Attenuation of cytogenetic effects by erythropoietin in human lymphocytes in vitro and P388 ascites tumor cells in vivo treated with irinotecan (CPT-11)

2010 ◽  
Vol 48 (1) ◽  
pp. 242-249 ◽  
Author(s):  
E. Digkas ◽  
D. Kareli ◽  
S. Chrisafi ◽  
T. Passadaki ◽  
E. Mantadakis ◽  
...  
1994 ◽  
Vol 17 (1) ◽  
pp. 50-54 ◽  
Author(s):  
Tetsu Shinkai ◽  
Tomohide Tamura ◽  
Tetsuro Sano ◽  
Akira Kojima ◽  
Kenji Eguchi ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Saskia Stier ◽  
Claudia Maletzki ◽  
Ulrike Klier ◽  
Michael Linnebacher

Toll-like receptors (TLRs), a family of pattern recognition receptors recognizing molecules expressed by pathogens, are typically expressed by immune cells. However, several recent studies revealed functional TLR expression also on tumor cells. Their expression is a two-sided coin for tumor cells. Not only tumor-promoting effects of TLR ligands are described but also direct oncopathic and immunostimulatory effects. To clarify TLRs’ role in colorectal cancer (CRC), we tested the impact of the TLR ligands LPS, Poly I:C, R848, and Taxol on primary human CRC cell lines (HROC40, HROC60, and HROC69)in vitroandin vivo(CT26). Taxol, not only a potent tumor-apoptosis-inducing, but also TLR4-activating chemotherapeutic compound, inhibited growth and viability of all cell lines, whereas the remaining TLR ligands had only marginal effects (R848 > LPS > Poly I:C). Combinations of the substances here did not improve the results, whereas antitumoral effects were dramatically boosted when human lymphocytes were added. Here, combining the TLR ligands often diminished antitumoral effects.In vivo, best tumor growth control was achieved by the combination of Taxol and R848. However, when combined with LPS, Taxol accelerated tumor growth. These data generally prove the potential of TLR ligands to control tumor growth and activate immune cells, but they also demonstrate the importance of choosing the right combinations.


2010 ◽  
Vol 25 (1) ◽  
pp. 111-116 ◽  
Author(s):  
Rondon Tosta Ramalho ◽  
Ricardo Dutra Aydos ◽  
Marney Pascoli Cereda

PURPOSE: To evaluate the antitumor effect of acetone cyanohydrin in Ehrlich ascites tumor cells in vitro. METHODS: The Ehrlich ascites tumor cells and lymphocytes were incubated with different concentrations of acetone cyanohydrin (0, 0.5, 1.0, 2.0, 10.0, 20.0 and 30.0 μg.mL-1), After 1, 2, 3, 4, 18 and 24 hours cell viability tests were performed by the trypan blue method. RESULTS: The results demonstrated a dose-dependent cytotoxic effect against the cells of Ehrlich ascites tumor. The concentrations of 20 and 30 μg.mL-1 was 100% of cell death in only 1 and 2 hours respectively. In lower doses of 0.5, 1.0 and 2.0 μg.mL-1 the cytotoxic effect was less intense, increasing gradually with time. CONCLUSIONS: At low concentrations of 0.5, 1.0 and 2.0 μg.mL-1, more than 90% of cell death was observed only after 24 hours of incubation which is the evidence that the tumor cell has the ability to poison cumulatively and irreversibly itself with the acetone cyanohydrin when compared with the results presented by human lymphocytes that the same doses and at the same time of incubation reached a maximum of 30% of cell death, suggesting an activity of rhodanese differentiated between the two cells.


1959 ◽  
Vol 37 (8) ◽  
pp. 1011-1023 ◽  
Author(s):  
A. R. P. Paterson

A nucleotide metabolite of 6-mercaptopurine has been isolated from Erhlich ascites carcinoma cells exposed to this compound under in vivo and in vitro conditions. By chemical and enzymatic methods, this nucleotide has been identified as 6-mercaptopurine nucleoside-5′-monophosphate.6-Mercaptopurine nucleotide is formed rapidly in the tumor cells in vivo, maximum concentrations being achieved within 0.5 hours after administration of the analogue. Treatment of the tumor cells with 6-mercaptopurine or with azaserine induced a twofold to threefold enhancement in their ability to synthesize 6-mercaptopurine nucleotide.Using isotopic techniques small amounts of 6-mercaptopurine nucleotide were detected in liver, intestine, and a solid tumor. The conversion of 6-mercaptopurine to the nucleotide form was also demonstrated in an ascitic form of Sarcoma 180.


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