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)

The ability of confluent monolayers of H-35 cells, originally obtained from a rat hepatoma, to synthesize prothrombin in response to vitamin K1 (phylloquinone) was studied. As demonstrated by radioimmunoassay, selective barium salt adsorption, and two coagulation assays which discriminate between precursor- and mature-prothrombin, these cells retained their ability to synthesize precursor prothrombin (preprothrombin) in the absence of exogenous phylloquinone (vitamin K). When phylloquinone was added to the medium (100 ng/ml), the existing intracellular concentration of preprothrombin was reduced to 50% within 1 hr after exposure to the vitamin and slowly declined thereafter to approximately 30% of control levels by 36 hr. Concomitant with the rapid loss of intracellular preprothrombin was the appearance of mature prothrombin in the medium. The appearance of prothrombin was biphasic: occurring during the initial 0-6 hr interval, and again at an increased rate during the next 18-24 hr interval. The amount of prothrombin appearing in the medium exceeded by severalfold the amount of precursor mobilized. These data demonstrate that monolayer cultures of H-35 hepatoma cells retain their ability to synthesize preprothrombin and other enzymes, responsible for post-translational modification of prothrombin and its subsequent secretion, under the influence of vitamin K.
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PMID:Vitamin K-dependent synthesis and modification of precursor prothrombin in cultured H-35 hepatoma cells. 18 12

Two regions of the hepatitis B virus (HBV) genome have been shown to display properties of a transcriptional enhancer. Enhancer 1 is active in most hepatoma lines examined as well as in some non-hepatocyte-derived cell lines. In contrast, enhancer 2 activity is strictly liver specific. In this study, we show that adenovirus E1A expression in the highly differentiated human hepatoma line Huh6 strongly inhibits HBV enhancer 2-stimulated transcription while having no effect on HBV enhancer 1 activity. A sequence motif in HBV enhancer 2 which is essential for its enhancer function is the target for E1A-mediated repression. The repression of HBV enhancer 2 activity is mediated through the N-terminal region of the E1A proteins known to bind a 300-kDa cellular protein. Our results suggest that HBV enhancer function may be modulated by a cellular mechanism similar to E1A-mediated transcriptional repression.
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PMID:Repression of liver-specific hepatitis B virus enhancer 2 activity by adenovirus E1A proteins. 133 30

Thirty two human livers were removed at autopsy. These included 7 with space-occupying or tumour-like lesions, namely one with multiple cysts, three with haemangiomas, a lobated liver with multiple nodules of focal nodular hyperplasia, one with a metastasis which also had a small haemangioma and one with a hepatocellular carcinoma. Fine particle barium diluted 2:1 with water was injected by hand to fill the arterial system. In the lobated liver, the portal system was also filled. High definition radiographs of liver slices showed arteriographic detail not visible on angiography. The arteriographic appearances were correlated with the macroscopic and microscopic pathology. Liver cysts compress the arteries and arterioles but an apparent halo on the whole liver radiograph was shown to be spurious on a 1 cm thick high definition film. The small vessel pattern of haemangiomas is well demonstrated accounting for the hyperechoic sonograms but hypoechoic areas may also occur due to involution of or haemorrhage into tumours. The small lesions of focal nodular hyperplasia had a poor arterial supply but filled from a portal venous injection. Metastases had a peripheral network of small vessels, central necrosis and normal sized peripheral arteries with no large artery entering the tumour. In hepatocellular carcinoma, a large artery was demonstrated entering the tumour which was considerably more vascular than the metastases. These features should aid in distinguishing these lesions on sonography.
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PMID:Radiological-pathological correlation of mass lesions in the liver. 166 81

Enhancer/promoter elements from two pancreas-specific genes, those encoding amylase and elastase, were ligated to the bacterial GPT gene. The resulting construct can be used to select for expression of gene products which activate these pancreas-specific promoters in hybrid cells. The selectable GPT construct was stably transferred into several cell lines either directly or by cotransfection with pSV2Neo. GPT was expressed when transferred to pancreatic cell lines but not when transferred to GPT-fibroblast (L) cells or hepatoma cells. When the transformed L cells and hepatoma cells were fused with pancreatic cell lines, GPT was activated in the hybrid cells. Endogenous pancreas-specific genes from the L-cell and hepatoma parents were also activated in the hybrids. In addition, a pancreas-specific nuclear protein, PTF1, was produced in pancreatic and hybrid cells, correlating with GPT expression. The transformed L cells and hepatoma cells thus contained a nonexpressed construct which could be activated in trans by factors present in pancreatic cells. The hepatoma hybrid also continued to produce albumin, demonstrating the coexpression of liver and pancreas-specific genes in the hybrid-cell population. Cell lines carrying the amylase/elastase/GPT construct may be useful as a selection system for cloning of pancreatic transcription activators.
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PMID:Transactivation of pancreas-specific gene sequences in somatic cell hybrids. 171 19

The extracellular matrix (ECM) promotes tissue morphogenesis, cell migration, and the differentiation of a variety of cell types. However, the mechanisms by which ECM causes differentiated gene expression have been unknown. In this report, we show that culturing the hepatocyte-derived cell line H2.35 on an ECM gel changes cell morphology and selectively stimulates the transcription of a subset of liver-specific genes, including serum albumin. Transcriptional activation by ECM also occurs with transfected plasmids bearing the transcriptional enhancer of the albumin gene. ECM substrates of different composition activated the albumin enhancer only when the ECM promoted a cuboidal, differentiated cell morphology. Enhancer activation by the ECM was mediated by two liver transcription factors, HNF3 alpha and eH-TF, which appear to be regulated differently by matrix. Specifically, we found that a collagen gel substratum caused a selective increase in the factor HNF3 alpha at the levels of mRNA accumulation and DNA-binding activity in nuclear extracts, both in H2.35 cells and in the hepatoma cell line HepG2. We conclude that the ECM can stimulate cell differentiation by selectively activating transcriptional regulatory factors and that such regulation occurs coordinately with ECM-promoted changes in cell shape.
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PMID:The extracellular matrix coordinately modulates liver transcription factors and hepatocyte morphology. 187 30

Twenty-five autopsy livers were studied for intrahepatic arterial anastomoses. Under fluoroscopy, barium suspension at various concentrations, with or without latex, was injected into the hepatic artery. One-centimeter axial or coronal liver sections were radiographed with high-resolution mammographic technique. All films were reviewed. Seven interconnecting arterial pathways were demonstrated: subcapsular and peripheral arcades, proximal and intermediate connecting vessels, periportal arterial rete and ring, a fine parenchymal network, and connections with the gallbladder arterial system. In the six cases where a branch artery was occluded, arterial filling of the entire liver was demonstrated. The authors conclude that these interconnecting networks could account for the infrequency of hepatic infarcts, are the anatomic basis for the intrahepatic spread of malignant lesions, the "duplication" and "triplication" patterns on arteriography, and may account for the outer streaks of the arteriographic "thread and streak" sign in portal vein invaded by hepatocellular carcinoma.
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PMID:Are the hepatic arteries "end arteries"? 203 21

Sensitivity to phenylephrine, isoproterenol, serotonin, oxytocin, acetylcholine and barium chloride of vas deferens uterus und fundus strip was studied comparatively in hepatectomized and sarcoma-45, sarcoma-M1, Walker carcinosarcoma and Zajdela ascites hepatoma bearing rats. The contractile response to monoamines and oxytocin was considerably lower or absent at certain periods after hepatectomy or tumour grafting. Effects of biogenic amine antagonists were also substantially altered. The response to isoproterenol, acetylcholine and barium chloride remained unchanged. Apparently a selective alteration of a response of visceral smooth muscles mediated through alpha-adrenergic and D-serotonin receptors occurred not only during the tumour growth but also in the case of active (extensive) proliferation of the normal tissue.
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PMID:[The monoaminergic receptors of the internal organs in rats with a tumor and after partial hepatectomy]. 217 98

A 64-year-old male, who had been diagnosed as having hepatocellular carcinoma, was admitted to hospital and underwent transcatheter arterial infusion therapy. CT and US examinations revealed a large tumor with air in its center. Barium meal examination of the duodenum showed a large filling defect with a central excavation. At endoscopic examination, a dark reddish tumor was seen protruding into the duodenal lumen. A biopsy specimen from this tumor revealed a hepatocellular carcinoma. The patient subsequently died of hepatic coma following gastrointestinal bleeding. An autopsy revealed that metastatic lymph nodes had infiltrated into the adjacent duodenum. Nine previous cases of duodenal metastasis from a hepatocellular carcinoma have been reported in the Japanese literature.
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PMID:[A case of hepatocellular carcinoma with a duodenal invasion from metastatic lymph node]. 254 41

Several murine monoclonal anti-human Factor VII antibodies were produced using hybridoma technology. Two noncompetitive monoclonal antibodies were used to examine by Western blotting the Factor VII cross-reactive material (CRM) in normal human plasma and three commercially available congenitally Factor VII-deficient plasmas, and to construct a facile "sandwich" immunoassay for plasma Factor VII. A second, previously undescribed, form of Factor VII CRM was detected in human plasma, which on Western blotting stained with an apparent intensity 5-8% that of Factor VII. This glycoprotein, tentatively called VII*, has a molecular weight 4,500 D less than Factor VII, lacks detectable Factor VII functional activity, does not bind to barium citrate, and is not recognized by a monoclonal antibody that recognizes Factor VII but not alpha-chymotrypsin-treated Factor VII. VII* was not proteolytically produced from Factor VII during in vitro coagulation or after infusion of human Factor VII into rabbits. As determined by Western blotting, the human hepatoma cell line, HepG2, cultured in the presence of vitamin K, secreted relatively greater levels of VII* in proportion to VII (75%) than that found in human plasma. Warfarin treatment of HepG2 cells decreased the quantity of VII secreted by 77%, whereas it only inhibited the secretion of VII* by 14%. Immunologic studies of the plasmas from a patient on chronic warfarin therapy and an individual given a short course of high dose warfarin therapy corroborated the in vitro synthetic studies obtained with HepG2 cells. The data are consistent with the production of VII* by posttranslational, proteolytic, modification of VII, that, at least in the HepG2 cells studied, occurs intracellularly. However, other mechanisms for the production of VII*, in particular, alternative RNA splicing of the transcript from a single gene, cannot be excluded.
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PMID:Monoclonal anti-human factor VII antibodies. Detection in plasma of a second protein antigenically and genetically related to factor VII. 299 51

A 70 year old man complaining of abdominal pain was admitted to our hospital and was suspected to have a gastric cancer with perforation by barium meal X-ray and by endoscopy. Ten days before, admission X-ray examination revealed the free air in the abdominal cavity but this patient didn't complain of any sign of peritonitis. He underwent left upper abdominal evisceration through upper median incision and median sternophrenicotomy. Resected specimen of the stomach had giant ulcer which looked like the gastric cancer. The pathological diagnosis of this lesion was liver cell carcinoma, Edmondson's grade 4, metastasis from the liver with lymph nodes and pancreatic involvement.
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PMID:[A case of gastric perforation due to invasive liver cell carcinoma to the stomach]. 301 75


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