Disease relevance of Carcinoma, Ehrlich Tumor

• While having no antitumor effect per se, caffeine substantially enhanced the antitumor effects of the phleomycins PLM-CHP and PLM-PEP, and the bleomycins BLM-CHP and Blenoxane in rats carrying Walker 256 carcinosarcoma and/or mice carrying Ehrlich ascites tumor, even at doses of phleomycin and bleomycin below the minimum effective level [1].
• Survival and toxicity studies show rhodium(II) pentanoate to possess the highest therapeutic index against the Ehrlich ascites tumor strain and also show that lengthening the carboxylate R chain beyond the pentanoate reduces the drugs' therapeutic efficacy [2].
• Metabolic effects of hyperthermia and ascorbic acid in Ehrlich ascites tumor cells [3].
• In the cytosol fraction of either Ehrlich ascites tumor, Yoshida ascites sarcoma or regenerating rat liver after partial hepatectomy, UDP reduction activity, in contrast to CDP reduction activity, is not sensitive to hydroxyurea [4].
• Also, the in vivo antineoplastic effects of methotrexate (at a concentration of 0.45 microg/g body weight) and its combination with caffeine (120 microg/g body weight), both on the survival time and the increase of the weight of tumor of BALB/c mice inoculated with Ehrlich ascites tumor cells was examined in the present study [5].

High impact information on Carcinoma, Ehrlich Tumor

• Enhancing effect of hydrocortisone acetate administration on the content of A-type particles in Ehrlich ascites tumor [6].
• The growth of a solid tumor induced by im implantation of Ehrlich ascites tumor cells in inbred CBA/J mice was retarded by treatment with an iron chelator, picolinic acid (PLA) [7].
• Experiments on the dose- and time-dependent changes in the survival of Ehrlich ascites tumor cells exposed to bleomycin were done to determine a useful regimen for the effective inactivation of the tumor cells [8].
• A crude extract of Ehrlich ascites tumor cell homogenate was found to contain three distinct bands of superoxide dismutase activity by polyacrylamide gel electrophoresis [9].
• Altered erythrocyte osmotic fragility in mice with Ehrlich ascites tumor [10].

Chemical compound and disease context of Carcinoma, Ehrlich Tumor

• Incorporation of tritiated uridine into DNA of Ehrlich ascites tumor cells [11].
• Protein synthesis in Ehrlich ascites tumor cells is inhibited when cellular calcium is depleted by the addition of EGTA to the growth medium [12].
• There was a progressive formation of strand breaks in mature DNA of Ehrlich ascites tumor cells that were treated with methotrexate [13].
• Three variants of the classical Ehrlich ascites tumor (EAT) cell have been studied by quantitative, sialic acid-specific, lectin-gold ultrastructural cytochemistry [14].
• The DIFs purified from spleen cells and Ehrlich ascites tumor cells exhibited neither interleukin 1 (IL-1) activity nor tumor necrosis factor (TNF) activity, though the unfractionated conditioned medium from spleen cells did exhibit them [15].

Biological context of Carcinoma, Ehrlich Tumor

• We report here that the addition of double-stranded RNA to an extract from Ehrlich ascites tumor cells which have been treated with an interferon preparation [or with the interferon inducer poly(I)-poly(C)] promotes the phosphorylation by [gamma-32P]ATP of at least two proteins: P1 (molecular weight of 64,000) and P2 (molecular weight of 37,000) [16].
• The addition of 10 mM glycine to a physiological saline bathing Ehrlich ascites tumor cells is followed by a slow increase in cell volume that plateaus between 15 and 30 min at a level approximately equal to 17% greater than the control volume; this increase is not observed when glycine is added to cells suspended in a Na+-free saline [17].
• The bromodeoxyuridine differential chromatid labeling techniques were applied to the simultaneous in vivo examination of cell cycle kinetics and sister chromatid exchange (SCE) induction by various cancer chemotherapeutic agents in normal and Ehrlich ascites tumor cell populations [18].
• Role of methotrexate polyglutamylation and cellular energy metabolism in inhibition of methotrexate binding to dihydrofolate reductase by 5-formyltetrahydrofolate in Ehrlich ascites tumor cells in vitro [19].
• It is concluded that inhibition of the glycolysis of Ehrlich ascites tumor cells by Lonidamine results from an effect of the drug on the mitochondrially bound hexokinase [20].

Anatomical context of Carcinoma, Ehrlich Tumor

• Duramycin has no effect on glycolysis catalyzed by cell-free extracts of Ehrlich ascites tumor cells in the presence of mitochondrial ATPase but partially inhibits glycolysis when ADP and Pi are generated by ATPases of plasma membrane preparations [21].
• Pyruvate dehydrogenase was partially purified from Ehrlich ascites tumor cell mitochondria and its kinetic properties were determined [22].
• Membranes from Ehrlich ascites tumor cells possess an activity which, in the presence of farnesyl pyrophosphate, incorporates [14C]isopentenyl pyrophosphate into a product which is soluble in chloroform/ methanol and retained by DEAE-cellulose [23].
• Purification of the intermediate filament protein vimentin from Ehrlich ascites tumor cells [24].
• Hydrogen exchange in the formation of dihydroxyacetone phosphate from acyl dihydroxyacetone phosphate in O-alkyl lipid synthesis in Ehrlich ascites tumor cell microsomes [25].

Gene context of Carcinoma, Ehrlich Tumor

• Expression of P-glycoprotein and multidrug resistance associated protein in Ehrlich ascites tumor cells after fractionated irradiation [26].
• Using a mouse calcyclin affinity matrix, two proteins with molecular masses of about 36 kDa have been purified from Ehrlich ascites tumor cells [27].
• Conditioned media from BuA-treated Ehrlich ascites tumor cells showed a 30% decrease in VEGF concentration when compared with untreated cells [28].
• The ability of purified nuclear lamin A, lamin B, lamin C, and vimentin from Ehrlich ascites tumor cells to bind nucleic acids was investigated in vitro via a quantitative filter binding assay [29].
• A protein target of mouse calcyclin, p30, which we call calcyclin-binding protein (CacyBP), was identified in mouse brain and Ehrlich ascites tumor (EAT) cells [30].

Analytical, diagnostic and therapeutic context of Carcinoma, Ehrlich Tumor

• Non-phosphorylated and phosphorylated HSP25 monomers, as well as non-phosphorylated multimeric HSP25 particles, were isolated from Ehrlich ascites tumor cells by ammonium sulfate precipitation, column chromatography, and ultracentrifugation and tested for their actin polymerization-inhibiting activity [31].
• EXPERIMENTAL DESIGN: Mice with cerebrally inoculated Ehrlich ascites tumor (EHR2) cells were treated with combinations of etoposide + dexrazoxane + cerebral radiotherapy [32].
• Comparison of the hsp25 gene structure between P388 and Hsp25-expressing Ehrlich ascites tumor (EAT) cells by Southern blot analysis revealed no differences in the structural organization of the gene and no changes in its localization in the genome [33].
• Induction of cell arrest at G1/S and in G2 after treatment of Ehrlich ascites tumor cells with metallocene dichlorides and cis-platinum in vitro [34].
• Poly(ADP-ribose) polymerase from Ehrlich ascites tumor cells, partially purified by chromatography on DNA-agarose, was obtained as a more than 80% homogeneous preparation by isoelectric focusing in a sucrose gradient [35].

References