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

Plasma membrane fractions from normal colon cells and a transplantable colon adenocarcinoma were isolated and purified by differential and zonal density centrifugation. Enrichment of normal and adenocarcinoma plasma membranes was found in zonal fractions I and II (ZI and ZII) following centrifugation in an 18--50% sucrose gradient. The distribution of various marker enzymes in normal colon preparations suggested an apical origin for the membranes obtained in zonal fraction I while zonal fraction II appeared to contain basal-lateral membrane fragments. Enzymatic analysis of the plasma membrane derived from the colon tumor indicated that these fractions possess a more uniform distribution of Na-K+ ATPase perhaps reflecting a dedifferentiated state. The plasma membrane fractions isolated should prove useful for investigation of transport and other properties of vesicles derived from malignant and normal colon cells.
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PMID:Isolation and purification of normal and malignant colonic plasma membranes. 14 56

Immunopotentiated rats, which were injected with Propionibacterium acnes or BCG, had the 50% survival twice as long as those in untreated controls after intravenous inoculation of Sato lung carcinoma (SLC) cells. The amount of labeled tumor cells in the lung of the adjuvant-treated rats decreased significantly in the first 20 hr after intravenous injection of 51Cr-labeled tumor cells compared to that of control animals. The elevated activities of ATPase and acid phosphatase in the whole nucleated spleen cells as well as spleen lymphocytes separated by Ficoll-Conray gradient were also demonstrated in adjuvant-treated groups. These data suggested that the elevation of ATPase and acid phosphatase activities in nucleated spleen cells as well as spleen lymphocytes has an important role for the suppression of tumor growth in adjuvant-treated rats.
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PMID:Effect of Propionibacterium acnes or BCG on enzyme activities in spleen lymphocytes of Donryu strain rats. 14 84

Seven well differentiated chondrosarcomas of bone have been analyzed by electron microscopy, and the fine structural localization of adenosine triphosphatase and nonspecific alkaline phosphatase has been elucidated. On the basis of the fine structural appearance, two distinct cell types were shown to constitute the tumor tissue: chondrocyte-like cells and large "mitochondria-rich cells". Large, multinucleated cells in the tumor did not seem to correspond to osteoclasts but rather were likely to represent true neoplastic cells. Some chondrocyte-like cells appeared to be binucleated by virtue of deep, groove-like nuclear indentations. Adenosine triphosphatase and alkaline phosphatase were associated with the plasma membrane of both chondrocyte-like and mitochondria-rich cells suggesting that they might be of common origin. Normal chondroblasts and chondrocytes lack histochemically demonstrable adenosine triphosphatase on their plasma membrane. Presence of this enzyme in the tumor cells may indicate that they are histogenetically related to immature non-chondroid matrix forming cells (known to carry the enzymes).
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PMID:Contribution to the knowledge of the fine structure of chondrosarcoma of bone. With a note on the localization of alkaline phosphatase and "ATPase". 15 79

The oxidative phosphorylation and ATPase activity (initial and stimulated by DNP and Mg2+) in tumor mitochondria were investigated. The intact mitochondria of Zajdela hepatoma, in contrast to liver mitochondria, exhibit the ATPase activity which is slightly stimulated by 2,4-dinitrophenol and is markedly activated by Mg2+. The mitochondria from transplantable solid tumors (adenocarcinoma 755, Iensen sarcoma, sarcoma 45) despite satisfactory morphological integrity under electron microscopy are biochemically less intact than the mitochondria of hepatoma. ATPase of these mitochondria is also slightly stimulated by 2,4-dinitrophenol and significantly by Mg2+. The ATPase activity of thymus mitochondria, the normal tissue with sufficiently high proliferative activity, corresponds to that of tumor mitochondria. The total amount of enzyme in mitochondria of tumors investigated and thymus is not lowered, since the ATPase activity in the presence of both DNP and Mg2+ corresponds to the ATPase activity of liver mitochondria. The Mg2+ ATPase activity of tumor mitochondria is not sensitive or is only partly sensitive to oligomycin. The data obtained are indicative of a high lability of the phosphorylating system in tumor and thymus mitochondria. A possibility of reorganization of the energy mechanism of tumor mitochondria and some normal tissues in connection with increased metabolism requiring high energy consumption, is discussed.
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PMID:[Some peculiarities of ATPase in tumor mitochondria]. 15 49

To better assess the significance of enzyme-deficient foci as putative premalignant lesions, parallel histochemical analyses of RNase and ATPase activities were carried out in serial sections of livers from rats fed 4-dimethylaminoazobenzene. The results showed that focal losses of RNase and canalicular ATPase activities occur simultaneously in congruent areas of liver parenchyma at early stages of carcinogenesis. Such foci presumably represent altered cells capable of progressing to neoplasia since the changes observed in this new cell population persist in developing tumors.
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PMID:Histochemical comparison of focal losses of RNase and ATPase activities in preneoplastic rat livers. 15 7

Effect of BCG, coenzyme Q10, or their combination on ATPase activity in spleen lymphocytes of tumor-bearing rats was investigated in relation to changes in the content of individual coenzyme Q homologs in these cells. Contents of both coenzyme Q9 and Q10 in spleen lymphocytes significantly decreased in the late stage of Donryu rats bearing Sato lung carcinoma. Oligomycin-sensitive ATPase activity in spleen lymphocytes was also significantly depressed in this stage. The depressed, oligomycin-sensitive ATPase activity was significantly recovered by a 3-time intramuscular administration of coenzyme Q10 emulsified with ethanol and saline, and the decreased contents of coenzymes Q9 and Q10 were slightly restored by this treatment. This enzyme activity was also significantly recovered by an intravenous administration of BCG, and was elevated more by the combined treatment with BCG and the emulsified coenzyme Q10. These results suggest that the combined treatment with BCG and emulsified coenzyme Q10 can contribute to the improvement of the depressed bioenergetics in lymphocytes of tumor-bearing animals, and that this combined effect of BCG and emulsified coenzyme Q10 might be based on the combination of their individual activating effect on lymphocytes.
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PMID:Combined effect of BCG and coenzyme Q10 on ATP-ase activity and coenzyme Q content in spleen lymphocytes of tumor-bearing rats. 15 9

Ca2+ uptake into Ehrlich ascites tumor cells was studied at 0 degrees C in the presence of mitochondrial inhibitors, conditions that minimized complications caused by sequestration of Ca2+ into organelles or by excretion. Under these conditions Ruthenium Red inhibited Ca2+ uptake, but other previously implicated ions, such as Pi or Mg2+, had no effect. Valinomycin either inhibited or slightly stimulated Ca2+ uptake depending on the presence of excess K+ on the outside or inside of the cell, respectively. Nigericin inhibited Ca2+ transport. Based on these data we propose an electrogenic uptake of Ca2+, possibly via a Ca2+/H+ antiport mechanism. The observation that glucose inhibited Ca2+ uptake suggested that in Ehrlich ascites tumor cells an energy-driven Ca2+ expulsion mechanism is operative, similar to that in erythrocytes. Plasma membrane preparations of ascites tumor cells were found to contain a Ca2+-dependent ATPase. These preparations, when incorporated into liposomes in an inside-out orientation, catalyzed an ATP-dependent uptake of Ca2+.
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PMID:Ca2+ translocation in Ehrlich ascites tumor cells. 15 90

The effect of CMNQ was studied on mitochondria isolated from S-180 ascites tumor cells. It was found that the primary metabolic event upon addition of CMNQ to S-180 mitochondria was a stimulation of oxygen uptake. The oxygen utilization rate was maximized at about 50 nmoles CMNQ/mg protein; at doses higher than this, inhibition of respiration was observed relative to the stimulation of respiration produced by CCCP. It was also up to 50 nmoles CMNQ/mg protein. S-180 ATPase activity is stimulated maximally by 125 nmoles CMNQ/mg protein; at doses higher than this, slight inhibition of the ATPase activity relative to the stimulation produced by CCCP is seen. In vivo treatment of CMNQ to tumor bearing animals leads to a significant reduction of in vitro S-180 cellular respiration rates. The data presented in this work coupled with previously published reports involving CMNQ support the proposal for a mitochondrial level of action for this bioreductive alkylating antineoplastic agent.
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PMID:Effects of the bioreductive alkylating agent 2,3-bis(chloromethyl)-1,4-naphthoquinone on coupled mitochondria isolated from sarcoma 180 ascites cells. 16 26

The formation of cellular aggregates (foci) in CV-1 cells following infection with Yaba tumor poxvirus is dependent upon cell passage level, temperatue of incubation, and calcium concentration in the medium. Resistance of older cells can be reversed by maintaining calcium at 0.1 mM or by adding cortisone acetate (1 mug/ml), hydrocortisone, or estradiol-17beta to the cultures. In susceptible cells, foci formation was inhibited slightly by methyltestosterone and inhibited completely by dexamethasone, aldosterone and progesterone. Activities and patterns of enzymes associated with cytoplasmic membranes (alkaline phosphatase, mononucleotidase, and Na+-K+-adenosine triphosphatase) and lysosomes (beta-glucuronidase and acid phosphatase) of the younger susceptible and the older resistant CV-1 cells differed. These differences apparently occurred in concert with phenotypic changes in the membranes that reduced the mobility of older resistant cells. In susceptible culture, unifected cells migrated to the infected cell and participated in foci formation. Reduction of the calcium content to 0.1 mM apparently removed some of the constraints on mobility of the resistant cells. Although the hormones may have had a similar effect, the changes in enzyme patterns indicated basic alterations in protein synthesis. The development of resistance to foci formation occurred between the 45th and 50th passage level. Hormonal reversal of this resistance resulted in enzyme profiles that reflected the pattern of young susceptible cells.
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PMID:Alterations of enzymes associated with plasma membranes and cellular organelles during infection of CV-1 cells with Yaba tumor poxvirus. 16 62

Plasma membranes isolated from Yoshida ascites hepatoma AH-130 by a modification of the method of T.K. Ray (Biochim. Biophys. Acta 196:1, 1970), were subfractionated into three fractions having densities (d) 1.12, 1.14 and 1.16 by discontinuous sucrose density-gradient. Membrane subfractions were characterized by electron-microscopy, by assay of marker enzymes and by lipid composition. All subfractions appeared to be essentially free from whole mitochondria, lysosomes and nuclei. Subfraction d 1.16 had the highest 5'-nucleotidase, Mg++-ATPase and (Na+ +K+)-ATPase activities; cytochrome c oxidase was undetectable in any fraction and glucose-6-phosphatase was measurable only in fraction d 1.14 and 1.16. Cyclic AMP phosphodiesterase was nearly equally distributed in the fractions. Adenylate cyclase, 5'-nucleotidase and Mg++-ATPase activities of tumor membrane were lower with respect to liver plasma membrane, while cyclic AMP phosphodiesterase and (Na" +K+)-ATPase were found to have similar activities in the two membrane preparations. With respect to liver membrane, hepatoma membrane contained a higher amount of glycolipids and a higher amount of phospholipids accounted for mainly by sphingomyelin, phosphatidylserine and phosphatidic acid. The possible significance of the decrease of adenylate activity in the hepatoma membrane is briefly discussed.
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PMID:Isolation and characterization of the plasma membrane from Yoshida hepatoma cells. 16 55


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