The disorder of gene expression in hepatomas was studied by following certain metabolic alterations (enzyme stimulation, nucleic acid labeling) after glucocorticoid treatment and analyzing the site of action of glucocorticoids. Compared to normal liver, the MC-29 virus-derived transplantable hepatoma (VTH) responded abnormally to glucocorticoids, which failed to stimulate the activity of certain enzymes (glucose-6-phosphatase, aryl hydrocarbon hydroxylase) or to inhibit DNA synthesis. Since the binding capacity of the cytosol steroid receptor was the same in liver and VTH but the interaction between the steroid receptor and DNA was reduced in VTH, it was concluded that structural alterations of chromatin nonhistones--including processed steroid receptor--may be responsible for the lack of physiological responses to steroids in VTH. Furthermore, the increased proportion or repetitive sequences in VTH DNA may be a feature of the disorder of gene regulation in malignant cells.
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The molecular mechanisms underlying the failure of steroids to stimulate glucose-6-Pase and arylhydrocarbonhydroxylase activities in the MC-29-virus-derived transplantable hepatoma (VTH) were investigated. Following cellular uptake of 3H-Cortisol, its subcellular distribution, binding to a specific cytoplasmic receptor and the interaction between steroid-bound receptor and DNA were compared in VTH and in normal chicken liver. No appreciable difference was observed either in 3H-Cortisol uptake or in binding to cytoplasmic receptors.
View Article and Find Full Text PDFBasic and stimulated intracellular cAMP concentrations were measured in normal chicken liver and MC-29-virus-derived transplantable hepatoma (VTH) slices after in vitro incubation. Data indicated the preservation of catecholamine receptor but a loss of glucagon receptor in VTH. Comparing the relative stimulatory action of various catecholamines on cAMP concentration it was concluded that as in normal liver a predominantly beta 2-adrenergic receptor exists in the VTH, but its response to adrenaline is greater.
View Article and Find Full Text PDFChromatin alterations and gene function disorder in MC-29 virus-derived hepatoma.
J Toxicol Environ Health
October 1979
The disorder of gene expression in hepatomas was studied by following certain metabolic alterations (enzyme stimulation, nucleic acid labeling) after glucocorticoid treatment and analyzing the site of action of glucocorticoids. Compared to normal liver, the MC-29 virus-derived transplantable hepatoma (VTH) responded abnormally to glucocorticoids, which failed to stimulate the activity of certain enzymes (glucose-6-phosphatase, aryl hydrocarbon hydroxylase) or to inhibit DNA synthesis. Since the binding capacity of the cytosol steroid receptor was the same in liver and VTH but the interaction between the steroid receptor and DNA was reduced in VTH, it was concluded that structural alterations of chromatin nonhistones--including processed steroid receptor--may be responsible for the lack of physiological responses to steroids in VTH.
View Article and Find Full Text PDFInfluence of immune status on virus-derived transplantable hepatoma in chickens.
J Toxicol Environ Health
October 1979
The transplantable MC-29 virus-derived hepatoma is a suitable model for studying the influence of immune status on virus-derived hepatomas in chickens. It was found that both humoral and cellular immunologic reactions have a role in the pathogenesis of virus-derived hepatomas and that virus-derived hepatomas can be influenced by nonspecific immunostimulation. The lymphoid system was profoundly altered in hepatoma-bearing chickens; this cannot be neglected when studying correlations between immune reactions and carcinogenesis.
View Article and Find Full Text PDFMorphological and biological features of MC-29 virus-induced liver tumors in chicken.
Prog Biochem Pharmacol
June 1978
Further comparative studies on the biological and biochemical features of virus-derived transplantable and chemically induced hepatomas may contribute to the knowledge of human hepatomas. Evidence for the reprogramming of gene expression found in chemically induced transplantable hepatomas [22] was also found in this virus-derived hepatoma.
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