis B virus infection in infants with exposure. Previously, the Centers for Disease Control recommended screening pregnant women considered at high risk of hepatitis B infection to detect newborns who would benefit from postnatal immunizations directed at preventing the HBV carrier state. Because of the poor sensitivity of high-risk criteria in distinguishing pregnant women who harbor the hepatitis B virus, these recommendations have recently been revised to call for the routine screening of all pregnant women in the United States.
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PMID:Hepatitis B in pregnancy. 266 19

Chronic infection with hepatitis B virus (HBV) accounts for 1-10% of hepatocellular carcinoma (HCC) in low-risk countries and for 56-94% in high-risk populations. However, although HBV is perhaps the second most important human carcinogen so far identified, chronic HBV infection is neither a sufficient nor a necessary cause of HCC. Other factors must be causally related to HCC, and some of them have been identified: aflatoxins, tobacco smoking, and use of alcohol and oral contraceptives. The evidence for an association between these factors and HCC is reviewed, as well as their joint effects. Finally, prospects for epidemiological research on HCC, and specifically the assessment of viral and chemical interactions, are discussed.
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PMID:Prospects for epidemiological studies on hepatocellular cancer as a model for assessing viral and chemical interactions. 284 66

Chronic infection with hepatitis B virus (HBV) is closely associated with the etio-pathogenesis of primary hepatocellular carcinoma (PHC). It has been proposed that infection with HBV early in life, frequently transmitted by an HBV-carrier mother, leads to persistent infection with HBV, which in turn is associated with the development of chronic active hepatitis (CAH), post-necrotic cirrhosis and PHC. If this view is correct, then there should be clustering of chronic carriers of HBV in families of patients with chronic liver disease. We tested this hypothesis in Korea by collecting serum from 132 patients with these chronic liver diseases admitted to the Seoul National University Hospital and 664 of their first-degree relatives. Controls (636) were members of two churches in Seoul and a rural village population; 261 of the controls were between the ages of 30 and 59, the age range that included 95% of the cases of chronic liver disease. Sera were assayed for hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs) and antibody to hepatitis B core antigen (anti-HBc). Almost all cases showed evidence of present or past infection with HBV; 80% were HBsAg(+) and 14% were anti-HBs(+); 100% of 47 cases of PHC, 100% of 35 cases of cirrhosis, and 94% of 50 cases of CAH were anti-HBc(+); 6% of males and 4% of females in control population (30-59 years of age) were HBsAg(+), 71% were anti-HBc(+), and 51% were anti-HBs(+). HBsAg(+) patients with chronic liver disease tended to be younger than HBsAg(-) patients with anti-HBs or anti-HBc antibodies. Mothers of patients with more frequently (HBsAg(+) (9 of 33) than age-matched women in the control population (0 of 34) or wives of patients (5 of 68). Five of 23 fathers were also HBsAg(+) compared with 1 of 25 age-matched controls. As first observed in Africa, there was a deficit of anti-HBs in the fathers of cases compared with the controls. Siblings of patients were frequently HBsAg(+) (45% of 154), with the highest prevalence in brothers (53%). Family history shows that five fathers, two mothers and five brothers of cases have died of PHC. These data are compatible with the hypothesis tested and lend further support to the view that prevention of infection with HBV will lead to a marked decrease in the incidence of CAH, cirrhosis and PHC in areas where these diseases are endemic. Members of the families of patients with these diseases are at high risk of developing persistent infection with HBV and chronic liver disease. It would be appropriate to focus preventive strategies on infants and children in such families.
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PMID:Hepatitis B virus and primary hepatocellular carcinoma: family studies in Korea. 628 79

Hepatitis C can cause a range of hepatic histopathology. The virus may cause an acute hepatitis indistinguishable from any other acute viral hepatitis, but it is more likely to be associated with steatosis, bile duct injury, and portal lymphoid aggregates. Chronic infection with hepatitis C can range from mild nonspecific changes, presumably representing a hepatitis C carrier state, to end-stage liver disease with cirrhosis and hepatocellular carcinoma. Between these are chronic hepatitis of varying severity. Steatosis, portal lymphoid aggregates, and bile duct injury, while not specific, are very characteristic of chronic hepatitis C. Reputed precursors of hepatocellular carcinoma, including liver cell dysplasia and adenomatous hyperplasia, frequently follow the development of cirrhosis and are presumed to predispose to the development of malignancy. New techniques for localizing the virus in liver tissue will undoubtedly lead to greater understanding of the pathogenesis of hepatitis C-related diseases.
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PMID:Histopathology of hepatitis C virus infection. 759 46

Chronic infection with the hepatitis B virus is a major health problem worldwide. The only established therapy is interferon-alpha, with an efficacy of only 30-40% in highly selected patients. Nucleoside analogues do not show a significant clinical benefit. Molecular therapeutic strategies aimed at blocking gene expression include antisense DNA/RNA and ribozymes acting at the posttranscriptional level and triple helix formation blocking at the transcriptional level. In vitro, antisense oligodeoxynucleotides inhibit viral replication and gene expression in human hepatoma cell lines. In vivo, an antisense oligodeoxynucleotide directed against the 5'-region of the pre-S gene of the duck hepatitis B virus inhibited viral replication and gene expression in ducks. In vitro, ribozymes accurately cleave HBV substrate RNA. Triple helix formation is another very promising molecular approach. Results in hepadnaviral infection are not yet available, however.
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PMID:Molecular therapeutic strategies in hepatitis B virus infection. 786 75

Chronic infection with hepatitis B virus (HBV) is accompanied by an increasing risk of developing hepatocellular carcinoma. There are indications that the HBx protein of HBV is involved in the process of tumour formation. HBx also transactivates several transcription factor binding sites. Recently, we reported that HBx can use a tumour promotor pathway for transactivation. In particular, we found that transactivation of the binding motif for transcription factor AP-1 (JUN/FOS) by HBx is dependent on functional protein kinase C (PKC), as indicated by abolition of the transcriptional stimulation following downregulation or inhibition of the enzyme. Moreover, HBx activates PKC, probably via increasing the endogenous PKC activator sn-1,2-diacylglycerol (DAG). Here we extend these data and report on the time course of PKC activation. We found that activation of PKC by HBx is transient and differs from activation of PKC by the ras oncogene product or phorbol ester in that it does not lead to rapid downregulation of the enzyme subsequent to the activation. Moreover, we provide evidence that an increase in cellular DAG is observable not only as an early event in response to HBx but also in cell lines transformed after transfection with HBV DNA and stably expressing HBx. Besides its important role in the regulation of cellular genes, PKC is also the intracellular receptor for tumour-promoting agents and an activator of proto-oncogenes, suggesting that our observations might provide an explanation for the oncogenic properties of HBx.
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PMID:The hepatitis B virus transactivator HBx causes elevation of diacylglycerol and activation of protein kinase C. 821 Jul 15


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