Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pH-dependent, saturable binding of hexokinase isozyme I from Ehrlich ascites carcinoma to plasma membrane and microsome preparations from the same tissue is demonstrated. This binding is enhanced by glucose 6-phosphate and may be considered as the sum of a glucose 6-phosphate-dependent binding and an independent binding. The half saturation concentration of hexokinase is about 0.4 unit per ml for both types of binding, and a maximal binding of 0.5-2.0 units per mg membrane protein is observed for both, although the pH optimum of the independent binding (5.4) is lower than that of the dependent binding (5.9). The half saturation concentration of glucose 6-phosphate required for the dependent binding is 0.05 mM at pH 6.1. 2-Deoxyglucose 6-phosphate competatively reverses the effect of glucose 6-phosphate on binding but does not diminish its inhibition of hexokinase activity.
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PMID:Glucose 6-phosphate-dependent binding of hexokinase to membranes of ascites tumor cells. 1 34

KB cells originally derived from epitheloid carcinoma of the nasopharynx were found to be contaminated with mycoplasma. The contaminated cells showed significantly higher glycolytic (EMP) and respiratory (TCA) rates when compared with non-contaminated or 'cured' cells. The activity of the hexose monophosphate (HMP) shunt, an alternative pathway of glucose metabolism, was shown to be reasonably higher than normal KB cell levels. Treatment involving combination of heat (41 degrees C) and kanamycin (350 microgram/cm3) for 21 hours was found to adequately and selectively inactivate the mycoplasmal population. Following cure, the metabolism of the cells fell well within normal ranges. The treatment showed no deleterious effects on the KB cell population. The possibility and the significance of an independent hexose monophosphate shunt activity in the mycoplasma population in addition to the already established partial TCA and EMP activities, and the overall significance of detection of carbohydrate metabolism in these organisms, are discussed.
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PMID:Metabolic consequences of mycoplasmal contamination of cell cultures. 10 31

After major abdominal surgery 32 patients received a parenteral nutrition for 6 days with 360 g of a carbohydrate mixture (levulose:glucose:xylitol = 2:1:1) and 100 g of an L-amino acid mixture/24 h. 16 patients with benign disease showed positive nitrogen balances, 16 patients with malignant diseases balanced or slightly negative nitrogen balances. Postoperatively, blood glucose levels did not require insulin. Less than 1.5% of the infused levulose, 2.0% of glucose and 2.4-4.1% of xylitol were found in urine. C3- and C4- complement levels in serum were below normal, transferrin showed a pathological decrease in carcinoma patients.
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PMID:[Calorie requirement after major abdominal surgery (author's transl)]. 11 34

The R3230AC mammary adenocarcinoma was not dependent on insulin; tumor growth was equal to or greater in diabetic rats than in intact animals. However, tumor growth was reduced when daily doses of insulin were administered. Treatment with estrogen inhibited growth of the R3230AC carcinoma, either in diabetic rats or in intact animals simultaneously treated with insulin. The effects of insulin plus estrogen treatment appeared to be additive in causing inhibition of tumor growth. Tumors from diabetic rats showed few metabolic alterations as reflected by little or no changes in the activities of selected glycolytic enzymes, pyruvate kinase, phosphofructokinase, and hexokinase, nor any striking changes in the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, representing the pentose phosphate pathway. A modest reduction in the ratio of utilization of (1-14C)glucose: (6-14C)glucose was seen in vitro by tumors from diabetic rats. It was concluded that insulin, along with estrogen and prolactin, should be considered as a hormonal factor that influences growth of this automonous, hormone-responsive adenocarcinoma.
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PMID:Influence of insulin on estrogen-induced responses in the r3230ac mammary carcinoma. 12 68

The endocrine pancreatic tissue from patients with severe primary chronic pancreatitis (n=6). secondary chronic pancreatitis due to duct obstruction by carcinoma (n=6) and non-diabetic, non-pancreatitic controls (n=4) was studied qualitatively and quantitatively using specific immunocytochemistry and electron microscopy. Grouping of variously sized islets in the sclerotic tissue (sclerosis islets), islet neoformation by ductuloinsular proliferation, and intrainsular fibrosis were the main qualitative findings. Immunocytochemical quantitation of the distribution of insulin (B), glucagon (A), somatostatin (D) and pancreatic polypeptide (PP) producing cells revealed a significant relative increase in the number of A cells and a decrease in the number of B cells of the sclerosis islets in primary chronic pancreatitis ((B-44.1+/-9.3%:A-38.3+/-2.4%:D-8.6+/-5.1%:PP-4.6+/-4.1%) as well as in secondary chronic pancreatitis B-38.0+/-14.3%:A-38.4+/-19.0%:D-9.1+/-5.8%:PP-14.5+/-23.4%) compared with controls (B-71.1+/-8.1%:A-24.3+/-5.5%:D-8.0+/-2.8%:PP-0.5+/-0.4%). The number of PP cells was significantly increased in primary chronic pancreatitis only. It is suggested that scarring of the exocrine pancreas affects islet composition, probably by impairment of the local circulation and of glucose diffusion, thus leading to reduction of the number and glucose sensitivity of B cells. The hyperplasia of A and PP cells appears to be a secondary phenomenon due to the loss of B cells.
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PMID:The endocrine pancreas in chronic pancreatitis. Immunocytochemical and ultrastructural studies. 14 59

The effects of estrogens on transport and incorporation of amino acids into the R3230AC mammary adenocarcinoma were studied in vivo and in vitro. Dissociated tumor cells from ovariectomized rats, like those from diabetic rats, displayed elevated transport of proline, representing entry by the A system; transport of phenylalanine (L system) was unaltered, as was glucose transport and its utilization. Administration of estradiol valerate decreased the entry of proline into tumor cells from intact, diabetic, or ovariectomized animals; the response to the steroid hormone was greater in ovariectomized or diabetic rats compared to intact animals. The time course of the effects of estrogen treatment was examined in diabetic rats. By 72 hr, transport of both proline and leucine was significantly decreased; incorporation of leucine into proteins and uridine into RNA was significantly reduced by 24 hr after injection of estradiol valerate. The effects of estrogen in vivo to reduce transport of amino acids and their incorporation into proteins appeared to correlate with the reduced tumor growth observed. Experiments were performed to examine the effects of 17 beta-estradiol in vitro on amino acid transport into dissociated cells from ovariectomized or diabetic rats. Under these experimental conditions, 17 beta-estradiol (10(-6)M) inhibited proline transport with little or no effect on leucine transport in cells from ovariectomized rats; in cells from diabetic rats, proline transport and leucine incorporation were significantly reduced by estradiol, whereas phenylalanine transport was slightly inhibited (approximately 20%). The effect of estradiol in vitro was also manifest in tumor cells obtained from diabetic rats treated in vivo with estradiol valerate; estradiol in vitro caused a further reduction in proline transport but not in leucine transport, results that imply some specificity to the action of estrogen on the A system. Since we had earlier shown that insulin action on transport in these tumor cells were directed towards the A system, we examined the effects of insulin, estradiol, and their combination in vitro on proline and leucine transport. Insulin (10(-8) M) stimulated proline transport; 17 beta-estradiol, at a selected lower level of 10(-8) M, inhibited proline transport. When both were added in vitro, estradiol (10(-8 M) was capable of significantly reducing the insulin (10(-8) M)-induced increase in proline transport. Leucine transport was not altered in any of these experiments. Together, these data suggest that estrogens are capable of inhibiting amino acid transport into the R3230AC mammary carcinoma, an effect that is compatible with reduced tumor growth. The possible relationship of estrogen and insulin at the level of amino acid transport remains to be elucidated.
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PMID:Effects of estrogen to alter amino acid transport in R3230AC mammary carcinomas and its relationship to insulin action. 15 4

The infusion of calcium results in the release of gastrin, calcitonin, and serotonin from certain nonbeta islet cell tumors of the pancreas, medullary carcinomas of the thyroid, and carcinoid tumors, respectively. In this study, intravenous infusion of either calcium chloride or calcium aluconate in a patient with an islet-cell carcinoma resulted in a simultaneous rise in plasma immunoreactive insulin and proinsulin, and concurrent hypoglycemia. After resection of the tumor, calcium infusion caused no change in these parameters. Similarly, calcium infusion caused no change in plasma insulin or glucose in normal volunteers. The response of this tumor suggests that calcium infusion may be a useful provocative test to detect insulin-secreting neoplasia. A derangement of the stimulus-secretion coupling mechanism for insulin in the tumor cells may be responsible for their abnormal sensitivity to calcium ion.
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PMID:Insulin and proinsulin release during calcium infusion in a patient with islet-cell tumor. 16 54

Rats (weight 150-200 g) bearing Walker-carcinoma showed tumour size dependent hypoglycemia, diminished mobilization of glycogen following glucagon stimulation and elevated values of the enzyme activity of glucose-6-(P)-ase. A further hormonal stimulation of this enzyme activity towards the values observed in normal rats after betamethasone stimulation was not possible. The values of the enzyme fructose-1,6-di-(P)-ase in liver of tumour bearing rats equalled those found in normal controls and did not show any rise after application of betamethasone. The serum levels of free fatty acids did not show any difference between normal controls and tumour bearing rats, and displayed an equal rise after intensive stimulation of peripheral lipolysis.
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PMID:[Biochemical investigations of cancer cachexia: I. Tumour induced changes of glycogenolysis and gluconeogenesis of Walker carcinoma bearing rats (author's transl)]. 17 91

Hypoglycemia in diabetes can be divided into 1) spontaneous hypoglycemic reactions due to absolute or relative overproduction of endogenous insulin or some other blood glucose-lowering substance, as in islet cell adenoma or carcinoma, latent or protodiabetic conditions, (extrapancreatic) tumors and pituitary and/or adrenal disorders; and 2) hypoglycemia caused by exogenous, i.e. therapeutic, measures. The problem of hypoglycemia in insulin-treated diabetics is far from being solved. As revealed by continuous blood glucose monitoring, nocturnal hypoglycemic attacks frequently escape attention especially in juvenile diabetics. Circadian variations in peripheral glucose utilization, rather than changes in plasma insulin activity, are likely to be involved in this mechanism. At least, this was the conclusion drawn from studies carried out by means of a glucose-controlled insulin and glucose infusion system (GCIGIS) -or artificial pancreas-which delivers short-acting insulin and glucose on demand intravenously. Hypoglycemic reactions in patients being treated with oral anti-diabetic agents, on the other hand, should be regarded primarily as one of the side reactions intrinsic to the mechanism of action of some of these drugs, e.g. sulfonylureas, which act mainly via stimulation of secretion of endogenous insulin reserves not responding properly to postprandial blood glucose increments. In the case of glibenclamide, at least partial resensitization of the defective glucose receptor of the beta-cell also becomes operative. A higher incidence of a characteristic type of hypoglycemic reaction was observed soon after glibenclamide therapy was introduced. Better understanding of the drug and dissemination of the information about it to doctors and patients has reduced the number of hypoglycemic reactions caused by glibenclamide to the same proportions as for other sulfonylureas. Hypoglyoemia following therapeutic hypophysectomy retains its position as one of the main hazards of this heroic therapy.
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PMID:Hypoglycemia in diabetics. 17 24

The levels of nicotinamide adenine dinucleotide (NAD) and NADH in blood of patients with cancer in various stages of development as well as their modification after glucose administration were determined in 188 respectively 77 cases. NAD was significantly decreased in patients with cervix and breast carcinoma but unaltered in patients with metastatic cancers (and lung carcinoma) comparatively with healthy subjects. At 48 hours after i.v. administration of glucose, NAD increased significantly in patients with cervix carcinoma but was unaltered in patients with metastatic cancers (an lung carcinoma). NADH in both cases has given little conclusive results.
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PMID:The levels of NAD and NADH in blood of patients with cancer. 18 70


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