Pharmacologic inhibitors of IkappaB kinase suppress growth and migration of mammary carcinosarcoma cells in vitro and prevent osteolytic bone metastasis in vivo. (65/243)

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Short-term metabolic fate of L-[13N]glutamate in the Walker 256 carcinosarcoma in vivo. (66/243)

In vivo studies with L-[13N]glutamate in the Walker 256 carcinosarcoma implanted under the renal capsule of female Sprague-Dawley rats demonstrate that uptake of glutamate and the rate of incorporation of the nitrogen label from this amino acid into metabolites is slower in the tumor than in nontumorous kidney tissue. Glutamate dehydrogenase, glutaminase, and alanine aminotransferase activities are significantly lower within the tumor than within the adjoining kidney. However, the tumor expresses high levels of aspartate aminotransferase, attesting to the importance of this enzyme in the metabolism of glutamate. Indeed, high performance liquid chromatographic analysis showed that the principal metabolic fate of label derived from L-[13N]glutamate in the tumor is incorporation into aspartate. Measurement of specific activity ratios of glutamate to aspartate shows that the transfer of nitrogen from glutamate to aspartate is rapid and that equilibration of label among components of the aspartate aminotransferase reaction is attained within minutes after tumor uptake. Analyses of the nontumorous portion of the implanted kidney also showed that aspartate is the major recipient of glutamate nitrogen. However, high performance liquid chromatographic analyses of deproteinized tissue revealed that glutamine and ammonia are also significant 13N-labeled metabolites formed from L-[13N]glutamate within the kidney. Proportionately lower amounts of these labeled metabolites were found in the tumor.  (+info)

The energy state of tumor-bearing rats. (67/243)

Rats bearing the Walker-256 carcinosarcoma have a profoundly altered liver metabolite content with significant increases in the concentrations of glucose 6-phosphate, fructose 1,6-bisphosphate, citrate, lactate, and alanine, while the concentrations of glucose, pyruvate, dihydroxyacetone phosphate, and glutamine are decreased. As a result of these changes both the cytosolic NAD+/NADH ratio and the cytosolic phosphorylation potential are significantly lowered while no changes are detected in either the cytosolic NADP+/NADPH ratio or the mitochondrial NAD+/NADH ratio. These hepatic changes are accompanied by marked increases in the circulating concentrations of lactate, non-esterified fatty acids, and triacylglycerols. The activities of both liver hexokinase and phosphofructokinase are also significantly elevated in the tumor-bearing rats. The changes observed both in the redox state and phosphorylation potential are in agreement with the energy imbalance associated with tumor burden.  (+info)

A morphological and phenotypic analysis of Walker 256 cells. (68/243)

A detailed morphological analysis of Walker 256 cells sensitive and resistant to cis-diamminedichloroplatinum(II) has been performed. Two cell populations are identified by electron microscopy of differing differentiation corresponding structurally to cells reported in experimentally induced metastases. Phenotyping of the cells using a number of monoclonal antibodies by immunocytochemistry and flow cytometry showed the absence of epithelial cell markers: however, the cells stained intensely for markers for germ and/or hematopoietic cells. Further studies utilizing monoclonal antibodies to lymphoid, myeloid, and monocytoid cells showed the cells to be monocytoid in origin. No evidence of cell heterogeneity was evident from the phenotypic experiments (a biphasic pattern was not observed). Enzyme histochemistry showed strong focal acid phosphatase activity suggestive of cells of hematopoietic origin. Thus the concept that these cells reflect an epithelial cell of origin is not substantiated by phenotyping with two methodologies.  (+info)

Action of tacrolimus on Wistar rat kidneys implanted with Walker 256 carcinosarcoma. (69/243)

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The effect of copaiba balsam on Walker 256 carcinoma inoculated into the vagina and uterine cervix of female rats. (70/243)

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Bilateral downregulation of Nav1.8 in dorsal root ganglia of rats with bone cancer pain induced by inoculation with Walker 256 breast tumor cells. (71/243)

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Effect of intravenous versus intraperitoneal glucose injection on systemic hemodynamics and blood flow rate in normal and tumor tissues in rats. (72/243)

The effect of i.v. versus i.p. glucose injections on blood flow rate of Walker 256 carcinoma and several normal tissues of unanesthetized, unrestrained female Sprague-Dawley rats was measured, using the radioactive microsphere technique prior to and 60 min after glucose administration (6 g/kg, i.v. or i.p.). Changes in systemic hemodynamics were also investigated in an attempt to further quantify the mechanisms responsible for tumor blood flow reduction. Most of the normal tissues showed either no modification or a decrease in the blood flow rate following i.v. or i.p. glucose injections. The response was more pronounced following i.p. injection. Most of the tissues studied also exhibited significant modification in cardiac output distribution. A decrease in blood flow rate and cardiac output distribution was also observed in the tumors following i.v. or i.p. injections. However, as observed in the normal tissues, the response was more pronounced following i.p. injection. Mechanisms for blood flow reduction include systemic effects such as reduction and redistribution of cardiac output. An additional systemic mechanism following i.p. injection includes hypovolemic hemoconcentration which was evident by an increase in blood hematocrit. In rats, unlike observations in mice, the change in hematocrit following i.p. injection is not as large and cannot account for the total blood flow reduction. Local mechanisms include an increase in red blood cell rigidity due to glucose itself and tissue acidosis.  (+info)