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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumour peracidity in otherwise moderately hyperacidulated tumours or tumour regions of DS carcinosarcoma-bearing Wistar rats attained by glucose infusion was substantially increased by simultaneous infusion of amygdalin and intratumoral i.m. or i.v. application of beta-glucosidase. Here the pH value of healthy tissue, measured at the sceletal muscle, remained unchanged. By means of the said process, tumour hyperacidulation has been raised to a level of deltapH =0.97; attaining a pH difference between tumourous and normal tissue of up to deltapH = 1.6. In one case, the slope of pH reduction in the tumour increased to 870%. Moreover, combined administration of glucose, amygdalin and beta-glucosidase evoked a significant cancerostatic effect hypogenesis, tumour regression) being comparable with the action of an Ifosfamid dosage of 150 mg-kg-1. However, i.m. and i.v. application of beta-glucosidase under narcosis results in an overall process that still remains somewhat too toxic. Hence optimizing studies are intended with the particular aim to further improve the comparability of this process.
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PMID:[Tumour hyperacidulation through intravenous glucose infusion enhanced by amygdalin and beta-glucosidase application (author's transl)]. 0 Sep 79

The mechanisms controlling secretion of glucagon and other pancreatic hormones were studied in a patient affected with multihormone-secreting islet-cell tumor. Fasting glucagon levels (3,000 pg./ml.) rose to 10 ng./ml. following arginine stimulation. While oral glucose load and intravenous glucose infusion did not suppress glucagon secretion, insulin administration induced a prompt depression in glucagon levels. Glucagon, insulin, and gastrin levels were suppressed by somatostatin while calcium infusion caused a paradoxical increase. It is suggested that only some of the stimulation-inhibition mechanisms were conserved in this case of glucagon-secreting pancreatic tumor.
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PMID:Suppression and stimulation mechanisms controlling glucagon secretion in a case of islet-cell tumor producing glucagon, insulin, and gastrin. 0 26

Glycolysis is not of importance for the process of carcinogenesis. It is very likely, however, that certain molecular-biological and genetic changes are produced which enable the malignant cell to develop an intensive glycolysis, for instance, to form specialized glycolytic isoenzymes already during oncogenesis, and may possible become effective in the primary tumour. As soon as the capacity of the cancer cell to intensive aerobic and anaerobic glycolysis has become manifest, this process is an irreversible one. The extent of glycolysis of a malignoma is greatly dependent on the degree of its dedifferentiation and vascularization (glucose supply), although a direct correlation between growth and the amount of lactic acid formed does not seem to exist. However, a certain utilization of glucose is essential for cell proliferation (supply of basic substances). In many cases there is a correlation between the extent of glycolysis measurable under optimal conditions in vitro (glycolytic power) in a malignant tumour and its growth rate recognizable in vivo. The formation of a strong capacity for glucose degradation via the Embden-Meyerhof pathway that cannot be fully utilized by the whole tumour in vivo is first of all designed to ensure survival and proliferation of cells even at extremely low levels of glucose supply. This process can be regarded as an adaptation of cancer cells to a situation of unsufficient supply. This circumstance endows the cancer cell with an essential advantage over the normal cell which enables or even promotes its invasive and destructive growth and metastatic dissemination. In this respect they differ, for instance, from benignant neoplasms. The possibility is discussed to control neoplastic growth by adjusting an optimal pH difference between normal and tumour tissue by combined administration of detoxicated drugs which are converted to their toxic forms only in the tumour by means of strongly pH-dependent exogenous enzymes.
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PMID:[Origination and importance of glycolysis for malignomas and utilization of this property in the chemotherapy of cancer (author's transl)]. 0 18

In this study, conditions for production, detection, and storage of heat-labile Escherichia coli enterotoxin (LT) in culture filtrates from E. coli H-10407 were defined by using the adrenal tumor cell assay system. An enriched medium containing 0.6% yeast extract, 2% Casamino Acids, and 0.25% glucose buffered at pH 8.5 produced the highest LT activity of the various test media. In E. coli strain H-10407, LT activity was markedly decreased if the initial pH of the culture media was reduced to pH 7.5 or less. In contrast to E. coli P-263, if strain H-10407 was grown in the presence of mitomycin C there was no increase in LT production. Crude-culture filtrates containing LT can be stored at 4 degrees C for several days without an appreciable loss of activity; however, for long-term storage lyophilization or freezing at -70 degrees C is recommended.
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PMID:Factors influencing heat-labile Escherichia coli enterotoxin activity. 0 63

Temperature measurements on Wistar rats with miniature-Hg-thermometer and laser-welded thermoelements lead to the following conclusions: 1. No change of temperature-profile, especially in the liver through glucose-infusion and hyperthermia, can be noticed. 2. Glucose-infusion causes hyperthermia of about 1.5 degrees C. 3. The temperature of the subcutaneous growing DS- carcinosarcoma lies under the norm and increases with the distance from the surface of the body. 4. Hyperthermia of 3 degrees C has no influence on tumor over-acidification. 5. The substance CEU has no pyrogenic effect on the rat but potentiates the decrease of the body-temperature caused by narcosis.
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PMID:[Temperature measurements in Wistar rats and DS carcinosarcoma under various conditions]. 1 31

The influence of intracellular pH (pHi) upon 5-fluorouracil (5-FU) uptake has been studied in slices of Walker 256 carcinosarcoma and rat liver. Alteration of pHi was achieved by the addition of either glucose alone or together with oxamic acid to the incubation medium. Results indicated that 5-FU uptake by the tumor slices was not dependent upon pHi, but was enhanced by the presence of glucose. Uptake of 5-FU by liver slices appeared to follow a pattern predictable from the pHi and the pK of the drug.
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PMID:Dissociation of 5-fluorouracil uptake from intracellular pH in Walker 256 carcinosarcoma. 1 65

High-resolution 31P nuclear magnetic resonance spectra at 145.7 MHz are reported for intact Ehrlich ascites tumor cells and their perchloric acid extracts. In the extracts it was possible to assign resonances to fructose 1,6-bisphosphates, dihydroxyacetone phosphate, ATP, ADP, AMP, Pi, NAD+, phosphorylcholine, glycero-3-phosphorylcholine, glycero-3-phosphorylethanolamine, and glyceraldehyde 3-phosphate from their chemical shifts, pH behavior, and spin couplings. All but glyceraldehyde 3-phosphate were observed and assigned in the intact cells. It was possible to show that the hydrolysis of fructose 1,6-bisphosphate to dihydroxyacetone phosphate and glyceraldehyde 3-phosphate is in equilibrium, that the dihydroxyacetone phosphate leads to glyceraldehyde 3-phosphate reaction is not, and that in the intact cell without added oxygen or glucose the reaction 2ADP in equilibrium ATP + AMP is in equilibrium. From the known pH dependence of the Pi resonance it was possible to show that during aerobic or anerobic glycolysis the difference between intracellular and extracellular pH values was less than 0.2 pH units. Upon oxygenation the ATP concentration increased while the ADP concentration fell. Introducing deoxyglucose depleted the ATP and resulted in an AMP signal and one from deoxyglucose 6-phosphate, which is transported and phosphorylated but not catabolized.
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PMID:31P nuclear magnetic resonance studies of Ehrlich ascites tumor cells. 1 72

Several anticancer chemicals containing a quinone group were found to stimulate the aerobic oxidation of NADPH by liver microsomes. The enzyme responsible for the above reaction was identified as NADPH-cytochrome c reductase (EC 1.6.2.4), one of the microsomal flavoproteins. The fact that a catalytic amount (20 micronM) of these anticancer chemicals was sufficient to oxidize all the NADPH (100 micronM) indicates that they function as electron carries from the flavoprotein to molecular oxygen. As a corollary, Mitomycin-C and Carbazilquinone stimulated oxygen uptake by Ehrlich ascites tumor cells in the presence of glucose that Daunomycin and Adriamycin failed to do so, although the reason for it remains to be elucidated. Carbazilquinone, in contrast to others, also stimulated the microsomal NADH oxidation.
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PMID:Stimulation of microsomal NADPH oxidation by quinone group-containing anticancer chemicals. 1 20

The pH profile in the intercapillary region of tumor tissue is calculated for normal (Case I) and enhanced glucose concentration in blood (Case II) which was increased by a factor of 4 for an extended period of time. The statement used, which takes into account the reduced lactic acid formation in the unsaturated region of cancer cell glycolysis, and the resulting solution of the lactic acid diffusion field equation are given. For Case II (conditions of cancer multistep therapy) and a capillary radius of 4 micrometer this yields the following pH values: Wall at venous end of the capillary 6.7 (or 6.5); at R greater than 12 micrometer, i.e. still in the vicinity of the capillary less than 6.3: at R approximately 60 micrometer a minimum of 5.9. This rather good pH homogeneity is the prerequisite that all lytic actions and activation mechanism induced by a temporary extreme hyperacidification of the tumor tissue can take place in the major portion of the intercapillary region with a strength of adequate uniformity. Conclusions were drawn from these results with respect to the further planning of cancer therapy. This refers to the utilization of processes serving to increase primary damage to tumor tissue through body defense mechanisms, inhibition of cell proliferation as well as the applicability of new anticancer drugs (CMT Selectines) that are rendered active only in strongly hyperacidified foci of cancer. Moreover, this includes the possible use for increasing the secondary damage to tumor tissue by way of the lysosomal cytolysis, by drastic decrease of microcirculation and the damage of the capillaries in tumor tissue.
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PMID:[Calculation of the pH profile in the intercapillary regions of tumour tissues before and after long-term glucose infusion into the blood stream (author's transl)]. 2 14

The mode of generation of free radicals of daunomycin, adriamycin, and carboquone in the NADPH-rat liver microsome system was studied at room temperature by electron spin resonance (ESR) spectroscopy. ESR signals of all these quinoid anticancer chemicals were detected when dissolved oxygen in the reaction mixture was consumed since the radicals are easilyaut oxidizable. All the radicals had an appreciable lifetime under anaerobic conditions. However, there were differences in the mode of their generation between daunomycin and adriamycin, on the one hand, and carboquone, on the other, with respect to the lag time and the effect of the amount of chemicals, pH of the medium, kind of electron donors, NADPH and NADH, and the presence of excess of DNA. Especially, ESR signal reappeared after the first signal had decreased considerably, in the case of daunomycin and adriamycin but not in carboquone. Intact Ehrlich ascites tumor cells also gave rise to an ESR signal of adriamycin and carboquone, but the former signal was prevented from appearing in the presence of glucose.
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PMID:Electron spin resonance study on the mode of generation of free radicals of daunomycin, adriamycin, and carboquone in NAD(P)H-microsome system. 2 73


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