Carcinoma Ehrlich cells

Wynder. E. L., Kmet, J.. Oungai, N., and Segi, M. An epidemiological investigation of gastric cancer. Cancer, 16 1461-1 6,1963. Yagashita, K., Takahashi, N., Yamamoto, H., Jinnouchi, H., Hiyoshi, S., and Miyakawa, T. Effects of tetraacetyl-bis-dehydroascorbic acid, a derivative of ascorbic acid, on Ehrlich cells and HeLa cells (human carcinoma cells). J. Nutr. Sci. Vitaminol., 22 419-427,1976. 

Byrnes RW, Antholine WE, Petering DH (1992) Oxidation-reduction reactions in Ehrlich cells treated with copper-neocuproine. Free Radic Biol Med 13 469-478 Capon DJ, Chen EY, Levinson AD, Seeburg PH, Goeddel DV (1983) Complete nucleotide sequences of the T24 human bladder carcinoma oncogene and its normal homologue. Nature 302 33-37... 

Ehrlich ascites carcinoma Whole cells 100 Wallach and Eylar,... 

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. 

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... 

Burlaka et al. (2004) used pristine C60 at 10 pM with visible light from a mercury lamp to produce some phototoxicity in Ehrlich carcinoma cells or rat thymocytes and used EPR spin-trapping techniques to demonstrate the formation of ROS. 

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-... 

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]. 

In die peripheral blood system, crocetin derivatives prevent an elevation in bilirubin levels [3] and also reduce elevated levels of serum cholesterol and triglyceride [4]. Anti-tumor activity of saffron is observed in mice transplanted with several types of tumor cell lines including sarcoma 180, Ehrlich ascites carcinoma, and Dalton s lymphoma ascites... 

Ehrlich ascites carcinoma cell <21> (<21> from intraperitoneal cavity [70]) [70]... 

Mukherjee, K. Ghosh, S. Ray, M. Ray, S. Purification and characterization of 3-phosphoglycerate kinase from Ehrlich ascites carcinoma cells. Indian J. Biochem. Biophys., 39, 332-341 (2002)... 

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. 

Amounts of Glucose by Ehrlich Ascites Carcinoma Cells, Cancer Res. (1966) 26,276. 

Considerable evidence has shown that selenium can inhibit the growth of experimentally transplanted tumors (65-74) One of the principal cell lines that has been used for many of these studies has been the Ehrlich ascites tumor cell (65-68) Abdullaev et al., (65) showed that the parenteral administration of sodium selenite at a dose of 1 ug per g body weight of the host retarded the growth of this tumor cell line. Additional studies also revealed that similar quantities of jelenium inhibited the growth of Guerin carcinoma, sarcomatous M neoplasms and L-1210 leukemic cells (65, 74) ... 

---