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Titolo:
DRUG-RESISTANCE MECHANISMS IN CHRONIC LYMPHOCYTIC-LEUKEMIA
Autore:
RIBRAG V; MASSADE L; FAUSSAT AM; DREYFUS F; BAYLE C; GOUYETTE A; MAIRE JP;
Indirizzi:
INST GUSTAVE ROUSSY,SERV MED C F-94805 VILLEJUIF FRANCE CNRS,URA 147,DEPT PHARMACOTOXICOL & PHARMACOGENET VILLEJUIF FRANCE INST GUSTAVE ROUSSY,HEMATOL LAB VILLEJUIF FRANCE HOP HOTEL DIEU,LAB CINET & CULTURES CELLULAIRES PARIS FRANCE HOP COCHIN,INSERM,U363,ICGM,SERV HEMATOL F-75674 PARIS FRANCE
Titolo Testata:
Leukemia
fascicolo: 12, volume: 10, anno: 1996,
pagine: 1944 - 1949
SICI:
0887-6924(1996)10:12<1944:DMICL>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
DNA TOPOISOMERASE-II; MULTIDRUG-RESISTANCE; GENE-EXPRESSION; P-GLYCOPROTEIN; CELLS; CLL; EPIPODOPHYLLOTOXINS; CHLORAMBUCIL; SENSITIVITY; SURVIVAL;
Keywords:
CLL; DRUG RESISTANCE; GLUTATHIONE SYSTEM; TOPOISOMERASE II; MDR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
V. Ribrag et al., "DRUG-RESISTANCE MECHANISMS IN CHRONIC LYMPHOCYTIC-LEUKEMIA", Leukemia, 10(12), 1996, pp. 1944-1949

Abstract

Peripheral blood samples from 18 patients with chronic lymphocytic leukemias (CLL) who were either untreated but who were later sensitive to chlorambucil (CLL S) or resistant to a combination containing doxorubicin, vincristine, cyclophosphamide and prednisone (CLL R) were studied for glutathione system, P-glycoprotein, PCNA and topoisomerase II expression. P-glycoprotein expression detected by an immunocytochemicaltechnique using MRK 16 antibody was present at the same level in CLL S and CLL R. The percentage of cells positive for P-gp was below 5% inall samples tested. Topoisomerase II alpha level was quantified by Western blot analysis. None of the 18 CLL samples had detectable topoisomerase II alpha protein. In addition, 12 CLL were tested for PCNA staining and no samples had more than 1% of positive cells at immunocytochemical detection indicating that CLL cells were not engaged in the cell cycle. Some differences were found between CLL S and CLL R in the glutathione system. Glutathione concentration (GSH) and GST activity wasthe same in CLL S and CLL R. The glutathione-S-transferase (GST) isoenzyme profile was different in the two CLL groups. The mean GST-pi andGST-alpha quantitation were twice as high as in CLL R compared to CLLS, but this difference did not reach statistical significance becauseof large variations between CLL samples. A significant correlation was observed between GST-pi expression and GST activity using CDNB as the substrate. GST-mu was detected in only one of seven CLL before therapy and in six of 11 resistant to chemotherapy. No correlation was found between P-glycoprotein expression, GST activity and the different GST isoenzymes studied. These results suggest that the glutathione system could play a role in the resistance of anticancer agents in chronic lymphocytic leukemia. The role of the other drug resistance mechanisms(P-glycoprotein and topoisomerase II alpha) seems to be of limited importance.

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Documento generato il 25/11/20 alle ore 04:19:19