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)

Woodchuck hepatitis virus (WHV) is a small, partially double-stranded DNA virus. Like the related human hepatitis B virus (HBV), WHV induces acute and chronic hepatitis and hepatocellular carcinoma (HCC) in its natural host. WHV DNA integration into c-myc and N-myc, resulting in deregulated expression of these genes, has been described previously in woodchuck HCC. We have analysed a woodchuck liver tumour in which WHV DNA was integrated in the c-myc gene. The virus insertion provoked multiple alterations in one c-myc allele, probably involving secondary deletions and mutations. Integrated viral DNA, including promotor and enhancer sequences, acted as an insertional mutagen, leading to enhanced expression of heterogenous c-myc transcripts ranging from 7.2 to 14 kb in size, strikingly longer than normal 2.3-kb c-myc RNA. These results provide an additional example in which the oncogenic activation of a myc gene by cis-acting effect of WHV insertion may play a critical role in virus-induced woodchuck HCC.
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PMID:Multiple rearrangements and activated expression of c-myc induced by woodchuck hepatitis virus integration in a primary liver tumour. 131 4

Our purpose was to ascertain whether alcohol abuse is a risk factor for the development of hepatocellular carcinoma in urban southern Africa blacks and, if so, to relate alcohol consumption to other possible risk factors such as persistent hepatitis-B-virus infection, smoking, male sex, in this subpopulation. A prospective, hospital-based, case-control format involving 101 patients with hepatocellular carcinoma and 101 controls was used. The mean age of the patients was 53.7 +/- 1.85 years and the male:female ratio 3.2:1. An increased risk was found, but only in urban men over the age of 40 years who habitually drank more than 80 g of ethanol daily. The risk remained after adjusting for chronic hepatitis-B infection, smoking, and sex (odds ratio 4.4, 95% confidence interval 1.3 to 16.6; p = 0.003). Smoking proved not to be a risk factor, either alone or in concert with alcohol consumption. Hepatitis-B infection was confirmed as a major risk in younger men and in women, but in urban men over the age of 40 years alcohol abuse was a greater risk. Current hepatitis-B infection and alcohol abuse were additive risks.
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PMID:Alcohol consumption as a risk factor for hepatocellular carcinoma in urban southern African blacks. 131 67

Between July 1986 and April 1989, 334 hospitalized adult Ethiopian patients with chronic liver disease were studied according to a protocol to define their clinical features and to identify risk factors with the aim of preventive intervention. Of these, 14 had chronic hepatitis, 208 cirrhosis and 112 hepatocellular carcinoma (HCC). Both clinical and histological diagnostic criteria were employed. A detailed questionnaire was used to document demographic and clinical data. A common clinical presentation among patients with chronic hepatitis was darkening of the face and hands with or without hypertrichosis of the face and blisters over the dorsi of the hands. This overt or latent form of porphyrea cutanea tarda (PCT) responds to chloroquine. Patients with cirrhosis of the liver commonly present for the first time with ascites, splenomegaly, haematemesis and/or melena from oesophageal varices, and mental changes due to hepatic encephalopathy. Overt or latent forms of PCT are also common features. Peculiar to these cirrhotics is the rarity of spider naevi, gynaecomastia, testicular atrophy, Dupuytren's contracture, parotid gland enlargement and clubbing of the fingers. Exhaustion, loss of appetite, rapid loss of weight, right upper quadrant and/or epigastric pain (all often of less than 6 months' duration, a big, hard, tender and grossly nodular liver with bruit, signs of portal hypertension, and/or hepatic encephalopathy, in a young male with a rapid down hill course characterize the Ethiopian patient with HCC. Serum anti-nuclear factor, anti-mitochondrial anti-bodies and anti-smooth muscle anti-bodies were absent in those with chronic hepatitis and were uncommon in the cirrhotics and HCC cases. One or more hepatitis B virus markers were found in 86% of chronic hepatitis, 88% cirrhosis and 78% HCC and the HBsAg carrier state was found in 36%, 29% and 23%, respectively. Among the HBsAg carriers, HBeAg positivity was less common than anti-HBe but anti-HDV was significantly higher than in the healthy general population. Alphafetoprotein (AFP) levels greater than 500 mg/ml were present in 16 (8%) cirrhotics and 58 (52%) patients with HCC. Histologically, 3 of the chronic hepatitis patients had progressed to cirrhosis, 8 of the cirrhotic patients had chronic active hepatitis and 85% of HCC cases occurred in a background of macronodular cirrhosis. Three cirrhotics developed HCC during follow-up.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic liver disease in Ethiopia: a clinical study with emphasis on identifying common causes. 131

Glucocorticoids have been shown to influence the severity of hepatitis B virus-related chronic hepatitis in human. However, very little is known about the effects of glucocorticoids on hepatitis B virus replication in vitro. In this report, we used a well-differentiated human hepatoma cell line, Hep3B, transfected with hepatitis B virus complementary DNA as a model to show that a glucocorticoid analog, dexamethasone, can directly stimulate the production of HBsAg and HBeAg. Elevation of 3.5-kb pregenomic RNA and all other viral RNAs in the transfected Hep3B cells after dexamethasone treatment supports the hypothesis that glucocorticoids directly stimulate hepatitis B virus gene expression in vitro. The concentration of dexamethasone for its half-maximal stimulatory activity toward HBsAg, HBeAg and all viral transcripts was approximately 10(-8) mol/L, close to the affinity of glucocorticoid receptors to [3H]-triamcinolone acetonide in Hep3B cells (approximately 10(-8) mol/L). Specific glucocorticoid antagonist RU38486 completely blocked dexamethasone-induced HBV gene expression, suggesting that the stimulatory effect of dexamethasone was mediated through specific glucocorticoid receptors.
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PMID:Glucocorticoid stimulates hepatitis B viral gene expression in cultured human hepatoma cells. 131 49

Immunohistochemical evaluation of Cu, Zn- and Mn-superoxide dismutase (SOD) activity in various viral liver diseases was performed by the peroxidase-conjugated antibody indirect method. Anti-human Cu, Zn-SOD (rabbit) and anti-human Mn-SOD (guinea-pig) derived and purified from SOD of human erythrocytes and placentas were used to determine SOD distribution in liver tissues. SOD in the liver tissues was detected in 68 inpatients of our unit. They consisted of 23 cases with chronic hepatitis caused by hepatitis B virus (13) and hepatitis C virus (10), 24 with liver cirrhosis caused by hepatitis B virus (5) and hepatitis C virus (19) (15: compensatory, 9: decompensatory) and 21 with hepatocellular carcinoma caused by hepatitis B virus (2) and hepatitis C virus (18) complicated of liver cirrhosis. In viral liver diseases, SODs in the liver tissues were distributed to hepatocytes mainly in the pattern of cytoplasmic diffusion. The incidence of immunohistochemical Cu, Zn-SOD and Mn-SOD were 47.8% and 56.5% in chronic hepatitis, 93.3% and 86.7% in compensated liver cirrhosis, 11.1% and 22.2% in decompensated liver cirrhosis, respectively. The aggression of viral liver disease was accompanied with the decrease of SOD concentration in the liver tissues. Hepatocellular carcinoma cells were negative for Mn-SOD in all cases, and weakly positive for Cu, Zn-SOD in 2 out of 21 cases. Comparatively strongly positive SOD findings were obtained from normal regions neighboring carcinomas. A close relationship between the depletion of SOD in liver tissues and carcinogenesis in viral liver diseases was observed.
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PMID:Relationship between superoxide dismutase (SOD) and viral liver diseases. 132 May 79

The antibodies to hepatitis C virus (HCV) were tested in 45 histologically confirmed cases of chronic liver disease. Twelve cases had chronic hepatitis, 24 cirrhosis and 9 hepatocellular carcinoma. Anti-HCV was detected in 6 patients. Two (16.67%) were suffering from chronic hepatitis, 3 (12.5%) had cirrhosis and one (11.11%) hepatocellular carcinoma. None of the anti-HCV positive cases had past history of blood transfusion. The patients of chronic liver disease in this study had a much higher prevalence of HBV infection which indicates that in northern Pakistan hepatitis C virus infection is not a common cause of chronic liver disease whereas HBV infection plays an aetiological role in a much larger number of these cases.
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PMID:Hepatitis C as a cause of chronic liver disease in northern Pakistan. 132 Dec 99

The prevalence of hepatitis virus markers in patients with chronic liver diseases from two countries has been studied: 68 patients (38 alcoholic hepatitis or cirrhosis, 30 chronic HBsAg-positive hepatitis) from Hungary as well as 109 patients (55 alcoholic liver disease, 45 chronic hepatitis or cryptogenic cirrhosis and 9 hepatoma) from Romania were examined for HBsAg, anti-HBs, anti-HBc, anti-HCV and anti-HDV, using the corresponding Abbott Elisa test systems. In alcoholic liver disease HBsAg occurred in 6/38 patients from Hungary and in 22/55 patients respectively, that is HBV markers occurred with significantly higher frequency in alcoholic patients from Romania (p less than 0.05). In the Hungarian group a total of 36 patients were HBsAg positive and out of them 5 had anti-HDV (13.9%), while out of 21 Romania HBsAg carriers 10 patients had anti-HDV (47.6%). Among 9 hepatoma patients 4 had HBsAg, 6 anti-HBs and 7 anti-HBc and 4 had anti-HCV and 3 had anti-HDV. One patient with hepatoma had both HBsAg and anti-HCV plus anti-HDV as well. Results suggest that the infection with hepatitis viruses in alcoholic liver diseases is more common in Romania than in Hungary, and the prevalence of delta virus infection in HBV carriers is also significantly higher in Romania than in Hungary.
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PMID:[Hepatitis virus (HBV, HCV, HDV) markers in chronic liver diseases. Comparative studies in two East-Central European countries]. 132 99

A patient with lichen planus (LP) who developed a hepatocellular carcinoma as a consequence of a postviral chronic hepatitis is described. Its possible noncoincidental association with LP is discussed on the basis of a recent large case-control study in which the association of LP with chronic, possibly postviral, liver disorders has been confirmed. In the same study 1 case out of 577 LP patients was found to have hepatocellular carcinoma versus none of the 1,031 controls, a prevalence which is higher than expected in a western population.
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PMID:Hepatocellular carcinoma and lichen planus: report of two cases. 132 53

Twenty-three patients with minute hepatocellular carcinoma, defined as a solitary lesion less than or equal to 2 cm, underwent hepatectomy at our institute during the 10 years between January, 1979 and December, 1988. Hepatitis B surface antigen was positive in 4 patients and the preoperative serum alpha-fetoprotein level was within the normal range in 7 patients and slightly elevated (20-200 ng/mL) in 14 patients. Liver cirrhosis was present in 16 patients and chronic hepatitis in 6 patients. The diagnosis was first suspected from the results of periodic examinations, including echography and the measurement of alpha-fetoprotein, in all except one patient. Minor hepatic resection was performed in 22 patients, and lobectomy in one patient in whom the tumor was located centrally in the liver. Three patients died of hepatic failure in hospital following surgery, and the survival rates of the other 20 patients at 1, 3, and 5 years were 90, 79, and 61 percent, respectively. The prognostic factors that influenced long-term survival were investigated by comparing the survival curves. The only factor associated with a significant difference in survival was the severity of concomitant liver disease. Thus, severe cirrhosis is the main obstacle against the long-term survival of patients with minute hepatocellular carcinoma.
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PMID:Hepatic resection for minute hepatocellular carcinoma. 132 59

For many years, epidemiological studies have demonstrated a strong link between chronic hepatitis B virus (HBV) infection and the development of primary hepatocellular carcinoma (PHC). Other hepatocarcinogens such as hepatitis C virus and aflatoxin also contribute to hepatocarcinogenesis either in conjunction with HBV infection or alone. Cellular and molecular biological studies are providing explanations for the HBV-PHC relationship, and models are now being formulated to further test the relative importance of various factors such as viral DNA integration, activation of oncogenes, genetic instability, loss of tumor suppressor genes, and trans-activating properties of HBV to the pathogenesis of PHC. Further research will probably define more than a single mechanism whereby chronic HBV infection results in PHC.
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PMID:Hepatitis B virus infection and primary hepatocellular carcinoma. 132 84


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