Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five cases of hepatocellular carcinoma in whom diagnosis was made when the tumor was relatively small, are described. In 2 cases, serum alpha-fetoprotein (AFP) strted to rise sharply, which enabled early detection and surgical removal of the tumor. Serum AFP was below 100 ng per ml, but above the upper normal limit by radioimmunoassay, and was unfluctuating for a considerable period of time before it began to rise in 2 cases. It was negative throughout in 1 case, who lived more than 4 years after the tumor had reached a detectable size. In 4 of 5 cases, the tumor seemed to have evolved during a stage of chronic hepatitis or its transition to cirrhosis. In 1 case with chronic schistosomiasis and advanced mixed macro- and micronodular cirrhosis, a 1.5-cm tumor was detected by celiac angiography. These observations on time relationship of oncogenesis may be generalized to modify the cirrhotic liver. Necessity is emphasized for the early detection of this type of carcinoma to monitor serum AFP in chronic hepatitis patients, particularly in those with unfluctuating, mildly abnormal levels of AFP.
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PMID:Clinical observations during a relatively early stage of hepatocellular carcinoma, with special reference to serum alpha-fetoprotein levels. 5 Feb 51

Alcohol and tobacco appear to act synergistically in the pathogenesis of epithelial cancers of the oropharynx (excluding lip), larynx, and esophagus. For the subsites within the upper aerodigestive tract, over 10,000 deaths in United States men during 1978 may be attributed to tobacco and alcohol consumption. The cancer sites for which tobacco and alcohol are major determinants occur with greater frequency in men, blacks, lower socioeconomic groups, and with increasing urbanization and increasing age (35--70 years). Because primary hepatocellular carcinoma occurs more commonly in patients with cirrhosis, chronic alcohol abuse is an important risk mechanism for carcinoma of the liver parenchyma. Although experimental animal studies have failed to demonstrate whether ethanol can independently initiate tumorigenesis, various alternative or associated biochemical and immunological mechanisms of action have been proposed.
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PMID:Alcohol as a co-factor in the etiology of cancer. 44 84

PAP technique and rabbit anti-X serum were used to detect the X protein in tumor and nontumor liver tissues from 34 patients with HCC. The positive rate of the X protein in both tissues were 94.1% and 84.4% respectively. Of the 34 patients with HCC, 27 were complicated by liver cirrhosis, in whom 92.6% were X protein positive in liver cells. It was found that almost all of the liver cells adjacent to the tumor tissue showed strong positive staining. The high frequency and predominant expression of X protein in HCC and liver cirrhosis tissues indicated that X protein may play an important role in hepatocarcinogenesis. X protein was detected in 17.2% of the patients with CAH, which suggested the risk of transformation from CAH to cirrhosis and/or HCC. X protein was first found in bile duct epithelial cells in 59.4% of the patients with HCC, and 6 of 34 HCC were combined with bile duct carcinoma, and some cancer cells were found positive for X protein. It seems that X protein may also be a potential factor in the oncogenesis of bile duct carcinoma.
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PMID:[Expression of hepatitis B virus X protein in tumor and nontumor tissues of patients with hepatocellular carcinoma (HCC)]. 132 50

Loss of tumor suppressor genes is involved in the mechanism of tumorigenesis of many solid tumors. We tested 9 hepatitis B virus (HBV)-positive and 10 HBV-negative hepatocellular carcinomas for loss of somatic heterozygosity using 14 polymorphic probes mapping to chromosomes 4, 11, 13, and 17. Losses were found on all chromosome arms tested. The highest frequency of loss was observed at the D13S1 locus (67%) at band 13q12. Losses were also observed at three other loci on 13q. Twenty-one % of informative cases showed loss on 17p using the probe pYNZ22 which maps near the p53 locus. Losses on 4q were infrequent with 17% found at one locus and no loss at two others. The retinoblastoma gene and the locus on 17p were only inactivated in our HBV-negative tumors, although the numbers were too small for statistical significance. For all loci tested, we found no significant differences in the frequency of losses with HBV status, ethnic background, cirrhosis, grade of tumor, or presence of hemochromatosis.
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PMID:Loss of somatic heterozygosity in hepatocellular carcinoma. 167 14

Infection with 100 Opisthorchis viverrini (OP) metacercariae prior to two injections of dihydroxy-di-n-propyl nitrosamine (DHPN) (1000 mg/kg body weight) brought about significant enhancement of resultant preneoplastic lesion development in Syrian hamster liver and pancreas tissue. Thus combined treatment with carcinogen and parasite was associated with pancreatic atypical (dysplastic) foci, hepatocellular nodules, cholangiofibrosis and cholangiocarcinomas. No such lesions were observed in carcinogen alone, parasite alone or untreated control groups. In addition, parasite induced hyperplastic gall bladder epithelium was found to include areas of putative preneoplastic cells only in the DHPN-OP combined group. The results strongly suggest that pancreatitis and biliary cirrhosis associated with liver fluke infestation are responsible for the observed enhancement of carcinogenesis, and that the resultant increased proliferation plays a major role in tumorigenesis.
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PMID:Enhancement of DHPN induced hepatocellular, cholangiocellular and pancreatic carcinogenesis by Opisthorchis viverrini infestation in Syrian golden hamsters. 283 5

The ubiquitous problem of cirrhosis may be complicated by the development of primary liver cell carcinoma, with rates of incidence so high in certain parts of the world as to make it a candidate for the most common cancer in humans. When cirrhosis reaches the macronodular stage, the risk of developing liver cell carcinoma increases, and at this point liver cell dysplasia may be seen in biopsy. Alcoholics, who classically have a micronodular cirrhosis, may attain the macronodular pattern through better clinical management, abstinence, and longer survival. Hepatitis B-related cirrhosis, on the other hand, is most often macronodular. Recent DNA hybridization studies strongly favor a viral role in oncogenesis, and this possibility is supported by the serologic and epidemiologic evidence complied in the last decade. Liver cell malignant tumors tend to recapitulate the characteristics of normal liver, namely, growth in cords, uniformity of cytologic appearances, and bile production, but also present distinctive histologic and immunohistochemical patterns that are unique to a malignant liver cell population. The other primary malignant tumors of the liver, arising in bile ducts, blood vessels, and mesenchymal elements, all carry their individual epidemiology and morphology, but in general invoke, as does liver cell carcinoma, the concept of a series of step by step cell-carcinogen and cell-carcinogen interactions by which normal cells give rise to malignant populations.
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PMID:The epidemiology and morphology of primary malignant liver tumors. 625 64

Chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections lead to cirrhosis and increase the risk for the development of hepatocellular carcinoma (HCC). Angiogenesis is an essential step in oncogenesis and contributes to tumor progression in adult organs; however, to what extent angiogenesis occurs in the liver during chronic viral hepatitis has not been studied. Ninety-nine matched patients affected by chronic hepatitis due to either HBV or HCV were studied together with 13 controls (5 patients were affected by familial hyperbilirubinemia with normal liver histology; 6 patients with stage II primary biliary cirrhosis; and 2 patients with pseudo inflammatory tumor). Microvessel density was assessed in liver biopsies by immunostaining using two different antibodies against endothelial cell antigens, QB-END/10 and Factor VIII. In addition, the liver homogenates and sera of HCV- or HBV-positive patients and controls were tested for their capacity to stimulate the migration and proliferation of freshly isolated human endothelial cells in vitro. Evidence of angiogenesis was significantly more frequent in HCV-positive patients compared with HBV-infected subjects or controls (74% vs. 39% vs. 8%) (chi2 = 20.78; P < .0001) (HCV+ vs. HBV+ vs. controls). The degree of microvessel density was also higher in HCV- than in HBV-positive patients or controls (chi2 = 12.28; P < .005). In addition, HCV-positive sera and liver homogenates stimulated a higher migration and proliferation of human endothelial cells in vitro compared with HBV-positive or control sera and liver homogenates. These observations indicate that angiogenesis is particularly linked to HCV infection, suggesting a possible contribution to HCV-related liver oncogenesis.
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PMID:Chronic viral hepatitis induced by hepatitis C but not hepatitis B virus infection correlates with increased liver angiogenesis. 898 96

The BCR gene is located on human chromosome 22. The normal cellular BCR gene encodes a 160,000-dalton phosphoprotein associated with a serine/threonine kinase activity. The BCR protein is involved in signal transduction. We investigated the expression of the BCR protein in hepatocellular carcinoma (HCC), surrounding noncancerous liver tissue, liver cirrhosis (LC), chronic hepatitis (CH), and normal liver with immunohistochemistry and a western blot analysis. BCR immunoreactivity was detected using a monoclonal antibody. In normal liver, and both CH and LC without association of HCC, the immunoreactivity of the BCR protein was minimal. In contrast, 73% (22 of 30) of noncancerous liver tissue adjacent to the HCC and 40% (12 of 30) of HCC expressed BCR protein; this difference was statistically significant (P < 0.01). The expression of the BCR protein expression correlated with the degree of histological differentiation of HCC (P < 0.05). In addition, the amplification of BCR protein in noncancerous cells was supported by the detection of specific protein using a western blot analysis. In two cases, the expression of BCR protein occurred only in overtly malignant HCC cells. As a result, the expression of the BCR protein may be associated with oncogenesis in human HCC.
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PMID:Amplification of BCR protein associated with oncogenesis in human hepatocellular carcinoma. 914 44

Prolonged infection of hepatitis B virus (HBV) is reported to cause hepatocellular carcinoma (HCC) via liver cirrhosis. However, it is still unknown whether the HCC is induced by the HBV DNA integration or by inflammatory stimulation during the phase of liver cirrhosis. The aim of this study is to determine the intracellular or intranuclear distribution of HBV DNA with a highly sensitive assay. Here we directly detected the integration of HBV DNA by fluorescence in situ polymerase chain reaction (FISPCR). Since FISPCR products directly incorporate rhodamine-4-dUTP, the nucleus of Alexander cells integrated with HBV gene reacted with the HBV primers emits obvious fluorescence. The fluorescence values which were measured with an imaging analyzer show a significant difference between Alexander cells as compared to the controls. In conclusion, the target sequences of HBV were specifically amplified as fluorescent DNA after the present FISPCR procedure. This method could provide a novel and simple strategy for determining the quantitative role of viral DNA integration in oncogenesis.
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PMID:Direct detection of hepatitis B virus gene integrated in the Alexander cell using fluorescence in situ polymerase chain reaction. 921 72

Oncogenesis is a multifactorial process in which environmental, genetic and infectious factors are variably involved. A possible role of specific viruses has been suggested in at least 15% of human cancers. Hepatitis C virus (HCV), which is both hepato- and lymphotropic, is responsible for various liver disorders, i.e. chronic hepatitis, cirrhosis and hepatocelluar carcinoma, as well as for a constellation of extrahepatic immune-mediated manifestations, among which is mixed cryoglobulinaemia. This is a systemic disorder secondary to a chronic, benign B-lymphocyte proliferation, which in some subjects may evolve to a malignant non-Hodgkin's lymphoma (NHL). Interestingly, recent studies reported the appearance of malignant B-cell neoplasias in patients with type C chronic hepatitis; moreover, in a significant number (from 22% to 50%) of 'idiopathic' NHLs, the presence of HCV infection has been demonstrated. The presence of a geographical etherogeneity in the prevalence of HCV-positive NHL suggests that other co-factors, i.e. genetic and environmental, could be involved in the lymphomagenesis. HCV may exert its oncogenic potential in two different directions, leading to liver cancer or B-cell lymphoma.
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PMID:Viruses and cancers: possible role of hepatitis C virus. 935 39


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