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)

Tissue factor (TF) is a lipoprotein cofactor that markedly enhances the proteolytic activation of factors IX and X by factor VIIa. The functional activity of TF is inhibited by serum in a time- and temperature-dependent fashion. The inhibitory effect is also dependent on the presence of calcium ions and can be reversed by calcium chelation (EDTA) and dilution, thus excluding direct proteolytic destruction of TF as the mechanism for inhibition. Using crude TF, serum immunodepleted of factor VII, and serum depleted of the vitamin K-dependent coagulation factors by BaSO4 absorption, it is shown that TF factor inhibition requires the presence of VII(a), X(a), and an additional moiety contained in barium-absorbed serum. When each of the other required components were at saturating concentrations, half-maximal inhibition of TF occurred in reaction mixtures containing 2% (vol/vol) of TF at a factor VII(a) concentration of 4 ng/mL (80 pmol/L), a factor X concentration of 50 ng/mL (850 pmol/L), and a concentration of barium-absorbed serum of 2.5% (vol/vol). Catalytically active factor Xa appeared to be required for the generation of optimal TF inhibition. The results are consistent with the conclusions of Hjort that barium-absorbed serum contains a moiety that inhibits the VIIa-Ca2+-TF complex. The role of factor X(a) in the generation of the inhibitory phenomenon remains to be elucidated. The inhibitor present in serum (plasma) may in part be produced by the liver in vivo since cultured human hepatoma cells (HepG2) secrete this inhibitory activity in vitro.
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PMID:Characterization of the inhibition of tissue factor in serum. 302 56

A 31-yr-old man, who had received left hepatic lobectomy for a ruptured hepatocellular carcinoma 17 months previously, began to have elevation of serum alpha-fetoprotein and occult gastrointestinal bleeding. Abdominal computed tomography, angiography, ultrasonography, upper gastrointestinal panendoscopy, colon-fiberscopy and endoscopic retrograde cholangiopancreaticography failed to disclose any recurrent intrahepatic tumor or bleeder in the gastrointestinal tract. However, a barium meal study revealed an intussusception with a suspicious nodular lesion in the proximal jejunum as the leading edge, which, after laparotomy, was proven to be a metastatic hepatocellular carcinoma and the cause of the gastrointestinal bleeding. The serosal side of this lesion was free from cancer involvement and there was no peritoneal implantation or lymph node involvement. The metastasis is probably hematogenous. The extremely unusual location involved by hepatocellular carcinoma in this patient signifies the ubiquitous nature of metastasis in this cancer.
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PMID:Metastasis of hepatocellular carcinoma to the proximal jejunum manifested by occult gastrointestinal bleeding. 302 29

The gene for the iron-binding protein transferrin is transcribed at a high level in liver hepatocytes but is also active in several other cell types, including oligodendrocytes in the brain. Enhancer elements between bp -560 and -44 of the transferrin gene promoter specifically activated transcription from a heterologous promoter in transgenic mouse liver and brain. Within this region, a potent cis-acting element between bp -98 and -83 was found to be essential for gene activity in both cultured hepatocytes and transgenic mouse liver. The -98 to -83 element contains a CCAAT sequence and is specifically bound by a nuclear factor from mouse liver that is homologous to rat liver C/EBP (CAAT enhancer-binding protein). Point mutations within this binding site inhibit factor binding and abolish transcription in transfected hepatoma cells. When placed in the context of the 3,000-bp transferrin promoter, the C/EBP binding site mutation causes a complete loss of transcription in transgenic mouse liver; however, transgene expression in the brain of the same animals was unaffected. These results suggest a modular structure for the transferrin promoter and demonstrate that deletions or specific point mutations can be used to generate transgene promoters with an activity more restricted than that of their endogenous counterparts.
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PMID:A C/EBP-binding site in the transferrin promoter is essential for expression in the liver but not the brain of transgenic mice. 824 83

We have purified the DNA binding protein E1BF (Enhancer 1 Binding Factor) from the nuclei of Morris hepatoma 3924A. This protein, which consists of two polypeptides of 72 kDa and 85 kDa, binds to several DNA sequences involved in the regulation of rDNA transcription. UV-crosslinking studies show that interaction of the protein with DNA is primarily through the 72 kDa polypeptide. Purified E1BF can also modulate pol I-directed transcription in a cell-free systems derived from rat and mouse. E1BF is related to the human autoantigen Ku as demonstrated by immunological cross-reactivity with monoclonal antibodies directed against Ku p70 in Western blot and gel mobility shift assays.
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PMID:Characterization of the factor E1BF from a rat hepatoma that modulates ribosomal RNA gene transcription and its relationship to the human Ku autoantigen. 843 24

The authors describe an extremely rare case of extrahepatic hepatocellular carcinoma. The patient was a 70-year-old man who was examined by a local doctor because of abdominal discomfort. Barium meal examination demonstrated a defect occupying the lesser curvature of the stomach from the middle of the corpus to the fornix. On an abdominal computed tomography (CT) scan, the lesion, 10 cm in diameter, touched the lower surface of the caudate lobe of the liver. Under laparotomy, the tumor was found between the caudate lobe of the liver and posterior wall of the gastric corpus. As the tumor appeared to be connected with the caudate lobe by a pedicle, only the tumor was resected. Histological examination showed the tumor to be hepatocellular carcinoma of Edmondson's grade III-IV, pedunculated type.
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PMID:Hepatocellular carcinoma presenting as extrahepatic mass on computed tomography. 908 79

Oesophageal carcinoma is a major cause of cancer death in certain parts of the world. Early detection provides the only chance of cure. In this study, one female and nine male patients with superficial oesophageal carcinoma were investigated to determine the pertinent clinical and pathological features. All male patients were smokers and six patients drank various amounts of alcohol on a daily basis. Histologically, five cases were confined within the mucosal layer and five within the submucosal layer. All five mucosal cancer cases and two of the five submucosal cancer cases were asymptomatic. Endoscopically, all five mucosal cancer patients had flat lesions, whereas the five submucosal cancer tumours appeared either protruding or depressed. Barium oesophagography failed to demonstrate the lesions in four of five mucosal cancer and one of five submucosal cancer cases. Endoscopic ultrasonography correctly detected the depth of cancer invasion in six out of eight superficial oesophageal carcinoma cases. All patients received a one-stage operation that included oesophagectomy and lymph node dissection. All five mucosal cancer patients had no lymph node involvement and have experienced no tumour recurrence. Among them, one who had concomitant hepatocellular carcinoma died early. Of the five submucosal cancer cases, four died 1-5 years after the operation. It is concluded that oesophageal carcinoma is curable in its early stage. Physicians should be alert while performing endoscopic examination. We believe that the dyeing technique is a useful adjunct to endoscopic examination.
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PMID:Diagnosis and treatment of superficial oesophageal carcinoma. 950 85

Enhancer II (ENII) of hepatitis B virus (HBV) is one of the essential cis-elements for the transcriptional regulation of HBV gene expression. Its function is highly liver-specific, suggesting that liver-enriched transcriptional factors play critical roles in regulating the activity of ENII. In this report, a novel hepatocyte transcription factor, which binds specifically to the B1 region (AACGACCGACCTTGAG) within the major functional unit (B unit) of ENII, has been cloned from a human liver cDNA library by yeast one-hybrid screening, and demonstrated to trans-activate ENII via the B1 region. We named this factor hB1F, for human B1-binding factor. Amino acid analysis revealed this factor structurally belongs to nuclear receptor superfamily. Based on the sequence similarities, hB1F is characterized to be a novel human homolog of the orphan receptor fushi tarazu factor I (FTZ-F1). Using reverse transcription-polymerase chain reaction, a splicing isoform of hB1F (hB1F-2) was identified, which has an extra 46 amino acid residues in the A/B region. Examination of the tissue distribution has revealed an abundant 5.2-kilobase transcript of hB1F is present specifically in human pancreas and liver. Interestingly, an additional transcript of 3.8 kilobases was found to be present in hepatoma cells HepG2. Fluorescent in situ hybridization has mapped the gene locus of hB1F to the region q31-32.1 of human chromosome 1. Altogether, this study provides the first report that a novel human homolog of FTZ-F1 binds and regulates ENII of HBV. The potential roles of this FTZ-F1 homolog in tissue-specific gene regulation, in embryonic development, as well as in liver carcinogenesis are discussed.
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PMID:Cloning and characterization of a novel human hepatocyte transcription factor, hB1F, which binds and activates enhancer II of hepatitis B virus. 978 8

An 82-year-old black woman with a history of hepatocellular carcinoma presented with gastrointestinal bleeding. Barium enema and fibrocolonoscopy revealed a 4-cm polypoid mass at the level of the ascending colon with evidence of active bleeding. Biopsies of the lesion proved it to be metastatic hepatocellular carcinoma. Exploratory laparotomy revealed no further dissemination of the tumor, and the patient underwent an ileocolectomy. The serosal side of the colonic lesion was free from tumor, and there was no peritoneal implantation, direct extension, or lymph node involvement. This case represents an extremely rare presentation of metastatic hepatocellular carcinoma.
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PMID:Metastasis of hepatocellular carcinoma to the right colon manifested by gastrointestinal bleeding. 1007 95

We have previously observed that all human hepatocellular carcinomas (HCCs) from HBV carriers examined had the integrated X region. In this study, HBV DNA was isolated from an integration site in one HCC that had a single, very small integrated viral DNA including the X region, but it had no expression of X gene as poly(A)RNA. It was found that HBV DNA was present between alphoid repetitive sequences, and it included Enhancer and X regions, encompassing the adr sequence from 910 to 1811. Nucleotides for 8 amino acids at the 3' end, a stop codon of X gene and a poly(A) signal downstream of X gene were lost by integration, and nucleotides for 7 amino acids and a stop codon were substituted by a connected alphoid sequence. When this cloned HBV DNA was transfected with an expression vector to an immortalized mouse liver epithelial cell line, MLE-10, malignant transformation occurred. Transformants having expressed poly(A)RNA of the X gene showed anchorage-independent growth in soft agar and tumor formation in the subcutis of nude mice. The mRNA level of EGFR was found to be remarkably enhanced in X-transformed cells, in contrast with the absence of this mRNA in parental and ras-transformed MLE-10. Our data provide evidence that the Enhancer-X region alone is the key contributor to the malignant change of pre-malignant liver cells in HBV carriers through activation of some specific genes, such as EGFR.
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PMID:Malignant transformation and EGFR activation of immortalized mouse liver epithelial cells caused by HBV enhancer-X from a human hepatocellular carcinoma. 1069 24

The type I interferons (IFNs) are a group of closely related cytokines which have different signal transduction pathways and different biological activities. Using transient transfection of human hepatoma cells with reporter plasmids containing the firefly/renilla luciferase genes under the control of the HBV-Enhancer (Enh) I, Enh II and core promoter we have investigated the biological activities of 10 recombinant (r) type I IFNs on transcription. Low concentrations of IFN (0.025 ng/ml) had a significant and specific inhibitory effect but the potencies of the different recombinant type I IFNs differed markedly with IFNalpha8 and IFNbeta being six-fold more potent than the least effective subtype (IFNalpha1). However, the addition of IFNalpha5-the subtype produced predominantly in the human liver-did not cause any synergistic effects.The non-natural consensus IFN displayed a more pronounced inhibition of HBV-regulated transcription than IFNalpha8 or IFNalpha2 but not IFNbeta. The INF-induced inhibitory effect was not dependent on the presence of the HBV-Enh1 and in particular of an interferon stimulated response element (ISRE)-like sequence. The characterization of different effects among type I interferons on HBV-regulatory elements may implicate an IFN-subtype-specific role for the pathogenesis and treatment of HBV-infection.
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PMID:Different activities of type I interferons on hepatitis B virus core promoter regulated transcription. 1199 74


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