scholarly journals INHIBITION OF EHRLICH ASCITES TUMOUR (EAT) CELLS PROLIFERATION THROUGH CHITOSAN-MEDIATED REGULATION OF ACTIVITY OF THE AKT PATHWAY

2014 ◽  
Vol 19 (1) ◽  
pp. 33-40
Author(s):  
Jan Ignacak ◽  
◽  
Maria Wiśniewska-Wrona ◽  
Joanna Dulinska-Litewka ◽  
Iwona Palka ◽  
...  
Keyword(s):  
Akt Pathway ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Regulation Of Activity ◽  
Eat Cells

scholarly journals Interferon alters the pattern of secreted proteins from Ehrlich ascites-tumour cells

1989 ◽  
Vol 261 (1) ◽  
pp. 57-61 ◽  
Author(s):  
S Tominaga ◽  
K Tominaga
Keyword(s):  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Culture Fluid ◽  
Two Dimensional Gel Electrophoresis ◽  
Gag Proteins ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Molecular Masses ◽  
Eat Cells

Treatment of Ehrlich ascites-tumour (EAT) cells with interferon (IFN) abolished their ability to secrete a 32 kDa protein that was secreted by growing EAT cells. These IFN-treated cells secreted two proteins (molecular masses 100 and 89 kDa as estimated by SDS/polyacrylamide-gel electrophoresis) that were not detected in two-dimensional gel electrophoresis of the culture fluid of untreated EAT cells. The sequence of 20 amino acids from the N-terminal end of the 32 kDa protein was very similar to portions of sequences of mouse proviral gag proteins.

Ehrlich ascites tumour cells show tissue-specific adherence and modify their shape upon contact with embryonic fibroblasts and myotubes

1990 ◽  
Vol 97 (3) ◽  
pp. 433-438
Author(s):  
E. Wojciak ◽  
W. Korohoda
Keyword(s):  
Direct Interaction ◽  
Cell Spreading ◽  
Ascites Tumour ◽  
L1210 Cells ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
A Cell ◽  
Eat Cells ◽  
Embryo Fibroblasts ◽  
And Migration

Adhesiveness of Ehrlich ascites tumour (EAT) cells to glass, to mouse peritoneal membrane, living and aldehyde-fixed mouse embryo fibroblasts and chick embryo fibroblasts, myoblasts and myotubes was investigated. The ascitic EAT cells (and leukaemia L1210 cells) did not adhere to glass and peritoneum but readily adhered to embryo fibroblasts, myoblasts and myotubes. The attachment was followed by cell spreading and migration. Fixation of fibroblasts or myogenic cells with aldehydes did not prevent ascitic cells from attaching but reduced the rate of spreading. Only direct interaction of ascitic cells with embryo myoblasts or fibroblasts induced changes in tumour cell adhesiveness followed by cell spreading and locomotion. These results are discussed in relation to an observation that ascitic cells growing as a cell suspension intraperitoneally grow as a solid tumour when injected subcutaneously.

Effects produced by Royal Jelly on haematopoiesis: relation with host resistance against Ehrlich ascites tumour challenge

2005 ◽  
Vol 5 (4) ◽  
pp. 679-688 ◽  
Author(s):  
Claudia Bincoletto ◽  
Samara Eberlin ◽  
Camila A.V. Figueiredo ◽  
Marcos B. Luengo ◽  
Mary L.S. Queiroz
Keyword(s):  
Host Resistance ◽  
Royal Jelly ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour

scholarly journals The transport and oxidation of succinate by Ehrlich ascites-tumour cells

1976 ◽  
Vol 160 (1) ◽  
pp. 121-123 ◽  
Author(s):  
T L Spencer
Keyword(s):  
Ph Dependence ◽  
Organic Anion ◽  
Tumour Cells ◽  
Cell Integrity ◽  
Carrier System ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Ascites Tumour Cells ◽  
Ehrlich Ascites Tumour Cells

The transport and oxidation of succinate by functionally intact Ehrlich ascites-tumour cells was investigated. On the basis of pH dependence and inhibitor sensitivity it was concluded that succinate may be transported across the cell membrane by the organic anion carrier system. Thus the ability of isolated Ehrlich cells to oxidize succinate is real, and is not necessarily a result of damage to cell integrity.

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