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

Lipid content and composition of DNA, histone and nonhistone proteins of Ehrlich ascites tumor cell chromatin were investigated. All fractions contained varying amounts of lipids, mostly neutral lipids, with different quantitative distribution. The DNA fraction was characterized by elevated total cholesterol level (37%); the histone fraction by high glycerol ester content (62%); and the nonhistone protein fraction by high percentage of glycerol ethers (22%). The results suggest that neutral lipids are integral parts of tumor cell nucleoproteins.
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PMID:Neutral lipids in DNA, histone and nonhistone fractions of Ehrlich ascites tumor cell chromatin. 55 6

Daunomycin was coupled via its amino group to omega-carboxypentyl agarose (CH-Sepharose 4B). Nonhistone proteins from rat leukemia cells (DBLA-6) were fractionated on a column of the adsorbent. The adsorption of nonhistone proteins to the column was increased by high salt concentration (4 M NaCl) and was reversed by 20% glycerol (v/v), indicating a hydrophobic interaction. Complexity of the chromatographic patterns may reflect the occurrence of several species of binding protein in the tumor cells used. Thus the hydrophobic chromatography in the presence of a high concentration of salt was a useful method for fractionation of nonhistone proteins under non-rigorous conditions.
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PMID:Fractionation of nonhistone proeins on a column of daunomycin-CH-Sepharose 4B. 62 48

When heated to 45 degrees C for 20 min Ehrlich ascites tumor and NK-lymphoma cells are irreversibly damaged, so that they lose transplantability. The presence of 7-8% glycerol during heat treatment protects EAT cells completely and NK-lymphoma cells partly against this injury.
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PMID:Glycerin prevents the 'heat-death' of Ehrlich ascites tumor cells. 66 46

[1-14C]Glycerol was injected into the peritoneal cavity of mice bearing Ehrlich ascites tumor cells and the lipids were extracted from the cells after selected periods. 1-O-Alkyl-2-acyl-3-acetyl-glycerols and 1,2-diacyl-3-acetylglycerols were prepared from the ethanolamine and choline phosphoglycerides and fractionated by AgNO3-impregnated thin-layer chromatography into seven molecular species. Bands 1--7 obtained in this way can be designed as saturated, monoene, diene (11), diene (02), triene, tetraene and pentaene + hexaene species, respectively. Band 7, composed mainly of hexaene species, was predominant among those derived from ether phospholipids. The predominant species was band 4 (saturated/linoleate) in both diacyl ethanolamine and choline phospholipids. The specific radioactivities of the fractionated species were determined. In diacyl or alkyl ether compounds of ethanolamine and choline phosphoglycerides, disaturated species turned over very rapidly, while in alkyl ether ethanolamine phosphglyceride, hexaene + pentaene molecular species turned over rapidly. In diacyl compounds of the ethanolamine phosphoglyceride, hexaene molecular species also turned over at a high rate. In diacyl ethanolamine or choline phosphoglycerides, dienoic species turned over rather slowly.
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PMID:Incorporation rates of [1-14C]glycerol into the molecular species of alkyl ether phospholipids of Ehrlich ascites tumor cells in vivo. 68 34

When glycerol was added to tobacco smoke condensate in acetone solvent, the topical carcinogenicity and the ability to produce epithelial hyperplasia in mice was reduced. Two doses of condensate were applied, combined with 2 concentrations of added glycerol. Age-standardized results show that glycerol reduced the incidence of tumours and malignant tumours and of hyperplasia in animals not developing skin tumours. The relative incidences of malignant tumours, benign tumours, hyperplasia and unaffected skin suggest that there is a sequential relationship (i.e. normal skin to hyperplasia to benign neoplasia to malignant neoplasia) which is impeded by glycerol. There was no systemic effect attributable to the condensate.
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PMID:Effect of glycerol on local and systemic carcinogenicity of topically applied tobacco condensate. 69 39

Proteins from plasmatic membrane of ascites and solid 20-methylcholantrene induced tumours cells in inbred mice and rats were obtained by isolation of vesicles of tumor cell membranes produced in glycerol solution. The tumour cells were not broken. In a syngeneic system the inoculation of the prepared protein with adjuvant resulted in protection of 50 to 100% of animals against challenge with a syngeneic tumour cells. The same results were obtained with Ehrlich ascites tumour. The lymphocyte cytotoxicity and blastic transformation of lymphocytes in immunized animals suggested a cellular cytotoxic immunity mediated by tumour specific antigen or perhaps by fetal antigen.
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PMID:[Growth control of experimental tumour. I. Host protection against tumour by previous inoculation of plasmatic membrane of tumour cell (author's transl)]. 72 35

Previous studies from this laboratory on the mechanism of O-alkyl bond formation using a microsomal system from Tetrahymena pyriformis have shown that O-alkyl lipid synthesized from dihydroxyacetone phosphate has exchanged one hydrogen stereospecifically from the 1-sn position of the glycerol moiety. Indirect evidence suggested that acyldihydroxyacetone phosphate, an intermediate in )-alkyl lipid synthesis, is probably not the locus of the exchange. In the present study in was shown that stable acyldihydroxyacetone phosphate incubated in the presence of tritiated water and Tetrahymena microsomes does not become tritiated. When hexadecanol is added to the system O-alkyl lipid is produced which has incorporated one atom of hydrogen for each mole of hexadecanol at all time periods examined. Experiments in Ehrlich ascites tumor cells have shown that the hydrogen exchange also occurs in a mammalian system. The results indicate that the mechanism of O-alkyl lipid ether bond formation involves a hydrogen exchange and that this exchange occurs after the formation of acyldihydroxyacetone phosphate.
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PMID:The formation of tritiated O-alkyl lipid from acyldihydroxyacetone phosphate in the presence of tritiated water. 80 79

Nuclear DNA-dependent RNA polymerases were isolated from Ehrlich ascites carcinoma, TA3 ascites adenocarcinoma, and mouse liver and tested for inhibition by glycerol. The results confirm the finding of Smith and Duerksen ((1975) Biochem. Biophys. Res. Commun. 67, 916-923) that glycerol may inhibit nuclear RNA polymerase II, but because different grades of glycerol inhibited mouse liver RNA polymerase IIa to different extents, it is suggested that an inhibitory contaminant is present. RNA polymerases IIa and IIb from the two tumors and mouse liver were proportionately inhibited by A.C.S. reagent-grade glycerol at concentrations above 10%. RNA polymerase Ia from liver and the TA3 tumor was not inhibited by any concentration of glycerol tested (2-32.3%), but RNA polymerase Ia from Ehrlich carcinoma was inhibited by glycerol concentrations above 16%.
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PMID:Inhibition of nuclear DNA-dependent RNA polymerases from mouse ascites tumors and liver by glycerol. 91 4

1. Radioactive precursors of phospholipids, i.e., 32Pi, [1-14C]glycerol, [2-3H]glycerol, and [1-14C]acetate, were individually injected into the peritoneal cavity of mice bearing Ehrlich ascites tumor cells and the rates of incorporation were estimated. 2. Although [2-3H]glycerol was not practically incorporated into ether phospholipids, the other three radioactive precursors were incorporated into diacyl, 1-O-alkenyl-2-acryl-, and 1-O-alkyl-2-acryl-GPE (GPC). 3. In the experiments on 32Pi or [1-14C]acetate incorporation, 1-O-alkyl compounds in the ethanolamine phosphoglyceride fraction showed high specific activities in comparison with 1-acyl compounds. In the case of [1-14C]glycerol incorporation, a high rate of incorporation into 1-O-alkyl compounds was not found. In the choline phosphoglyceride fraction, a high rate of incorporation of the above precursors into 1-O-alkyl compounds was not observed. 4. The specific activities of 1-O-alkenyl compounds were fairly low compared with those of 1-acyl- and 1-O-acyl- and 1-O-alkyl compounds throughout the incorporation experiments with [1-14C]glycerol and [1-14C]acetate, but in 32Pi incorporation, 1-O-alkenyl compounds showed higher specific activities than 1-acyl compounds in ethanolamine phosphoglyceride, suggesting an exchange reaction of the phosphorylethanolamine moiety. 5. From the above findings, it appears that alkyl ether phospholipids of ethanolamine from may have a significant role in ascites tumor cells, based on their rapid turnover.
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PMID:Phospholipid metabolism in ehrlich ascites tumor cells. II. Turnover rate of ether phospholipids. 101 Aug 41

1. Radioactive precursors, 32 PI, [1-14C]glycerol, and [1-14C]acetate, were individually injected into the peritoneal cavity of mice bearing Ehrlich ascites tumor, and the rates of incorporation into phospholipid fraction of Ehrlich ascites tumor cells were estimated. Although no distinct difference in specific activities was observed between phosphatidylinositol and other phospholipid classes as regards the incorporation of [1-14C]acetate of [1-14C]glycerol, a higher rate of incorporation of 32Pi into phosphatidylinositol was observed. The specific activity of phosphatidylinositol reached more than ten times that of phosphatidylcholine in the first hour. 2. The radioactivities incorporated into the phospholipids of Ehrlich ascites tumor cells and liver were estimated after simultaneous injection 32Pi and [2-3H]inositol. The incorporation of 32Pi into phosphatidylinositol of liver was similar in specific activity to those of other phospholipids. The ratio (3H/32Pi) of phosphatidylinositol only slightly in the ascites tumor cells, while an appreciable decrease of the ratio was observed in the liver during the first 3 hr. 3. These results suggest that phosphatidylinositol synthesis through pathways other than de novo synthesis is rapid in ascites tumor cells.
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PMID:Phospholipid metabolism in Ehrlich ascites tumor cells. I. Turnover rate of phosphatidylinositol. 127 Apr 11


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