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)

To clarify the potential role for HCV in the development of chronic liver disease in Yatsuka town with a high morbidity of liver disease, epidemiological studies were taken in 459 subjects of Yatsuka town compared with 219 subjects of Mihonoseki town with a low one. In Yatsuka town, the mortality rate of liver cirrhosis was three times higher than the overall rate in Simane prefecture, and the rate of liver cancer rapidly increased in recent years. Age and sex-matched epidemiological studies showed a significantly higher incidence of hepatic dysfunction compared with Mihonoseki town (11.5% vs 3.7%, P less than 0.01). The prevalence of HCV antibody was significantly higher in Yatsuka town than Mihonoseki town (16.6% vs 3.7%, P less than 0.001), although there were no differences in frequencies of HBs antigen and habitual alcohol drinker between the two districts. These data strongly suggest that the high prevalence of HCV may be associated with the high morbidity of chronic liver disease, especially hepatocellular carcinoma in Yatsuka town.
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PMID:[Prevalence of HCV antibodies in Yatsuka town of Simane prefecture, Japan]. 159 74

In recent years a strong case has been made in support of a viral aetiology for at least some primary hepatocellular carcinoma (PHC) in areas of low incidence. By pooling routinely collected cancer registration and infection data, study of the relationship between hepatitis B virus (HBV) infection and the incidence of PHC in Scotland over the period 1972-1985 has confirmed this view. Over this period the incidence of PHC in men increased, there was a relationship between the incidence of notification of HBV infection and that of hepatocellular carcinoma in different parts of the country, and an increased risk attached to those chronically infected with the virus. Given the recent introduction of lower cost yeast derived vaccines, there may now be more scope for prevention both of primary liver cancer and of other liver disease.
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PMID:Primary hepatocellular carcinoma in an area of low incidence: evidence for a viral aetiology from routinely collected data. 164 50

N-(2-Hydroxypropyl)methacrylamide (HPMA) copolymers containing doxorubicin (DOX) and galactosamine can be targeted to the hepatocyte galactose receptor for organ-specific chemotherapy of primary and metastatic liver cancer. Here we report the dose-dependent pharmacokinetics of this macromolecular conjugate. Following intravenous administration to mice most efficient liver targeting was seen at low dose (0.05 mg DOX kg-1), with receptor saturation observed using higher bolus doses. Repeated low dose bolus injections did not cause down-regulation of the galactose receptor and targeted drug delivery rates of greater than or equal to 2 micrograms DOX g-1 liver h-1 were achieved. DOX is released from such conjugates intracellularly via action of lysosomal proteinases. It was shown that isolated rat liver lysosomal enzymes (Tritosomes) can release unmodified DOX from the peptidyl side chain Gly-Phe-Leu-Gly at a rate greater than or equal to 3 micrograms DOX g-1 liver h-1 i.e. the hydrolytic capacity is greater than the observed rate of drug delivery to the liver lysosomes in vivo. Although most conjugate would be captured by normal hepatocytes following intravenous administration, it was shown that the human hepatoma cell line HepG2 retains the galactose receptor, accumulating and processing the conjugate efficiently. Potential dose limiting toxicities of such drug conjugates could include cardio- or hepatotoxicity. Administration of conjugate reduced the 15 min heart level of DOX approximately 100-fold compared with that observed for an equivalent dose of free drug. Preliminary experiments showed that plasma levels of alkaline phosphatase, alanine transaminase and asparate transaminase did not change following administration of HPMA copolymer-daunorubicin (DNR) (10 mg DNR kg-1) indicating no significant heptatoxicity.
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PMID:N-(2-hydroxypropyl)methacrylamide copolymers targeted to the hepatocyte galactose-receptor: pharmacokinetics in DBA2 mice. 164 46

The importance of chronic hepatitis B virus (HBV) infection in the development of primary liver cancer has been established by epidemiological studies. However, the evidence for a direct role of the virus in liver carcinogenesis is still tentative. In addition, the findings of HBV DNA sequences in HBsAg-negative subjects with liver cancer has been reported, although it is controversial. Here we report the use of the polymerase chain reaction to detect HBV DNA in the serum and liver of HBsAg-negative patients. This technique allows both for the detection and cloning of HBV variants. In addition, the demonstration of HBV DNA and RNA molecules in HCC of HBsAg-negative individuals as determined by standard techniques reinforces the role of HBV in the pathogenesis of this tumor.
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PMID:The detection of hepatitis B virus (HBV) in HBsAG negative individuals with primary liver cancer. 165 Jun 88

Benign liver tumors occurring in young women were rarely reported in the medical literature before the introduction of oral contraceptives in the early 1960s. Subsequently, there were numerous case reports from the U.S. and other countries of liver tumors in women who used combined oral contraceptives. These reports, coupled with data from two U.S. case-control studies, indicate that the risk of hepatocellular adenoma increases sharply with increasing duration of oral contraceptive use. Case reports suggest that there may be a similar effect on the risk of focal nodular hyperplasia, but this is not established because there have been no case-control studies of the lesion. The incidence of benign liver disease attributable to oral contraceptive use in the U.S. is small because of the very low incidence of the disease. There have also been numerous case reports of malignant liver tumors in young women who used oral contraceptives. Seven case-control studies have been conducted--two in Great Britain, two in the U.S., one in Italy, one in several developing countries (conducted by the World Health Organization (WHO)), and one in South Africa. Data from the first five studies, all conducted in low risk populations, indicated an association of hepatocellular carcinoma (largely in the absence of liver cirrhosis) with oral contraceptive use. Because of small numbers estimates were unstable, but the risk did not appear to be increased appreciably for durations of use less than about five years. For longer durations, the risk appeared increased by five- to tenfold or more. There was little evidence of hepatitis B infection in the cases, but systematic determinations were not carried out. An increased risk of cholangiocarcinoma was not established, but few of these lesions were studied. Because the incidence of primary liver cancer in Northern Europe and the U.S. is low, the incidence attributable to oral contraceptive use is also likely to be low. The WHO study was carried out in eight countries, most of which have a high incidence of liver cancer and a high prevalence of a predisposing factor, hepatitis B infection. Similarly, the South African study was carried out among black women, and virtually all of the cases had serological evidence of hepatitis B infection. Both studies indicated no association of short-term oral contraceptive use with risk of hepatocellular carcinoma, and the WHO study indicated a lack of association with cholangiocarcinoma.
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PMID:The risk of liver neoplasia in relation to combined oral contraceptive use. 165 Dec 5

Superoxide dismutase (SOD) activity and content of lipid peroxides (LPO) in human hepatocellular carcinoma (HCC) tissue were studied. It was observed that SOD activity and LPO content in HCC tissue were lower than those in normal liver tissue (P less than 0.001 respectively). The contents of copper, zinc and manganese in HCC tissue were also lower than those in normal liver tissue (P less than 0.001, P less than 0.05). Furthermore, LPO content in necrotic HCC tissue was higher than that in non-necrotic HCC tissue (P less than 0.05). The results suggest that deficiency of copper, zinc and manganese in HCC tissue may be a contributing factor that leads to impairment of SOD activity. Decreased SOD activity in liver cancer cells was a negative feedback of the multiplication of cancer cells loss of lipid peroxidation explains the malignancy of HCC, and enhanced lipid peroxidation in liver cancer cells may cause the necrosis of cancer cells.
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PMID:[Impaired superoxide dismutase activity and decreased content of lipid peroxides in hepatocellular carcinoma tissue]. 165 38

A 36-year-old woman was admitted to our hospital because of general fatigue. The physical and laboratory findings on admission revealed splenomegaly, pancytopenia, hypocoagulopathy, liver hypofunction with a hepaplastin test of 55% and ICG Rmax of 0.6 mg/kg/min. Diagnostic imaging showed a hypoechoic mass 1.5 in diameter a low density area on the CT scan and a faint tumor stain on the AAG in the posterior inferior area of the liver. On a diagnosis of hepatocellular carcinoma with liver cirrhosis and hypersplenism, partial hepatectomy and splenectomy were performed. The resected hepatic specimen revealed a small liver cancer of 1.9 x 1.5 x 1.3 cm with liver cirrhosis. The specimen consisted of a firm rubbery mass. Macroscopically, the tumor appeared oval and was lobulated with a thin capsule. A fibrous scar was observed in the central area. Microscopically, malignant hepatocytes showed various shapes, ranging from polygonal to spindle form, with eosinophilic granular cytoplasm and were surrounded by abundant fibrous stroma. Orcein stain, revealed that these malignant hepatocytes contained many black granules of copper-binding protein. Immunoperoxidase staining for alpha 1-antitrypsin was also positive in the malignant hepatocytes. However, within this lamellar fibrous regions, there were many cords of tumor cells in which nucleoli were absent and abortive biliary differentiation was suggested. Consequently this tumor was diagnosed as an atypical fibrolamellar hepatocellular carcinoma. We think that this case is the 3rd case reported in Japan and the 2nd case in a Japanese person.
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PMID:Fibrolamellar carcinoma of the liver--a case report. 165 47

The expression of HBx protein in liver tissues from 48 cases of different liver diseases, including 32 cases of hepatocellular carcinoma (HCC), 10 of chronic hepatitis (CH), 2 of angioma and 4 cases of normal liver was studied. These samples were tested for HBx protein, HBsAg by modified ABC method. Positive rates of HBx in cancer and adjacent liver tissue were 75.0% and 62.5%, and positive rates of HBsAg were 37.5% and 78.1% respectively. The occurrence of HBx in the absence of HBsAg was more frequently observed in tissues from HCC (46.9%) than CH (0%). The results showed that expression of HBx was more active than that of HBsAg, and it is suggested that HBx might be a useful marker for the diagnosis of liver cancer.
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PMID:[The HBx protein expression in liver cancer]. 165 95

Chromosomal translocation, deletion, and inversion/duplication directly linked to hepatitis B virus (HBV) DNA integration occur frequently in host DNA of human hepatocellular carcinomas. To test the possible recombinogenic effect of HBV DNA, we have utilized an in vitro recombination assay. Fragments containing the region spanning DR1, which is believed to be the origin of viral replication and a preferred site in the viral genome for integration, increased the recombination events reproducibly in the presence of extracts from actively dividing cells (e.g., hepatocellular carcinoma) but not resting cells (e.g., normal liver). Moreover, in these extracts we have found a protein(s) that specifically binds to these HBV DNA fragments. These results support the notion that in some instances integrated HBV DNAs cause further genomic instability, possibly involving specific cellular protein(s). The fact that extracts from nondividing, normal liver did not increase recombination events suggests that genomic instability depends upon active cellular growth, a feature more commonly found subsequent to HBV-induced hepatocellular injury than in healthy liver. Our results offer an explanation for the high incidence of liver cancer that accompanies chronic hepatitis and add HBV to the list of agents that can cause genetic recombination.
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PMID:Evidence for increased in vitro recombination with insertion of human hepatitis B virus DNA. 165 66

The incidence of the two principle types of liver cancer (hepatocellular carcinoma and cholangiocarcinoma) in five different areas of Thailand was compared with the prevalence of exposure to the main risk factors in samples of the population. Cholangiocarcinoma showed striking variations in incidence, which correlated closely with markers of exposure to the liver fluke, Opisthorchis viverrini. However, there was little geographic variation in incidence of hepatocellular carcinoma or in prevalence of the major risk factors (chronic carriage of hepatitis B virus and exposure to aflatoxin), and apparently there was little relationship between them.
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PMID:The role of infection by Opisthorchis viverrini, hepatitis B virus, and aflatoxin exposure in the etiology of liver cancer in Thailand. A correlation study. 165 55


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