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)

Lymphokine-activated killer activity and natural killer activity in hepatocellular carcinoma patients were assessed. Maximum lymphokine-activated killer activity was induced at 3 to 5 days of incubation, and lymphokine-activated killer activity tended to increase in a manner dose dependent of recombinant interleukin-2. However, the maximum increase of lymphokine-activated killer activity in hepatocellular carcinoma was not as high as that of normal subjects or liver cirrhosis patients. Lymphokine-activated killer activity was impaired in hepatocellular carcinoma as compared to that in normal subjects. Hepatocellular carcinoma seemed to consist of two groups: i.e. a high-lymphokine-activated killer activity group and a low-lymphokine-activated killer activity group. Reduction of natural killer activity was also observed in hepatocellular carcinoma as compared with that in normal subjects and patients with liver cirrhosis. No correlation could be demonstrated between natural killer activity and lymphokine-activated killer activity in normal subjects, liver cirrhosis patients and hepatocellular carcinoma patients. With regard to the presence of HBsAg or alpha-fetoprotein concentration in the sera, there was no significant difference in natural killer and lymphokine-activated killer activity in hepatocellular carcinoma patients. Patients with a small mass lesion showed a low lymphokine-activated killer activity, and depressed lymphokine-activated killer activity was not necessarily related to tumor size. In comparison with the high-lymphokine-activated killer group, the low-lymphokine-activated killer group showed a significant decrease in gamma-interferon production and a preserved function of indocyanine green clearance.
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PMID:Defective function of lymphokine-activated killer cells and natural killer cells in patients with hepatocellular carcinoma. 253 90

Biosynthesis of C1r and C1s subcomponents has been studied using monocytes and macrophages, hepatocytes and hepatoma cell lines or fibroblasts. Both proteins have been detected in supernatants and cell lysates as proenzymic monocatenar molecules. C1r and C1s were secreted by stimulated monocytes and by Hep G2 cells, according to a 1:1 stoichiometry. Monocyte C1s secretion was enhanced by lymphokines, such as alpha- or gamma-interferon or by placental soluble factors. Expression of both proteins was coordinately modulated by a newly purified 14 kDa lymphokine at a pretranslational level. Data from in vitro RNA translation are discussed.
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PMID:Biosynthesis of C1r and C1s subcomponents. 255 84

Therapy for chronic hepatitis B virus (HBV) infection is primarily directed at those patients with evidence of replicative infection because they are most at risk for developing chronic hepatitis, cirrhosis, and possibly hepatocellular carcinoma (HCC). Although a number of agents or therapeutic approaches have been tested against HBV infection, only a few have been subjected to controlled clinical trial. Corticosteroid therapy, particularly if prolonged, may be harmful and should be avoided. Adenine arabinoside monophosphate (Ara-AMP) has potent inhibitory effects on HBV replication, but its use is limited by severe neurotoxicity. At present, prolonged treatment with alpha interferon offers the most promise as a beneficial therapy for chronic type B hepatitis. Alpha interferon consistently induces permanent clearance of hepatitis B e antigen (HBeAg) and HBV DNA from serum more often than in untreated patients. Present efforts are directed at determining the factors predictive of a favorable response to interferon, and attempting to increase the response rate by using alpha interferon in combination with other antiviral or immunomodulatory agents.
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PMID:Treatment of chronic type B hepatitis. 262 Mar 10

Over the 12 years since the first introduction of interferon for the treatment of chronic hepatitis B, progress has apparently been slow. Nevertheless, it now appears that at least one third of chronic hepatitis virus carriers, particularly those with more severe disease, and a similar, perhaps greater, proportion of those with chronic parenteral non-A, non-B hepatitis, can be successfully treated with alpha-interferon. In the not too distant future, controlled trials of alpha-interferons in these situations will be complete and they will be a yardstick by which other future therapies can be judged. Already a number of trials are in progress to determine which agents might, in addition to interferon, augment the response rates. The situation clinically is analogous to that for tuberculosis in the 1950s and for cancer chemotherapy only a decade or so ago. The prospects of prevention of the progression to cirrhosis, and perhaps in the long term reduction in the incidence of hepatocellular carcinoma, are exciting, and with the introduction of a number of new cytokines available through recombinant technology, each with novel antiviral activities, the future prospects are exciting indeed.
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PMID:Treatment of acute and chronic viral hepatitis. 265 45

Immunohistochemical examinations were carried out for the study of cytochrome P-450 implication in the human hepatic disorders. An isozyme of human hepatic P-450 (P-450-HM1) with the m.w. of 51,000 was purified from human autopsied liver. Antibody against P-450-HM1 was prepared in rabbits, of which specificity was confirmed by Western blot. Eighty-three livers (27 autopsies and 56 biopsies, M:F = 63:20), which were either normal or of various hepatic disorders such as acute or chronic hepatitis, cirrhosis and hepatocellular carcinomas, were examined by the method of avidin-biotin-complex technique. It was revealed that immunoreactive hepatocytes were diffused throughout the lobule of the fetal liver. In the normal livers as well as those of acute and chronic hepatitis, positive hepatocytes were found in the centrilobular zone. Three of the 4 cases treated with beta-interferon showed faint staining; and the presence of positive individual hepatocytes was considered to be induced by steroid therapy. In the livers with chronic hepatitis and cirrhosis, hepatocytes near the perifibrous region and those trapped in the portal triad by thin fibrous connective tissue, as well as in the regenerating nodules, were strongly stained, which indicate that P-450-HM1 is expressed in the regenerating hepatocytes. Hepatocellular carcinomas, however, were devoid of immunohistochemistry. From these results, the antibody might be a useful tool for differentiating regenerating nodule from hepatocellular carcinoma.
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PMID:[Clinico-pathological studies of cytochrome P-450 on human hepatic disorders]. 276 18

Cell hybrids between malignant mouse hepatoma cells and normal rat fibroblasts with approximately one set of chromosomes from each parent exhibited remarkable karyotypic stability. Most chromosomes of both parents were retained even after prolonged culture in vitro. Normally, such hybrids showed suppression of the transformed phenotype and formed no colonies in soft agar. However, two hybrids, BS140 and BS181, formed a few colonies in soft agar when many cells were seeded, and also occasional foci of cells were detected piling up in monolayer cell cultures. We isolated soft agar colonies (a-subclones) and sub-clones from foci (h-subclones) of both hybrids, and, as a control, subclones of cells from random areas without foci of one hybrid (BS181 p-subclones). When tested for soft agar growth, cells from the a- and h-subclones of both BS140 and BS181 formed colonies at frequencies comparable to the malignant mouse hepatoma parent, whereas the control cells of the BS181 p-subclones (like the normal rat parental cells) yielded no soft agar colonies. All the cell lines were subjected to detailed karyotype analysis in G-banding, which resulted in the finding that cells from the original BS140 hybrid contained at least one copy of each rat chromosome, whereas BS140 a- and h-subclones had lost both copies of rat chromosome 5. Similarly, the original BS181 hybrid contained at least one copy of each rat chromosome, whereas BS181 a- and h-subclones displayed a deletion of the segment q22-23 of rat chromosome 5. In contrast, the control BS181 p-subclones contained one or two copies of non-deleted rat chromosome 5. The conclusion is that a gene for the suppression of anchorage independence is located in the segment 5q22-23. We propose to call this gene SAI1 (for suppression of anchorage independence). Using Southern blotting, we tested whether any of several gene probes, known to correspond to DNA sequences in rat chromosome 5, were homologous to sequences in the deletion. Only one probe, corresponding to the active alpha1-interferon gene, was shown to be located within the deletion. Hence, the SAI1 gene is closely linked to the alpha 1-interferon gene, and might be identical to this locus.
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PMID:A gene for the suppression of anchorage independence is located in rat chromosome 5 bands q22-23, and the rat alpha-interferon locus maps at the same region. 277 18

The effects of recombinant gamma interferon (rIFN-gamma) were tested on 4 different hepatocellular carcinoma (HCC) cell lines PLC/PRF/5, HepG2, Hep3B and SK-Hep1. Exposure of these HCC cells to 100/ml of rIFN-gamma induced high levels of major histocompatibility complex (MHC) class I expression on their membrane, but not class II antigens. The enhancement of class I antigen synthesis occurs without a corresponding increase in synthesis of HBsAg by HBV genome positive PLC/PRF/5 and Hep3B cells. A 5 log dose of rIFN-gamma also did not trigger the integrated HBV genome into active replication as indicated by a lack of HBcAg and HBeAg synthesis. These results point to a possible role for the use of rIFN-gamma to enhance tumour cell recognition by the host immune system via the increased MHC class I expression.
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PMID:Effect of recombinant gamma interferon on hepatocellular carcinoma cell lines. 283 43

Apolipoprotein CIII (apoCIII) is a major protein constituent of triglyceride-rich lipoproteins and is synthesized primarily in the liver. Cis-acting DNA elements required for liver-specific apoCIII gene transcription were identified with transient expression assays in the human hepatoma (HepG2) and epithelial carcinoma (HeLa) cell lines. In liver cells, 821 nucleotides of the human apoCIII gene 5'-flanking sequence were required for maximum levels of gene expression, while the proximal 110 nucleotides alone were sufficient. No expression was observed in similar studies with HeLa cells. The level of expression was modulated by a combination of positive and negative cis-acting sequences, which interact with distinct sets of proteins from liver and HeLa cell nuclear extracts. The proximal positive regulatory region shares homology with similarly located sequences of other genes strongly expressed in the liver, including alpha 1-antitrypsin and other apolipoprotein genes. The negative regulatory region is strikingly homologous to the human beta-interferon gene regulatory element. The distal positive region shares homology with some viral enhancers and has properties of a tissue-specific enhancer. The regulation of the apoCIII gene is complex but shares features with other genes, suggesting shuffling of regulatory elements as a common mechanism for cell type-specific gene expression.
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PMID:Human apolipoprotein CIII gene expression is regulated by positive and negative cis-acting elements and tissue-specific protein factors. 283 95

Human lymphoblastoid interferon, in an initial dose of 2.5 MU m-2 weekly i.m., was given with mitozantrone 12 mg m-2 i.v. every 3 weeks to 15 patients with hepatocellular carcinoma. The survival curve for these patients was worse than that of 15 patients previously treated with mitozantrone alone; there were more long-term survivors in those not given interferon; more side-effects were seen in the group given interferon. The addition of interferon to mitozantrone in the management of hepatocellular carcinoma is not recommended.
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PMID:Human lymphoblastoid interferon does not increase survival when added to mitozantrone in the treatment of hepatocellular carcinomas. 285 13

In this study, we examined the activity of recombinant interferon (IFN)-gamma against Plasmodium berghei exoerythrocytic forms (EEF) grown in vitro within the highly differentiated human hepatoma cell line HEPG2. We assayed the effect of IFN-gamma on parasite growth by DNA hybridization using a P. berghei specific DNA probe. The specific activity of IFN-gamma against EEF is very high, and depends upon the time of lymphokine addition. When IFN-gamma is added to HEPG2 cells containing intracellular EEF, 6 hr after sporozoite invasion, parasite DNA replication is inhibited by approximately 75% at 10(3) U/ml and 50% at 1 U/ml. This treatment can either abolish or greatly reduce the infectivity of EEF for mice. When added earlier, 3 hr after completion of sporozoite invasion, IFN-gamma inhibits parasite replication to an even greater degree. The highest levels of inhibition were obtained when IFN-gamma was added 6 hr prior to sporozoite invasion (100% inhibition at 10(2) U/ml, approximately 55% inhibition at 0.1 U/ml, and 17% inhibition at 0.001 U/ml). We found that HEPG2 cells express approximately 44,000 surface receptors for IFN-gamma. These data are consistent with the view that IFN-gamma exerts its antimalarial activity by binding to surface receptors on hepatocytes and inducing intracellular changes unfavorable for parasite development. Tryptophan starvation does not appear to be involved in this process. These findings also support the idea that IFN-gamma, released from immune T cells upon encountering sporozoite antigen, may be an important effector mechanism in sterile immunity to sporozoite challenge.
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PMID:Interferon-gamma inhibits the intrahepatocytic development of malaria parasites in vitro. 295 45


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