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)

Hepatic cirrhosis is the most common cause of ascites. It is caused by liver failure leading to complex interrelated circulatory and renal changes resulting in retention of sodium and water and portal hypertension localising that sodium and water in the peritoneum. Ascites is an important development in cirrhosis as it implies a generally poor long term prognosis. Investigation is important as ascites is not always dueto cirrhosis, may bethe consequence of complications of cirrhosis such as hepatocellular carcinoma, and may be associated with infection which is fatal if untreated. Most patients respond to treatment with sodium restriction and diuretic drugs. This treatment takes time, and increasingly doctors use therapeutic paracentesis with sodium restriction and diuretics to prevent recurrence of ascites. Paracentesis, however, is not without complications, and it is particularly important to give colloid replacement to prevent hypovolaemia which can lead to renal failure. Patients who do not respond to this treatment may be helped by a TIPSS procedure or a peritoneovenous shunt. However, these patients usually have very poor liverfunction and the possibility of fiver transplantation should be considered. Infection is a very serious complication of ascites (spontaneous bacterial peritonitis) and carries a generally poor prognosis.Antibiotic prophylaxis is important to prevent recurrence and liver transpiantation shoulcl be considered.
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PMID:[ASCITES IN HEPATIC CIRRHOSIS: RECOGNITION INVESTIGATIONAND TREATMENT] 1221 41

Infection with hepatitis B and/or hepatitis C virus is strongly associated with hepatocellular carcinoma (HCC). HCC likely develops through a sequence of chronic inflammation to fibrosis to cirrhosis and, eventually, dysplasia. Medical therapies aimed at the prevention of HCC are predicated on the interruption of this sequence by means of antiviral therapy. In this review, the authors summarize the available experience with prophylactic medical therapies and a number of questions that remain unanswered. Overall, although it appears that interferon-alpha therapy is beneficial in the prevention of HCC in patients with viral hepatitis, more experience is required before definitive recommendations can be made.
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PMID:Role of antiviral therapy in the prevention of hepatocellular carcinoma. 1235 36

GP73 is a novel type II Golgi transmembrane protein that is expressed at high levels in the hepatocytes of patients with viral hepatitis (R. D. Kladney, G. A. Bulla, L. Guo, A. L. Mason, A. E. Tollefson, D. J. Simon, Z. Koutoubi, and C. J. Fimmel, 2000, Gene 249, 53-65) and is induced in cultured cells by infection with viruses including adenoviruses. Its biological function and the mechanisms by which its expression may be regulated by viral infection are unknown. Here we report that GP73 is induced at the RNA and protein level in human Hep3B hepatoma cells infected by human Ad5 and Ad2. Hep3B cells were infected with wild-type or mutant adenoviruses. GP73 expression was measured by RNase protection assay, immunoblotting, or immunofluorescence microscopy. GP73 RNA and protein levels were strikingly induced following infection. The rise in GP73 expression coincided with the appearance of the adenovirus E1A and DBP proteins and preceded the expression of the fiber protein, a marker of the late phase of infection. Infection did not affect the expression of giantin, GPP130, or golgin-84, three integral Golgi membrane proteins with structural similarities to GP73. Mapping studies using a panel of mutant adenoviruses demonstrated that the E1A C-terminus, specifically its CtBP interaction domain (CID), is required for GP73 expression. Subsequently, Hep3B cells were transiently transfected with plasmids expressing wild-type or mutant E1A proteins. These studies confirmed that E1A induced GP73 expression via the CID. Our studies establish GP73 as a novel adenovirus-induced cellular protein whose expression is regulated through the CID of the E1A protein.
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PMID:Upregulation of the Golgi protein GP73 by adenovirus infection requires the E1A CtBP interaction domain. 1235 26

Infection with hepatitis B virus may develop into a chronic carrier state, which may result in chronic hepatitis, cirrhosis and hepatocellular carcinoma, but the exact mechanism of the development of hepatocellular carcinoma is still not known. The question is whether it is hepatitis B virus itself or the cellular changes due to persistent hepatitis B virus infection that cause malignant changes? The purpose of this article was to describe the natural history of hepatitis B virus infection together with epidemiological, serological, and molecular data that show a connection between chronic hepatitis B virus infection and the development of hepatocellular carcinoma.
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PMID:[Hepatitis B--a viral oncogene?]. 1255 16

Congenital myasthenic syndromes are caused by different genetic defects affecting proteins expressed at the neuromuscular junction. Recently, the first molecular genetic defect resulting in a presynaptic congenital myasthenic syndrome has been reported: Recessive loss-of-function mutations in CHAT, the gene encoding choline acetyltransferase, were described in five congenital myasthenic syndrome families. In this study, we investigated three patients from two independent Turkish kinships. Clinically, all patients presented with moderate myasthenic symptoms including ptosis and muscle weakness with increased fatigability. Multiple episodes of sudden apnea were reported for all patients. One child suffering from a second, unrelated disorder, i.e. hepatocellular carcinoma, showed a severe myasthenic phenotype, requiring permanent ventilation. Genetically, we identified a novel missense mutation (I336T) in the CHAT gene homozygously in all three patients. Haplotype analysis revealed that the mutant allele cosegregates with the clinical phenotype in both families (maximum combined two-point LOD-score of 2.46 for D10S1793). In summary, we confirm that CHAT mutations are responsible for a clinically distinct form of congenital myasthenic syndrome, characterized by episodic apnea. Infections and stress may lead to a life-threatening failure of neuromuscular transmission in congenital myasthenic syndrome with episodic apnea. The observation of the same mutation (I336T) in two independent Turkish kinships may suggest a common origin, i.e. founder.
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PMID:Congenital myasthenic syndrome due to a novel missense mutation in the gene encoding choline acetyltransferase. 1260 6

Infection with hepatitis C virus (HCV) is characterized by inflammatory liver damage and a long viral persistence associated with an increased risk of developing hepatocellular carcinoma. Both in liver damage and in oncogenesis a disturbance of apoptosis has been implicated, although the underlying mechanisms in these apparently opposite processes are incompletely understood. HCV-triggered liver injury is mediated mainly by host immune mechanisms and eventually by direct cytopathic effects of HCV. Recent data shows that caspase activation, either triggered by death ligands, other cytokines, granzyme B or HCV proteins, is considerably upregulated in HCV-infected liver. Interestingly, caspase activation appears to correlate closely with the inflammatory response. Data about the role of single HCV proteins, either in cultured cells or transgenic animals models, however, are contradictory, as both pro- and anti-apoptotic effects have been observed. Nevertheless, apoptosis induction upon HCV infection may critically contribute to liver damage, while inhibition of apoptosis may result in HCV persistence and development of hepatocellular carcinoma.
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PMID:Apoptosis in hepatitis C virus infection. 1265 46

Infection of newborn woodchucks with woodchuck hepatitis virus (WHV) results in hepatocellular carcinoma (HCC). Since oxidative damage may be carcinogenic, we investigated the relationship between WHV infection and oxidative damage to hepatic lipids and DNA. Eastern woodchucks were infected with WHV. Hepatic lipid peroxidation was assessed in vitro in isolated hepatocytes by thiobarbituric acid reactive substances (TBARS). Oxidative DNA damage was assessed in vivo in snap-frozen livers by 8-hydroxy-2'-deoxyguanosine (8-OH-dG). The proliferation index (PI) and apoptotic index (AI) were also determined. WHV infection was associated with increased hepatic lipid peroxidation (0.51+/-0.04 nmols TBARS per mg protein for WHV+ hepatocytes vs. 0.38+/-0.04 for WHV negative controls, P<0.01). In contrast, the WHV+ livers exhibited less oxidative DNA damage than uninfected controls (11+/-5 vs. 38+/-8 8-OH-dG/10(6) dG, P<0.02). In WHV-infected animals PI and AI were increased, by >20-fold. We conclude that WHV infection is associated with increased in vitro lipid peroxidation and decreased in vivo oxidative DNA damage. The increased PI and AI in the WHV+livers suggest that rapid cell turnover dilutes 8-OH-dG concentration.
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PMID:Decreased oxidative DNA damage and accelerated cell turnover in woodchuck hepatitis virus infected liver. 1269 46

Infection with hepatitis C virus (HCV) is a major cause of transfusion-associated hepatitis, cirrhosis and hepatocellular carcinoma. The present study was conducted with an objective to evaluate the prevalence of anti-HCV antibody in New Delhi, India using a large number of healthy voluntary blood donors. A total of 15,898 healthy voluntary blood donors were subjected to anti-HCV testing (using a commercially available third generation anti-HCV ELISA kit) and 249 were found to be reactive for anti-HCV antibody, yielding an overall prevalence of 1.57%. No significant difference was found between the HCV positivity rate of male (1.57%; 238/15,152) vs. female (1.47%; 11/746) donors, family (1.58%; 213/13,521) vs. altruistic (1.51%; 36/2377) donors and first-time (1.55%; 180/11,605) vs. repeat (1.61%; 69/4293) donors. The age distribution of anti-HCV reactivity showed a maximum prevalence rate of 1.8% in the age group of 20-29 years. In addition, there was a clear trend of decreasing positivity for anti-HCV with increasing age and this trend was statistically significant. The results of the present study show that the prevalence of anti-HCV antibodies in the healthy voluntary blood donors of New Delhi, India is considerably higher than the reported seroprevalence of HCV in majority of the industrialized nations and this represents a large reservoir of infection capable of inflicting significant disease burden on the society. In addition, donors of New Delhi, India showed a trend of decreasing seroprevalence with increasing age, possibly implying a higher exposure rate to HCV in younger subjects.
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PMID:The prevalence of hepatitis C virus antibodies among the voluntary blood donors of New Delhi, India. 1295 45

Infection, including viral infection, still cause serious complication in the course of chemotherapy. Recognition of viral infections, monitoring, prophylaxis and treatment is aimed at reducing the number of infected patients, mitigating the cause of the disease and limiting deaths directly linked with infections in paediatric cancer patients. Viruses from the herpes group (HSV, VZV, EBV, CMV) are particularly dangerous. They can cause not only asymptomatic and local infectious but also general diseases and can reactivate, especially after BMT. Hepatoropic viruses (HBV, HCV) often lead to breaks in chemotherapy, while chronic viral hepatitis can lead to fibrosis, cirrhosis and even primary hepatocellular carcinoma. CMV, RSV, adenovirus influenza and parainfluenza virus cause diffuse interstitial pneumonitis and are also associated with a high rate of mortality. In this paper, we present the most frequency viral infection in children with malignant diseases, their methods of diagnosis and treatment.
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PMID:[Viral infection in children with malignant diseases]. 1457 9

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. Infection with the hepatitis B virus (HBV) is one of the high-risk factors for the development of HCC, particularly in Asia and Africa. Other risk factors include hepatitis C virus (HCV) infection and, to a certain extent, exposure to a liver-specific carcinogen such as aflatoxin B, and alcohol consumption. In the present retrospective study, we analysed the clinical profile and aetiological role of HBV and HCV in HCC. A total of 40 cases of HCC (33 males and 7 females, age range 22-80 years) were seen from January 1999 to June 2001 at our institute. A detailed history of age, sex, past history of liver disease, clinical symptoms and presenting complaints was recorded. The most common presenting complaints were abdominal distention, pedal oedema and pain abdomen. Underlying cirrhosis of the liver was seen in 30 cases (75%), Child's A in 6, Child's B in 11 and Child's C in 13 cases. A history of alcoholism was present in 6 patients. All the patients were tested for HBsAg and anti-HCV by ELISA. HBsAg and anti-HCV was positive in 19 (47.5%) and 8 patients (20%), respectively. The diagnosis in the majority of cases was derived by FNAC and in a few by imaging techniques plus alfa-fetoprotein (AFP) evaluation. The diagnosis was confirmed by FNAC in 34, CT scan and AFP in 2, and ultrasound abdomen and AFP in 4 cases. We conclude that viral infection (HBV > HCV) is still a major aetiological factor and the incidence of HCV infection appears to be increasing. The majority of the cases of HCC studied had a cirrhotic background.
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PMID:Clinical and aetiological profile of hepatoma at a tertiary care centre. 1460 25


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