Ehrlich-Ascites

L Na -iiidepeiideiit Braiiched-chaiii and aromatic amino acids Ehrlich ascites cells Chinese hamster ovary cells Hepatocytes... 

Ehrlich ascites tumor agar, collagen glucose 2.4... 

Osterreich, S., Schunck, H., Benndorf, R., Bielka, H. (1991). Cisplatin induces the small heat shock protein hsp25 and thermotolerance in Ehrlich ascites tumor cells. Biochem. Biophys. Res. Comm. 180,243-248. 

Kim et al. (1987) showed that the prolonged retention time of Ara-C in the peritoneal cavity after intraperitoneal administration of the drug in liposomal form as discussed above resulted in better therapeutic effects on intraperitoneally inoculated L1210 cells, as compared to the free drug. The activity of intraperitoneally administered cDDP on Ehrlich ascites carcinoma in mice was increased after encapsulation in neutral liposomes (Sur et al., 1983). The in vivo studies revealed improved antitumor activity and a lower toxicity sifter administration of cDDP liposomes compared to free drug. 

Perfluoroalkyl)-5 -deoxy-5 -fluoro- and 5-(perfluoroalkyl)-2, 5 -di-deoxy-5 -fluoro-uridines were prepared " from 840 and 834, respectively, using perfluoroalkyl-copper complexes. Among them, 5 -deoxy-5 -fluoro-(846) and 2, 5 -dideoxy-5 -fluoro-5-(perfluoroethyl)uridine (839) were particularly effective against Ehrlich ascites carcinoma. 5-Hydroxyl (847) and 5-amino or 5-alkylamino (5-NHMe, -NHBu, -NHCH2Ph, -morpholino, -piperidino, and -pyrrolo) analogs (848) of 840 were prepared. The a anomer of 5 -deoxy-5 -fluorouridine (840) was also synthesized. "... 

Iliakis G. 1984. The mutagenicity of alpha particles in ehrlich ascites tumor cells. Radiat Res 99 52-58. 

Ir(CO)2(aniline-dithiocarbamate) shows a moderate activity against Ehrlich ascites at 50 mg kg 1,704 The synthesis of air-unstable [Ir2(//-L)(cod)2], where H2L = RiSSH2(l,2-0-isopropylidene-2,5-dithio-a-D-ribofuranose, XySSH2(l,2-0-isopropylidene-3,5-dithio-a-Z)-xylofuranose), is described.705... 

Elephantopus mollis is interesting because it elaborates a series of cytotoxic antitumor germacranolides including molephantinin and phantomolin, which are cytotoxic in vitro and in vivo against Ehrlich ascites carcinoma and Walker 256 carcinosarcoma in rodents (104,105). Molephantinin mitigates DNA and protein synthesis in Ehrlich ascites carcinoma cells and DNA synthesis. What is the activity of molephantinin on apoptosis (106)1... 

Hall IH, Liou YF, Lee KH. Antitumor agents LII The effects of molephantinin on nucleic acid and protein synthesis of Ehrlich ascites cells. J Pharm Sci 1982 71 687-690. 

ATPase activity of P-glycoprotein related to emergence of drug resistance in Ehrlich ascites tumor cell lines, Biochim. Biophys. Acta 1997,... 

Panniers, R., and Henshaw, E. C. (1983). A GDP/GTP exchange factor essential for eukaryotic initiation factor 2 cycling in Ehrlich ascites tumor cells and its regulation by eukaryotic initiation factor 2 phosphorylation. J. Biol. Chem. 258, 7928—7934. 

Grassetti, D.R., and Murray, J.F. (December 1967) The effect of 2,2 -dithiodipyridine on thiols and oxi-dizable substrates of Ehrlich ascites cells and of normal mouse tissues. Biochem. Pharmacol. 16(12), 2387-2393. 

Xanthothricin 308 stimulated oxidation of NADH and NAD-linked substrates by rat liver mitochondria, yeast mitochondria, and Ehrlich ascites tumor cells (74MI1, 74MI3). It also stimulated mitochondrial oxidation of succinate, pyruvate, or malate. The antibiotic xanthothricin was obtained... 

Agranofl, B. W., Hajra, A. K. The acyl dihydroxyacetone phosphate pathway for glycerolipid biosynthesis in mouse liver and Ehrlich ascites tumor cells. Proc. Natl. Acad. Sci. U.S. 68, 411-415 (1971). 

Sugibayashi K, Akimoto M, Morimoto Y (1979a) Drug-carrier property of albumin microspheres in chemotherapy III. Effect of microsphere-entrapped 5-fluorouracil on ehrlich ascites-carcinoma in mice. J Pharmacobio-Dynam 2 350-355. 

A protein highly homologous to the S100 proteins has been isolated from Ehrlich ascites tumor cells it has subsequently been shown to be nearly identical with human calcyclin. The fluorescence intensity from the three tyrosine residues is enhanced on the binding of Ca2+.(l58)... 

In different organs of the rat [128], Ehrlich ascites tumor cells [144], trout testis [127], calf thymus [145], and carp testis [146], H4 is modified mainly as the N -dimethyllysine, while H3 is modified as N -monomethyllysine, N -dimethylly-sine and N -trimethyllysine with the N -dimethyllysine predominating. Pea seedling H4 is not methylated and H3 exits as N -mono- and N -dimethyllysine with N -trimethyllysine not being detectable [147,148]. 

The temporal sequence of H3 and H4 methylation after synthesis has been examined in Ehrlich ascites tumor cells [144] and trout testis [149]. Methylation lagged histone synthesis, and the histone was methylated after being bound to DNA. H4 methylation follows the stepwise acetylations and deacetylations [149]. It was suggested that methylation was involved in final arrangement of H3 and H4 on newly replicated DNA [144] and might be involved in histone interactions with other proteins such as histone kinases [149]. 

Gregory, R.I. et al. (2002) Inhibition of histone deacetylases alters allelic chromatin conformation at the imprinted U2afl-rsl locus in mouse embryonic stem cells. J. Biol. Chem. 277, 11728-11734. Thomas, G., Lange, H.W., and Hempel, K. (1975) Kinetics of histone methylation in vivo and its relation to the cell cycle in Ehrlich ascites tumor cells. Eur. J. Biochem. 51, 609-615. 

Phenanthrenebiguanides possess 384) some activity against cancer. The effect of biguanides on plasma protein surface has been investigated 294, 610) with a view to the possibility of finding anti-tumor ents. Aryl-and naphthyl-biguanides exhibit 625) a slight anti-neoplastic activity in vitro in Ehrlich ascites carcinoma. 

Woerdenbag et al also evaluated the influence of chiral center configurations present in artemisinin (1) structure on the proliferation of Ehrlich ascites tumor (ETA) cells. Compounds 11-hydroxyartemisinin (47) and 11-hydroxy-11-epi-artemisinin (48) (Fig. 4) were synthesized and the... 

Woerdenbag HI, Moskal TA, Pras N, Malingre TM, El-Feraly FS, Kampinga HH, Konings AWT. (1993) Cytotoxicity of artemisinin-related endoperox-ides to Ehrlich ascites tumor cells. J Nat Prod 56 849-856. 

Sheeja K, Kuttan G. (2007) Modulation of natural killer activity, antibody dependent cellular toxicity, and antibody dependent complement mediated cytotoxicity by andrographolide in normal and Ehrlich ascites carcinoma bearing mice. Integr Cancer Ther 6 66-73. 

Conversion of 4-aminopyrazolo [3,4-d] pyrimidine (VIII) to its ribonucleotide by mouse tumours and host tissues has been observed [118,119]. Although no evidence of the anabolism of A -methyladenine (111) [120] to the ribonucleotide was obtained in mice with Ehrlich ascites carcinoma [121, 122], it is anabolized by bacteria [123. 124] and the enzyme responsible was partially purified from Salmonella typhimurium [125]. Human epidermoid carcinoma No. 2 cells resistant to 2-fluoroadenine (H.Ep.-2/FA) have lost adenine phosphoribosyl-... 

Chromatographic evidence has been obtained for the formation of 6-thioguanosine di- and triphosphates in Ehrlich ascites cells [197] and their formation is supported by the demonstrated incorporation of thioguanine into nucleic acids as thioguanylic acid [198]. The incorporation of both the a- and 3-anomers of 2 -deoxythioguanosine (XXXVI) [199] into DNA without... 

Cordycepin-1-oxide (XLVIIl) is activated in Ehrlich ascites cells by reduction to cordycepin [220] and a similar A -oxide reduction probably underlies the action of 6-mercaptopurine-3-oxide (XLIX) [221]. 

The first step of this sequence, which is not unique to de novo purine nucleotide biosynthesis, is the synthesis of 5-phosphoribosylpyrophosphate (PRPP) from ribose-5-phosphate and adenosine triphosphate. Phosphoribosyl-pyrophosphate synthetase, the enzyme that catalyses this reaction [278], is under feedback control by adenosine triphosphate [279]. Cordycepin interferes with thede novo pathway [229, 280, 281), and cordycepin triphosphate inhibits the synthesis of PRPP in extracts from Ehrlich ascites tumour cells [282]. Formycin [283], probably as the triphosphate, 9-0-D-xylofuranosyladenine [157] triphosphate, and decoyinine (LXXlll) [284-286] (p. 89) also inhibit the synthesis of PRPP in tumour cells, and this is held to be the blockade most important to their cytotoxic action. It has been suggested but not established that tubercidin (triphosphate) may also be an inhibitor of this reaction [193]. 

The effect of 6-mercaptopurine on the incorporation of a number of C-labelled compounds into soluble purine nucleotides and into RNA and DNA has been studied in leukemia L1210, Ehrlich ascites carcinoma, and solid sarcoma 180. At a level of 6-mercaptopurine that markedly inhibited the incorporation of formate and glycine, the utilization of adenine or 2-aminoadenine was not affected. There was no inhibition of the incorporation of 5(or 4)-aminoimidazole-4(5)-carboxamide (AIC) into adenine derivatives and no marked or consistent inhibition of its incorporation into guanine derivatives. The conversion of AIC to purines in ascites cells was not inhibited at levels of 6-mercaptopurine 8-20 times those that produced 50 per cent or greater inhibition of de novo synthesis [292]. Furthermore, AIC reverses the inhibition of growth of S180 cells (AH/5) in culture by 6-mercaptopurine [293]. These results suggest that in all these systems, in vitro and in vivo, the principal site at which 6-mercaptopurine inhibits nucleic acid biosynthesis is prior to the formation of AIC, and that the interconversion of purine ribonucleotides (see below) is not the primary site of action [292]. Presumably, this early step is the conversion of PRPP to 5-phosphoribosylamine inhibited allosterically by 6-mercaptopurine ribonucleotide (feedback inhibition is not observed in cells that cannot convert 6-mercaptopurine to its ribonucleotide [244]. 

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