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 incorporation of lysophosphatidylcholine into biological membranes and its effect on some membrane-bound enzymes of mitochondria and microsomes from rat liver and hepatoma were studied. It was shown that in the presence of lipid-exchange proteins of the liver a far greater amount of lysophosphatidylcholine is incorporated into the membranes than in the-iv absence. The increase of the lysophosphatidylcholine content in the membranes has no effect on the activity of mitochondrial monoamine oxidase, inhibits the activity of microsomal cytochrome P-450 and activates glucose-6-phosphatase.
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PMID:[New method of lysophospholipid incorporation into biological membranes. Effect of lysophosphatidylcholine on the activity of membrane-bound enzymes]. 626 66

Out of 56 thioacetamide (TAA)-fed rats hepatocellular carcinoma were found in four instances after 300, 360, 450 and 495 days in the present experiment. Of the four tumours, two showed lung metastasis. The size of TAA-treated hepatocyte nucleoli increased greatly after several weeks of feeding. Two enzymes, succinate dehydrogenase and glucose-6-phosphatase were found in both cytoplasma and nucleoli of hepatocytes of which nucleolar localizations are quite new. In hepatocellular carcinoma, malignant cells lost glucose-6-phosphatase activity completely in cytoplasm and nucleoli though succinate dehydrogenase activity was present in these organelles.
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PMID:Thioacetamide-induced hepatocarcinoma in rat. 626 62

The correlation between the cytochemistry (glycoprotein, glycogen, glucose-6-phosphatase, catalase, alkaline phosphatase) and the growth rate of the fast-growing Morris hepatoma 3924A and the slow-growing Morris hepatoma 9618A was studied by utracytochemical techniques. By the chromic acid-phosphotungstic acid technique, acid glycoprotein is stained in glycocalyx, Golgi saccules and vesicles, and secretory granules of the tumor cells of both hepatomas. However, the hepatoma 3924A cells contain thicker glycocalyx and more numerous glycoprotein-rich granules than hepatoma 9618A cells. Abundant alpha and beta glycogen particles are found in hepatoma 3924A. Moderate glucose-6-phosphatase activity is observed in the cisternae of endoplasmic reticulum and nuclear envelope of hepatoma 9618A, but it is totally absent in hepatoma 3924A. High catalase activity is present in numerous peroxisomes of hepatoma 9618A. Hepatoma 3924A contains only a few catalase-positive microperoxisomes. Weak to moderate alkaline phosphatase is present in the plasma membrane and nuclear envelope of hepatoma 9618A cells, while hepatoma 3924A shows no activity of the enzyme. All the cytochemical parameters except glycoprotein show an inverse relationship with the growth rate of the hepatomas. The higher intracellular glycoprotein content of hepatoma 3924A may be related to differences in cell coat secretion (composition and activity) from the slower-growing hepatoma 9618A
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PMID:Correlation between growth rate and cytochemistry in Morris hepatomas. 627 86

Liver cells obtained from newborn mice homozygous for any one of several overlapping deletions in chromosome 7 fail to express a number of liver-specific differentiated traits. Among these is the activity of the membrane-bound liver-specific enzyme glucose-6-phosphatase (Glc-6-Pase; D-glucose-6-phosphate phosphohydrolase, EC 3.1.3.9). Previous studies have led to the suggestion that the region of the genome covered by these deletions includes genes that normally regulate the expression of structural genes encoding liver-specific enzymes and proteins mapping elsewhere in the genome. To find out whether the deficiency of Glc-6-Pase may be caused by the deletion of the relevant structural gene, mouse liver cells homozygous for the deletion c14CoS were hybridized with 2S Faza rat hepatoma cells, and the hybrid cell cultures were analyzed for mouse and rat Glc-6-Pase activity. Hybrids showed expression of mouse Glc-6-Pase activity, proving that the structural gene for this enzyme is not included in the deletion c14CoS in chromosome 7. In the hybrid cells the rat hepatoma genome apparently contributes a factor that activates the structural gene of the mouse and corrects its failure of expression, which most likely resulted from the deletion of an essential regulatory or processing gene. By using as a marker glucose-6-phosphate isomerase (Glc-6-PIase; glucosephosphate isomerase, D-glucose-6-phosphate ketolisomerase, EC 5.3.1.9), known to map on chromosome 7, this entire chromosome could be excluded as a possible carrier of the Glc-6-Pase structural gene. In addition, the structural genes for Glc-6-Pase and for tyrosine aminotransferase (TyrATase; L-tyrosine:2-oxoglutarate aminotransferase, EC 2.6.1.5), another enzyme deficient in lethal deletion homozygotes, were shown to map on two different chromosomes. Together with our previous studies of TyrATase gene regulation, the present experiments suggest that the region of the mouse genome defined by the deletions includes one or more genes regulating the expression of several structural genes that map on different chromosomes and that encode liver-cell-type specific traits.
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PMID:Correction of a genetically caused enzyme defect by somatic cell hybridization. 657 48

Basophilic hepatic foci, nodules, and trabecular hepatocellular carcinomas, collectively referred to as focal hepatic lesions, were induced by single injections of 5.0 micrograms of diethylnitrosamine (DEN) per gram body weight in 15-day-old C57BL/6J X C3HeB/FeJ F1 (B6C3 F1) mice. Groups of eight experimental and eight control mice were killed at 3 days and at 1, 2, 4, 10, 20, 28, 36 and 41 weeks after injection. The only observable acute hepatic toxic effect of DEN, a mild steatosis, was noted at 3 days, but this had disappeared by 7 days following injection. Basophilic foci, composed entirely of altered hepatocytes, were first noted, when very small, at 10 weeks. At later times, some of the foci also contained small collections of proliferated ductules, apparently a result of secondary ingrowth from nearby interlobular bile ducts. The hepatocytes within basophilic foci were characterized by their abundant cytoplasmic RNA, a high nuclear to cytoplasmic ratio (two times greater than normal), which gave them a "crowded appearance," and decreased glucose-6-phosphatase activity. During the course of the study, basophilic foci appeared to increase in size and number. Cytologic anaplasia also became more evident, ultimately culminating in the development of typical trabecular hepatocellular carcinomas by 44 weeks. Invasion of hepatic veins by basophilic foci, first noted at 10 weeks, was prominent by 20 weeks and indicated that many of the lesions manifested this characteristic of malignancy well in advance of the anaplastic features that are also diagnostic of hepatocellular carcinoma. The high growth rates of basophilic foci were confirmed by their greatly increased 3H-thymidine labeling indices, which were 20 times greater than background hepatocytes at 20 weeks following DEN injection. Tumor progression during the course of the study was also suggested by a doubling of labeling indices of hepatocytes in the basophilic foci between 20 to 28 weeks. (The term tumor progression is used in a broad biological sense to encompass any or all of the qualitative and quantitative changes describing the stepwise development of initiated cells to highly malignant neoplasms. This definition differs from the more clinical usage which restricts the process to qualitative changes during the late stages in the development of fully autonomous neoplasms.) An analysis of the number and size of transections through basophilic foci and in some cases, actual reconstructions of the foci from serial sections, indicated that, in aggregate, they grew exponentially between 10 to 36 weeks, with a volume doubling time of 2.5 weeks. The combined morphologic and kinetic data support the view that trabecular hepatocellular carcinomas develop from basophilic foci. Because of their ease of quantitation on conventional H&E stained sections, their rather uniformly spherical shapes, and the high probability of their clonal origin, the induced focal hepatic lesions should provide a useful model for studying tumor growth kinetics during carcinogenesis.
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PMID:Preneoplastic and neoplastic progression during hepatocarcinogenesis in mice injected with diethylnitrosamine in infancy. 687 10

Male inbred Fischer rats were fed a diet containing 5 p.p.m. aflatoxin for 1, 3, 4 1/2 and 6 weeks at which times groups were killed for histological and histochemical study. Aflatoxin produced a scattered individual cell necrosis of parenchymal cells by 1 week. At 3 weeks small basophilic proliferative foci were seen which increased in size and abundance to 6 weeks. These foci showed starvation-resistant glycogen, variable depletion of glucose-6-phosphatase, succinic dehydrogenase, aniline hydrogenase, membrane ATPase and acid phosphatase. At 6 weeks the foci showed the presence of gamma glutamyl transpeptidase and glucose-6-phosphate dehydrogenase. The basophilic foci were not preceded by other focal histological and histochemical change. The basophilic proliferative lesions are observed when an irreversible change has been induced in the liver. The role of such lesions in the histogenesis of hepatocellular carcinoma is discussed.
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PMID:Histochemical studies on the early proliferative lesion induced in the rat liver by aflatoxin. 724 Dec 69

Plasma membranes have been isolated from chicken liver and from Mc-29 virus induced transplantable hepatoma. The purity of membrane preparations has been checked by electron microscopy and by determination of the activity of some enzymes: 5'-nucleotidase, Na+, K+-ATP-ase, Mg2+-ATP-ase, alkaline beta-glycerophosphatase and glucose-6-phosphatase. In hepatoma membranes the activity of 5'-nucleotidase, Na+, K+-ATP-ase and Mg2+-ATP-ase was lower, that of alkaline phosphatase higher, than in liver membrane preparation. The incorporation rate of glucosamine-14C into UDP-N-acetylglucosamine and into plasma membrane glucosamine have been studied as well. The rate of synthesis of UDP-N-acetylglucosamine was faster in liver than in tumor cells. The labeling of hepatoma plasma membranes with glucosamine-14C occurred more slowly than that of liver ones. The rate of transfer of N-acetylglucosamine from UDP-N-acetylglucosamine to membrane-bound glucosamine is lower in hepatoma, than in liver cells.
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PMID:Isolation and partial characterization of plasma membranes from chicken liver and from Mc-29 virus induced transplantable hepatoma. 745 56

A human hepatocyte line (HHY41) was established from normal human liver tissue. This cell line was derived from a primary culture of human hepatocytes maintained between two layers of collagen gel for 4 weeks. It differs from other human hepatocyte lines in that transfection with the simian virus 40 gene was not used for cellular transformation and nonhepatocellular coculture cells were not present. HHY41 cells have proliferated freely in serum and hormone-supplemented medium after more than 1 year in continuous culture, exhibiting typical morphological characteristics of hepatocytes. HHY41 cells retain glucose-6-phosphatase activity. They also retain the ability to secrete liver-specific proteins such as albumin, transferrin, and alpha-fetoprotein. Northern blot analysis confirmed the presence of albumin mRNA. Cytochromes P450 induced by polycyclic aromatic hydrocarbons are maintained in these cells. Detection of cell surface antigens revealed that HHY41 cells express alpha 1 beta 1-integrin, which is expressed by normal hepatocytes and not by bile duct epithelial cells. High-molecular-weight cytokeratin, a marker for bile duct cells, is also absent in HHY41. Cytogenetic analysis showed hyperdiploid karyotype with a consistent deletion in the short arm of chromosome 1. HHY41 can be considered a new human hepatocyte line which retains liver-specific functions of differentiated hepatocytes. Derived from normal liver tissue, not a hepatocellular carcinoma, it provides a new model system for studying the regulation of cell growth and differentiated functions in human hepatocytes.
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PMID:Establishment of a human hepatocyte line derived from primary culture in a collagen gel sandwich culture system. 749 48

Four separate continuous lines of human hepatocytes (HH01, HH02, HH09, HH25) were developed from normal liver tissue by subjecting cocultures of human hepatocytes with rat liver epithelial cells in a highly enriched medium to frequent subculturing. The addition of conditioned medium from either the human hepatoma line Hep G2 or one of these stable human hepatocyte lines (HH09) appeared to facilitate establishment of line HH25. These human hepatocyte lines have been in continuous culture for 2 to 5 yr and consist of approximately 95% human cells by analysis of cell surface antigens. Cytogenetic analysis also confirmed the human origin of these cells and showed clonal origin with abnormal ploidy. Cells in these human hepatocyte lines retain morphological features of hepatocytes by both light and electron microscopy. They also retain glucose-6-phosphatase activity and secrete proteins characteristic of hepatocytes, such as albumin, alpha-fetoprotein and transferrin. After incubation with 13 mumol/L dibenz(a,h) anthracene for 24 hr, each line had detectable activity of aryl hydrocarbon hydroxylase, ethoxyresorufin O-deethylase and methoxyresorufin O-demethylase. Thus, these human hepatocyte lines retain important differentiated characteristics of hepatocytes. Derived from normal liver tissue, they appear to be immortalized. They provide a new model system for studying human hepatocellular drug metabolism. These lines may also be useful for studying the regulation of synthesis of albumin, alpha-fetoprotein and other proteins in human hepatocytes, determining the effects of cytokines and growth factors and designing systems to effect gene transfer into human hepatocytes for the purpose of gene therapy.
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PMID:Characterization of human hepatocyte lines derived from normal liver tissue. 751 62

Preneoplastic and neoplastic liver cell lesions, induced by EHEN (N-ethyl-N-hydroxyethylnitrosamine) in rats, were investigated to establish the numbers of simultaneously expressed altered enzyme phenotypes within the lesion cells. The lesions were divided into 5 classes on the basis of altered expression in one or more of the following 5 enzymes: glutathione S-transferase placental form, glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, adenosine triphosphatase, and gamma-glutamyl transpeptidase. Class 1 lesions contained cells expressing one altered enzyme. Similarly, class 2, 3, 4 and 5 lesions had cells simultaneously expressing 2, 3, 4, and 5 enzyme alterations, respectively. Four histopathological categories of lesions, ACF (altered cell foci) (274 lesions), HN (hyperplastic nodules) (47 lesions), HCC (hepatocellular carcinomas) (99 lesions) and THC (transplanted hepatocellular carcinomas) (5 lesions) were studied. Proliferation potential was assessed in terms of 5-bromo-2'-deoxyuridine (BrdU) incorporation. The distribution profiles of classes 1 to 5 showed a clear reciprocal change from low class (1 to 2 enzymes) predominance in ACF to high class (4 to 5 enzymes) predominance in HN. Increase of BrdU labeling indices was clearly correlated with progression from HN to HCC. Only a small population of class 5 ACF showed a high BrdU labeling index, indicating particular potential for further development. Thus, the stages of EHEN-induced neoplasia were found to be characterized by gradual increase in the number of altered enzyme phenotypes, with acquisition of proliferative potential being associated with further progression towards malignant conversion.
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PMID:Number of simultaneously expressed enzyme alterations correlates with progression of N-ethyl-N-hydroxyethylnitrosamine-induced hepatocarcinogenesis in rats. 790 86


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