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)

The concentration of Hepatitis C Virus (HCV) in the blood is increased by alcohol drinking and decreased by abstinence. These facts suggested that alcohol abuse may enhance the replication of HCV. The effects of alcohol on HCV replication may be related to increased development of chronic hepatitis to liver cirrhosis and hepatocellular carcinoma in HCV marker positive heavy drinker. These results indicated that HCV positive heavy drinkers must keep abstinence and that these patients have to be treated with interferon.
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PMID:[Effects of interferon treatment in alcoholic liver injury]. 752 33

We designed a multicenter cross-sectional study to evaluate the role of alcohol abuse, the hepatitis viruses and other pathogenic factors in cirrhosis and hepatocellular carcinoma. A total of 1,829 consecutive cirrhosis patients, with or without HCC, was enrolled over 6 mo in 21 centers throughout Italy. The etiological categories and diagnostic criteria were preestablished. The median age of the patients was 59 yr (range, 13 to 85 yr); 63.6% of the patients were graded as Child class A, 23.4% as Child class B and 13% as Child class C. Hepatitis C virus antibodies were found in 72.1% of cases (47.7% alone, 21.2% with alcohol abuse, 3.2% with hepatitis B virus); HBsAg was present in 13.8% (4.2% alone, 3.2% with hepatitis D virus, 3.2% with hepatitis C virus, 3% with alcohol abuse), alcohol abuse with no concomitant viral infection was recorded in 8.7%, primary biliary cirrhosis was found in 1.8%, other causes were found in 1.4% and cryptogenic cirrhosis was only present in 5.3%. Hepatocellular carcinoma was detected in 11.9% of patients (217 cases). The presence of hepatocellular carcinoma was more frequent in males than females (14.7% vs. 7.3%; p < 0.001) and increased with worsening Child class (8.3% in Child class A, 16.9% in Child class B, 19.9% in Child class C, p < 0.001). The highest prevalences of hepatocellular carcinoma were observed in hepatitis B virus infection, with or without alcohol abuse (20% and 16%, respectively) and in hepatitis C virus cirrhosis, with or without alcohol abuse (16% and 10.3%, p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenic factors in cirrhosis with and without hepatocellular carcinoma: a multicenter Italian study. 752 73

A double case control study evaluated the role of hepatitis C virus (HCV) and hepatitis B virus (HBV), alcohol drinking, and tobacco smoking as potential risk factors for cepatocellular carcinoma (HCC). Fifty-one patients with HCC, 34 of whom had underlying cirrhosis, were analyzed against 51 hospital controls and 34 patients with cirrhosis, respectively. Sera from patients of all three groups were tested for HBV markers and anti-HCV antibodies. The polymerase chain reaction technique was used to detect HCV RNA in the anti-HCV-positive samples. Alcohol drinking and smoking habits were recorded for all patients. HCC risk was significantly related to the presence of hepatitis B surface antigen (HBsAg) [relative risk (RR) = 18], HCV infection (RR = 8), and alcohol abuse (RR = 4). When the presence of cirrhosis was taken into account, only HBsAg positivity was significantly associated with HCC development (RR = 6.7), indicating that HCV infection and alcohol abuse are related to HCC indirectly through the cirrhotic process. No significant interaction between HCV and HBV infection in the causation of HCC was found. Through the computation of population-attributable risk, it was found that 46% of the HCC cases in Greece could be attributed to HBsAg positivity but only 4% to HCV infection. In conclusion, HBV infection is the major risk factor in the development of HCC in Greece, either by inducing cirrhosis or by direct oncogenic effect. HCV infection is also related to HCC development, albeit indirectly through the cirrhotic process.
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PMID:The leading role of hepatitis B and C viruses as risk factors for the development of hepatocellular carcinoma. A case control study. 779 31

gamma-Glutamyltransferase (GGT) is a glutathione-metabolizing enzyme whose activity variations in serum and organs are valuable markers of preneoplastic processes, alcohol abuse and induction by drugs. To elucidate the implication of GGT in various metabolic pathways, we established a stable transfected V79 cell line highly producing the human GGT. A full length cDNA, encoding the human hepatoma Hep G2 GGT, was subcloned into an expression vector under the control of the SV40 early promoter and was used to transfect V79 cells. A cell line was selected, exhibiting a GGT activity of 2 units per mg of protein, one of the highest levels reported to date. The recombinant GGT purified from this cell line showed the expected heterodimeric structure, with two subunits existing as sialylated and differentially glycosylated isoforms, with mean molecular masses of 80 and 29 kDa. Catalytic features were found to be identical to those of human serum and Hep G2 GGTs. Thus, the newly engineered cell line should be useful for the production of human GGT and as a potential alternative model for pharmacological studies.
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PMID:Establishment of a V79 transfected cell line highly producing recombinant human gamma-glutamyltransferase. 790 24

The hepatic microsomal ethanol-oxidizing system (MEOS) has been well characterized as an important pathway in ethanol metabolism. Cytochrome P450 2E1 (CYP 2E1), the principal component of MEOS, is ethanol inducible and has been implicated in hepatotoxicity associated with alcohol abuse and exposure to organic solvents. Results of chronic in vivo experiments have shown that ethanol induction of hepatic CYP 2E1 occurs by a two-step mechanism. The first step of induction is associated with low blood alcohol concentrations (BACs) and appears to be post-transcriptional, whereas high BACs observed in step-two induction are associated with increased CYP 2E1 gene transcription. The mechanisms underlying these induction steps are under intense investigation. Progress in this area has been limited due to lack of hepatic cell culture models that express CYP 2E1. We report here an in vitro tissue culture cell model, the FGC-4 hepatoma cell line, that exhibits basal levels of CYP 2E1 apoprotein that are inducible by ethanol treatment. Total cellular RNA and microsomal fractions were isolated from control or ethanol-treated confluent cells, and CYP 2E1 mRNA and apoprotein levels were characterized by northern blot or immunoblot analysis, respectively. Initial experiments on isolated microsomes revealed detectable levels of CYP 2E1 apoprotein in control cells that were induced 5-fold in cells treated with 100 mM ethanol for 24 hr. Concentration-response experiments demonstrated that the maximal 24-hr induction in CYP 2E1 apoprotein level was 5-fold and was attained at a concentration of 10 mM ethanol. Interestingly, while the steady-state mRNA levels encoding CYP 2E1 were detectable, they remained unchanged in identically treated cells. Furthermore, there was no observed increase in CYP 2E1 mRNA levels in an extended time course to 72 hr or at higher alcohol concentrations (up to 1500 mM), providing preliminary evidence that the induction is post-transcriptional. The time course of CYP 2E1 apoprotein induction by exposure to 100 mM ethanol demonstrated maximal induction at 8 hr. Measurement of CYP 2E1 apoprotein levels after removal of ethanol from pretreated cells demonstrated the half-life of the apoprotein to be 12.7 hr, in good agreement with previous reports using primary hepatocytes. The half-life of the induced protein after ethanol removal in the presence of cyclohexamide (10 micrograms/mL) was biphasic with a rapid 1.8 hr first phase followed by a slower 44.7 hr second phase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Characterization of cytochrome P450 2E1 induction in a rat hepatoma FGC-4 cell model by ethanol. 798 Jun 52

To identify factors that might be useful as prognostic indexes for the risk of hepatocellular carcinoma in Italian patients with genetic hemochromatosis, 152 homozygotes were studied prospectively for 1 to 229 mo. Factors that were considered in estimating the risk of developing hepatocellular carcinoma were age, sex, cirrhosis (Child class), HBsAg, antibodies to HBsAg, antibodies to HBcAg, hepatitis C antibodies, alcohol abuse and the amount of iron removed during therapeutic phlebotomy to produce iron depletion. At diagnosis, cirrhosis was present in 97 patients and absent in 55. During follow-up, hepatocellular carcinoma developed in 28 of the 97 patients with cirrhosis but in none of those without. Among patients with cirrhosis, the cumulative probability of being free of hepatocellular carcinoma at 10 yr was 70%. For patients with and without HBsAg the probabilities of being free of liver cancer at 10 yr were, respectively, 54% and 75%; for those with and without history of alcoholism, 58% and 78%; and for those younger and older than 55 yr, 90% and 54%. In patients with cirrhosis, multivariate analysis using proportional-hazards (Cox) regression found that the only factors contributing significantly to the estimation of a prognostic index were age, presence of HBsAg and alcohol abuse. Age over 55 yr increased the relative risk of hepatocellular carcinoma 13.3-fold (p < 0.001), the presence of HBsAg increased it 4.9-fold (p < 0.02) and alcohol abuse increased it 2.3-fold (p < 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic factors for hepatocellular carcinoma in genetic hemochromatosis. 798 40

Data on the prevalence of chronic liver disease, derived from selected series of hospitalized patients or from mortality registers, underestimate the prevalence of chronic liver disease. The Dionysos Study is a cohort study that investigated for the first time the prevalence of chronic liver disease in a general population. All the citizens of two towns in northern Italy, Campogalliano and Cormons, aged 12 to 65 yr were contacted by letter. From March 1991 through March 1993, 6,917 of a total of 10,150 citizens were enrolled (compliance, 69%). The standardized protocol for each enrollee included (a) a color-illustrated food questionnaire on dietary habits and alcohol intake; (b) a detailed medical history, including questions on risk factors for chronic liver disease; (c) a physical examination; and (d) blood tests for AST, ALT, gamma-glutamyltranspeptidase, mean cell volume, platelet count and hepatitis B virus and hepatitis C virus markers. Signs suggestive of chronic liver disease were seen in 21.3% of the subjects, and who then underwent further liver function tests, upper abdominal ultrasonography and, when necessary, liver biopsy. Persistent signs of chronic liver disease were present in 17.5% of the subjects, including 1.1% with cirrhosis and 0.07% with hepatocellular carcinoma. The prevalence rates of hepatitis B virus and hepatitis C virus positivity (second-generation enzyme-linked immunosorbent assay) were 1.3% and 3.2%, respectively. Alcohol abuse was the etiological agent in 23%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of chronic liver disease in the general population of northern Italy: the Dionysos Study. 798 43

In a consecutive series of 317 patients with hepatocellular carcinoma (HCC), 32 (10.1%) had 35 extrahepatic primary malignant neoplasms (PMNs) (3 patients had triple cancers). Twenty-five PMNs occurred before the diagnosis of HCC, 7 were synchronous and 3 metachronous. These 35 PMNs were: 6 cancers of the colon, 3 of the stomach, 1 of the rectum, 4 of the breast, 2 of the lung, 1 of the larynx, 3 of the prostate, 1 of the penis, 1 of the urinary bladder, 1 of the uterus, 2 of the skin, and the remaining 10 were immunoproliferative cancers, all of B cell origin (7 non-Hodgkin's lymphoma, 2 multiple myeloma, and 1 chronic lymphocytic leukemia). Thus, in this series, B-lymphocyte-derived neoplasms were the most frequent PMNs associated with HCC. These 10 patients showed no difference for age, male:female ratio, HCC cytotype, presence of cirrhosis, alcohol abuse, markers related to hepatitis B and C virus, and serum level of alpha-fetoprotein when compared with the 22 patients with HCC and other PMNs and the 285 with HCC alone. B cell neoplasms constitute half of the synchronous or metachronous cancers, and must, therefore, be kept in mind in the management of HCC patients.
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PMID:Extrahepatic primary malignant neoplasms associated with hepatocellular carcinoma: high occurrence of B cell tumors. 805 89

The prevalence of antibodies to hepatitis C virus (anti-HCV) was determined in 105 patients with biopsy-proven chronic liver disease and 128 comparison patients without any evidence of liver pathology living in Lima, Peru. Using a second-generation EIA screening and supplemental immunoblot assay, anti-HCV was detected in four of 13 patients with chronic hepatitis, in 11% of 85 patients with cirrhosis, and in none of seven patients with hepatocellular carcinoma. Only two (1.6%) comparison patients without liver disease had anti-HCV. Hepatitis B surface antigen (HBsAg) was found in 23% of patients with chronic hepatitis, 12% of patients with cirrhosis, and three of seven patients with hepatocellular carcinoma. There was no evidence of chronic viral hepatitis or alcohol abuse (reported by one-third of subjects) in 48% of chronic liver disease patients. These preliminary data suggest that among this South American population neither hepatitis B nor hepatitis C infection is the predominate cause of chronic liver disease and that other infectious or environmental factors may be important.
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PMID:Chronic liver disease in Peru: role of viral hepatitis. 815 7

A case of hepatocellular carcinoma (HCC), which developed during chemotherapy for chronic myelogenous leukemia (CML), is presented. A 55-year-old Japanese man, who had received an alkylating agent for 16 years, was diagnosed as having HCC with clinically evident splenic metastases. The patient died of the HCC rupture three months after diagnosis. The autopsy revealed the HCC to have developed from the non-cirrhotic liver. In the present case, DNA damage due to the long-term chemotherapy with the alkylating agent for CML may have endowed the HCC induced by post-transfusion hepatitis and alcohol abuse with an aggressive proliferative potential. This is the first report on HCC in association with CML.
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PMID:Hepatocellular carcinoma with splenic metastasis developing after 16 years of chemotherapy for chronic myelogenous leukemia: a case report. 815 58


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