Ascites tumor

Ehrlich ascites tumor agar, collagen glucose 2.4... 

The kind of detailed quantitative information the method can yield is well illustrated by the determination of the total dry weight of individual ascites tumor cells, the volume of each cell being less than 4 X 10" 9 cc. The total dry weight, mc, of a cell is given by... 

Ascites tumor cells, determination of dry weight of individual, 299, 300 Atomic absorption coefficient, 15 Atomic energy program, use of x-ray absorptiometry in, 96 Atomic number, significance proved by Moseley, 28, 29... 

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. 

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

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

Yarbro JW, Kennedy BJ, Barnum CP. Hydroxyurea inhibition of DNA synthesis in ascites tumor. Proc Natl Acad Sci USA 1965 53 1033-1035. 

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. 

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... 

B. Chance, D. Garfinkel, J. Higgins, and B. Hess, Metabolic control mechanisms A solution for the equations representing interaction between glycolysis and respiration in ascites tumor cells. 

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). 

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)... 

Fetner has also demonstrated chromatid breaks in a human tissue-culture cell line exposed to ozone at 8 ppm for 5 min. Other tissue-culture studies include that of Sachsenmaier et who noted tetraploidy and other chromosomal abnormalities in embryonic chick fibroblasts exposed to ozone and a decrease in transplantability of mouse ascites tumor cells. In addition, Pace et demonstrated an interference by ozone with mitotic activity in two tissue-culture cell lines. More recently, Booher et al. reported that lung cells exposed in culture to ozone concentrations as low as 0.3 ppm demonstrated an inhibition in growth that was proportional to the ozone concentration. 

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. 

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. 

At-Te colloid. Injected by an intraperitoneal route. Ascitic tumor. 

However, as we mentioned above, chemotherapy and immunotherapy are still the only weapons applicable either when solid tumors are delocalized over a large area of the body or when the tumors are liquid (ascites tumors like leukemias). 

DC059 Majumder, P. K., and M. Gupta. Effect of the seed extract of carrot Daucus carota Linn.) on the growth of Ehrlich ascites tumor in mice. Phytoter Res 1998 12(8) 584-585. 

Genotoxic Effects. Genotoxic Effects. HDI was demonstrated to be non-mutagenic against some Salmonella typhimurium strains with or without metabolic activation (Anderson et al. 1980). HDI also inhibited the growth of Ehrlich ascites tumor eells in female mice (Moos et al. 1971) and decreased the mutation frequency in Escherichia coli (Kawazoe et al. 1981). Calf thymus DNA incubated in vitro with 10.4 or 52 mol of HDI for 10 or 20 minutes produeed no evidence of intrastrand cross-links or DNA strand breaks (Peel et al. 1997). No studies were located that studied the genotoxic effects of HDI on human cells or that deseribed the ability of prepolymer forms of HDI to induce genotoxicity."... 

Moos GE, Mcquire JA, Kitchlew WA, et al. 1971. Inhibition of growth of erhlich ascites tumors in ICR-Ha Swiss mice by isocyanates. Cancer Res 31 937-941. 

Maruyama, T., Kataoka, N., Nagase, S., Nakada, H., Sato, H., and Sasaki, H. (1971). Identification of three-line electron spin resonance signal and its relationship to ascites tumors. Cancer Res. 31, 179-184. 

In animals, the first in vivo experiments were performed with bacterial extracts in a guinea pig sarcoma model by Gratia and Linz [88], and with LPS in mouse primary subcutaneous tumors by Shear and Turner [4], The antitumoral effect of LPS on the growth of subcutaneous or intramuscular tumors has been extensively investigated [61,147-153], On ascitic tumors, treatment with LPS was shown to be efficient in some cases [153-155] while failing in others [61,156],... 

Schoneich, J. (1967) The induction of chromosomal aberrations by hydrogen peroxide in strains of ascites tumors in mice. Mutat. Res., 4, 384-388... 

Not only have animals or isolated organs of animals been used to perform pharmacological studies, but also cells in culture. In a study done by Prof. Yamasaki25 at the University of Hiroshima (Figure 16.28), Ehrlich ascites tumor cells have been used to demonstrate the increase of glucose transport into the cell as a function of G115. 

Effect of standardized P. ginseng extract G115 on the glucose transport in Ehrlich ascites tumor cells. 

K. Yamasaki et al., Effects of the standardized ginseng extract G115 on the D-glucose transport by Ehrlich ascites tumor cells, Phytother. Res., 7, 200, 1993. 

Belkin et al. 29> were first to examine various polysaccharide fractions from higher plants for their antitumor activity. They could demonstrate that many of these fractions produced haemorrhagic necrosis in different tumor types. In most cases, the polysaccharides were injected intraperitoneally into mice carrying Sarkoma 37 ascites tumor. The result was a progressive increase in cell volume and in cytoplasmic vacuolization. Osswald 30) found that tragacanth, gum arabic, and CMC reduced tumor cells in Ehrlich ascites carcinoma in female NMRE mice. The effect depended upon the dose, the route of injection, and the molecular size of the polysaccharides administered. 

However, oral administration of these polysaccharides had no effect. Hemi-celluloses from different higher plants caused regression of solid Sarkoma 180 in mice but not of ascites tumor. Arabinoglucuronoxylan isolated from wheat-straw hemicellulose was completely devoid of activity, whereas arabinoglucoxylan was highly active (Nakahara 31)). 

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