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)

A cDNA clone, B4-2, was isolated from a natural killer (NK) minus T cell subtractive library. The B4-2 clone coded for an mRNA of 2061 bp in length. It encodes a deduced 327 aa protein with a calculated molecular mass of 35.2 kDa. Searching of B4-2 DNA and protein sequences against various databases revealed no high homology to other sequences. However, B4-2 has an unusually high proline content (13%), contains a putative nuclear targeting sequence, and has several SPXX motifs which are frequently found in gene regulatory proteins. One of the stretches of prolines in B4-2 closely resembles the ligand for proteins with SH3 domains. Northern hybridization data showed that B4-2 is not a lymphoid specific gene and is expressed in a hepatoma cell line and also weakly transcribed or absent in a variety of other cells. A polyclonal antiserum raised against recombinant B4-2 recognizes a 32-34 kDa protein in lymphocytes.
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PMID:Cloning a cDNA from human NK/T cells which codes for a protein with high proline content. 757 50

Hepatitis C can cause a range of hepatic histopathology. The virus may cause an acute hepatitis indistinguishable from any other acute viral hepatitis, but it is more likely to be associated with steatosis, bile duct injury, and portal lymphoid aggregates. Chronic infection with hepatitis C can range from mild nonspecific changes, presumably representing a hepatitis C carrier state, to end-stage liver disease with cirrhosis and hepatocellular carcinoma. Between these are chronic hepatitis of varying severity. Steatosis, portal lymphoid aggregates, and bile duct injury, while not specific, are very characteristic of chronic hepatitis C. Reputed precursors of hepatocellular carcinoma, including liver cell dysplasia and adenomatous hyperplasia, frequently follow the development of cirrhosis and are presumed to predispose to the development of malignancy. New techniques for localizing the virus in liver tissue will undoubtedly lead to greater understanding of the pathogenesis of hepatitis C-related diseases.
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PMID:Histopathology of hepatitis C virus infection. 759 46

Hepatitis C virus (HCV) is the main cause of non-A, non-B hepatitis around the world. It frequently leads to chronic hepatitis which may progress to cirrhosis and hepatocellular carcinoma (HCC). Characteristic, although not pathognomonic, histologic changes in chronic hepatitis C include bile duct damage and lymphoid aggregates in portal tracts. Hepatocyte and bile duct injury seem to be mediated by both a direct cytopathic effect of HCV and immune mechanisms, perhaps triggered by HCV. Most HCC are related to HCV, HBV, or both. HCV appears to persist and replicate in hepatocytes during malignant transformation, but it is not clear whether the virus plays a direct or indirect role in hepatocarcinogenesis.
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PMID:Pathobiologic effects of hepatitis C. 760 83

25 Amaryllidaceae alkaloids belonging to different skeletal types were evaluated for their cytotoxic activity against one murine non-tumoral cell line (LMTK) and two human tumoral cell lines (Molt4 and HepG2) according to established protocols. Significant differences of activity related with the type of skeleton of the tested alkaloids could be observed. Pretazettine (22) was among the most active compound among the 25 tested alkaloids on the Molt4 lymphoid cells, but was inactive against HepG2 hepatoma. On the other hand, lycorenine (11) was found to be the most cytotoxic compound against HepG2 hepatoma, even though it appears to be active against Molt4 cells. Almost all of the tested alkaloids showed cytotoxic activity against fibroblastic LMTK cells. Only mesembrenone (25) showed some specificity against Molt4 cells in comparison to LMTK cells.
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PMID:Cytotoxic activity of Amaryllidaceae alkaloids. 770 Oct

Hepatitis C is usually poorly symptomatic, particularly in the acute phase. After an incubation period ranging from 5 to 12 weeks, the symptoms are nonspecific and icterus is rarely present. Laboratory results are more suggestive, showing characteristic fluctuations in transaminases comprising periods with normal values. Chronic hepatitis is probable when elevation of transaminases persists for more than 6 months. Chronic virus C hepatitis is usually asymptomatic. Clinical manifestations are poorly specific and transaminase concentrations are generally little increased and variable in over 75% of the cases. Some histological lesions are more often observed in the chronic stage, particularly steatosis, presence of intraportal lymphoid nodules and bile duct involvement. The natural history is dominated by the risk of development to cirrhosis and hepatocellular carcinoma. A course to chronic hepatitis C is observed in 20 to 70% of cases, while the risk of developing cirrhosis is between 10 and 38% within approximately 20 years. Prognosis is then linked to decompensation of cirrhosis and especially to the development of hepatocellular carcinoma, within approximately 10 years after appearance of cirrhosis, with a prevalence of at least 20%. The association of other factors such a hepatitis B virus or alcohol can accelerate this course.
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PMID:[Hepatitis C]. 772 19

We developed transgenic rabbits with a DNA construct containing the proto-oncogene c-myc conjugated to the Ig kappa-chain enhancer gene, E kappa. One of four transgenic rabbits was mated to a normal rabbit and we used the offspring to develop a colony of rabbits carrying the E kappa-myc transgene in their germline. Of a total of 19 E kappa-myc transgenic rabbits, eight developed tumors. The tumors were characterized histologically and four were diagnosed as lymphoma, and one each was diagnosed as embryonic carcinoma, hepatoma, ovarian carcinoma and basal cell carcinoma. By Southern analysis, we showed the four lymphomas were of B-lymphoid lineage and by nucleotide sequence analysis we found three of them most likely used VH1 in their VDJ gene rearrangements. Cells from the embryonic carcinoma, the hepatoma and two of the B-lymphomas were adapted to tissue culture. We discuss the possibility that tumors of non-lymphoid origin develop in the E kappa-myc transgenic rabbits because of the potential for NF-kappa B to activate the kappa-enhancer in cells other than B-lymphoid lineage cells.
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PMID:Lymphoid and non-lymphoid tumors in E kappa-myc transgenic rabbits. 780 3

We recently identified a gene that is induced by lymphocyte activation (ILA). The sequence of the full-length 1.4-kb cDNA characterized ILA as a new member of the nerve growth factor/tumor necrosis factor (NGF/TNF) receptor family and the human homologue of the murine T-cell-specific receptor 4-1BB. The present study demonstrates ILA mRNA isoforms at 4.4, 4.0, and 1.8 kb in poly-A+ RNA from activated, but not from resting human peripheral blood T lymphocytes. A reverse transcriptase-polymerase chain reaction (RT-PCR) assay was used to study tissue distribution and regulation of ILA expression. The gene was induced in T lymphocytes by phytohemagglutinin (PHA), phorbol myristate acetate (PMA), and antibody to CD3, in B lymphocytes by PMA and antibodies to cell surface Ig, and in blood monocytes by interleukin-1 beta (IL-1 beta), lipopolysaccharide (LPS), and PMA. In T lymphocytes, ILA mRNA was detectable 1.5 hours after stimulation, reached maximal levels at 8 hours, and declined to background levels by 48 hours. Induction of ILA mRNA required protein synthesis and was primarily due to increased transcription. Actinomycin D reduced ILA mRNA levels in activated lymphocytes 50% within 30 minutes, demonstrating a relatively short half-life of this mRNA. Analysis of nonlymphoid cells showed that ILA mRNA was not detectable in resting cells. However, in contrast to the lymphoid-specific expression of the murine 4-1BB gene, ILA was detected in nonlymphoid cells, including epithelial and hepatoma cells after stimulation with IL-1 beta. ILA was not detectable in several brain derived cell lines. The ILA cDNA encodes a 30-kD protein as demonstrated by in vitro translation, and this protein is immunoprecipitated by antisera that were raised against ILA peptides or a glutathione-S-transferase fusion protein. Flow cytometry showed expression of ILA protein on a subset of activated T or B lymphocytes. In conclusion, activation-dependent expression of ILA is found not only in T lymphocytes, but also in B lymphocytes, monocytes, and diverse nonlymphoid cell types.
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PMID:ILA, the human 4-1BB homologue, is inducible in lymphoid and other cell lineages. 784 93

The human MDR3 (or MDR2) P-glycoprotein is probably involved in the transport of phospholipids from liver hepatocytes into bile (Smit et al. (1993) Cell 75, 451-462). In accordance with this function, MDR3 is highly expressed in human liver, but lower mRNA levels were also found in adrenal, heart, muscle and cells of the B-cell compartment. We have cloned and analyzed the MDR3 promoter region. It is GC-rich, and contains neither a TATA nor a CAAT box, but it does contain multiple putative SP1 binding sites, features also found in so-called housekeeping genes. RNase protection and primer extension analyses indicate that the MDR3 gene has multiple transcription start sites in a GC-rich region with considerable homology to the putative mouse mdr2 promoter. A 3 kb genomic fragment containing the MDR3 start sites directs transcription of a chloramphenicol acetyltransferase (CAT) reporter gene upon transient transfection in the human hepatoma cell line HepG2. This transcription is orientation dependent, and stimulated by a SV40 enhancer, indicating that the 3 kb insert contains the core promoter elements of the MDR3 gene. The promoter region contains several consensus sequences where known or putative liver-specific (C/EBP, HNF5) or lymphoid specific (Pu.1, ets-1) transcription factors may bind.
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PMID:Characterization of the promoter region of the human MDR3 P-glycoprotein gene. 789 60

The present study undertook to investigate the biological significance of human leucocyte antigen expression in hepatocellular carcinoma and to elucidate the role of potential modulating agents on human leucocyte antigen expression. These studies used several hepatic tumour-derived cell lines as in vitro model systems. The cell lines included PLC/PRF/5 (Alexander cell line), Hep3B, HepG2, TONG PHC, HA22T/VGH, HA59T/VGH and Mahlavu. The cell lines K562 and Raji were used as negative and positive controls, respectively. K562, a B lymphoid-derived cell line, was shown to express negligible amounts of human leucocyte antigens, while Raji, an erythromyeloid-derived cell line, expressed both class I and class II human leucocyte antigens as well as their respective invariant chains, beta 2-microglobulin and Ii. Using an ELISA, experiments performed on these cell lines confirmed the natural expression of class I and class II antigens by the HA22T/VGH and HA59T/VGH cell lines, whereas PLC/PRF/5 displayed class II surface antigens only. The effects of modulating agents such as interferon-gamma sodium butyrate and clofazimine on human leucocyte antigen expression were investigated using the HA22T/VGH, HA59T/VGH and TONG PHC cell lines. These agents increased class II and class II human leucocyte antigen expression on HA22T/VGH and TONG PHC cells, but had no effect on the HA59T/VGH cell line. The results suggest a potential use for these agents as modulators of human leucocyte antigen expression by human heptocellular cell lines.
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PMID:HLA expression in hepatocellular carcinoma cell lines. 805 Jan 84

Hepatitis C virus (HCV) frequently leads to chronic hepatitis, cirrhosis, and hepatocellular carcinoma, but the mechanism of liver injury is unknown. To determine whether replication of HCV is related to liver damage, we studied 17 liver biopsy specimens (six anti-HCV-positive chronic persistent hepatitis specimens, seven anti-HCV-positive chronic active hepatitis specimens, and four anti-HCV-negative controls) by reverse transcription followed by double polymerase chain reaction for the 5' nontranslated regions of the genomic and replicative strands of HCV. The histologic activity index as well as lymphoid aggregates in portal tracts, bile duct damage, and fatty change were assessed semiquantitatively. There was a statistically significant correlation between the presence of HCV RNA sequences in liver tissue and anti-HCV antibody in serum (P < .005). No correlation was detected between the histologic activity index or any individual histologic parameters and the presence of genomic or replicative strands of HCV. These findings suggest that a direct viropathic effect is less important than other mechanisms, such as the host immune response, in the pathogenesis of hepatocyte and bile duct injury in chronic hepatitis.
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PMID:Genomic and replicative hepatitis C virus RNA sequences and histologic activity in chronic hepatitis C. 811 15


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