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Overproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell lines.

BACKGROUNDImatinib mesylate, a BCR-ABL tyrosine kinase inhibitor, induces apoptosis in chronic myeloid leukemia cells. Resistance to imatinib is currently the most important concern of this treatment. One of the main mechanisms of this resistance is overexpression of BCR-ABL. METHODSIn the current s... Full description

Journal Title: Cancer January 1, 2005, Vol.103(1), pp.102-110
Main Author: Desplat, Vanessa
Other Authors: Belloc, Francis , Lagarde, Valérie , Boyer, Catherine , Melo, Junia V , Reiffers, Josy , Praloran, Vincent , Mahon, François-Xavier
Format: Electronic Article Electronic Article
Language: English
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ID: ISSN: 0008-543X
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title: Overproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell lines.
format: Article
creator:
  • Desplat, Vanessa
  • Belloc, Francis
  • Lagarde, Valérie
  • Boyer, Catherine
  • Melo, Junia V
  • Reiffers, Josy
  • Praloran, Vincent
  • Mahon, François-Xavier
subjects:
  • Antineoplastic Agents–Pharmacology
  • Apoptosis–Drug Effects
  • Benzamides–Genetics
  • Drug Resistance, Neoplasm–Genetics
  • Fusion Proteins, Bcr-Abl–Biosynthesis
  • Genes, Abl–Pathology
  • Humans–Pharmacology
  • Imatinib Mesylate–Pharmacology
  • Leukemia, Myelogenous, Chronic, BCR-Abl Positive–Pharmacology
  • Mitochondria–Pharmacology
  • Piperazines–Pharmacology
  • Pyrimidines–Pharmacology
  • Tumor Cells, Cultured–Pharmacology
  • Abridged
  • Antineoplastic Agents
  • Benzamides
  • Piperazines
  • Pyrimidines
  • Imatinib Mesylate
  • Fusion Proteins, Bcr-Abl
ispartof: Cancer, January 1, 2005, Vol.103(1), pp.102-110
description: BACKGROUNDImatinib mesylate, a BCR-ABL tyrosine kinase inhibitor, induces apoptosis in chronic myeloid leukemia cells. Resistance to imatinib is currently the most important concern of this treatment. One of the main mechanisms of this resistance is overexpression of BCR-ABL. METHODSIn the current study, the authors investigated the correlation between BCR-ABL overexpression and apoptosis in BaF/BCR-ABL and LAMA84 cell lines resistant to imatinib suddenly deprived of the inhibitor, and compared with their sensitive counterpart. RESULTSRemoval of imatinib from culture medium led to a decrease in Bcr-Abl protein expression by Day 5, which was sustained for > or = 3 weeks of imatinib deprivation. Apoptosis was observed after 3 days of imatinib deprivation in resistant lines accompanied by caspase activation, loss of membrane asymmetry (annexin V staining), and alteration of mitochondrial potential (dihexyloxacarbocyanine iodide [DiOC6]). Transient activation of the STAT5/Bcl-xL pathway and Akt kinase activity preceded these responses. CONCLUSIONSThus, imatinib removal led to apoptosis of BCR-ABL-overexpressing leukemic cells, a phenomenon that could be exploited to sensitize imatinib-resistant cells to the cytotoxic effect of other drugs.
language: eng
source:
identifier: ISSN: 0008-543X
fulltext: fulltext
issn:
  • 0008543X
  • 0008-543X
url: Link


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titleOverproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell lines.
creatorDesplat, Vanessa ; Belloc, Francis ; Lagarde, Valérie ; Boyer, Catherine ; Melo, Junia V ; Reiffers, Josy ; Praloran, Vincent ; Mahon, François-Xavier
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ispartofCancer, January 1, 2005, Vol.103(1), pp.102-110
identifierISSN: 0008-543X
subjectAntineoplastic Agents–Pharmacology ; Apoptosis–Drug Effects ; Benzamides–Genetics ; Drug Resistance, Neoplasm–Genetics ; Fusion Proteins, Bcr-Abl–Biosynthesis ; Genes, Abl–Pathology ; Humans–Pharmacology ; Imatinib Mesylate–Pharmacology ; Leukemia, Myelogenous, Chronic, BCR-Abl Positive–Pharmacology ; Mitochondria–Pharmacology ; Piperazines–Pharmacology ; Pyrimidines–Pharmacology ; Tumor Cells, Cultured–Pharmacology ; Abridged ; Antineoplastic Agents ; Benzamides ; Piperazines ; Pyrimidines ; Imatinib Mesylate ; Fusion Proteins, Bcr-Abl
descriptionBACKGROUNDImatinib mesylate, a BCR-ABL tyrosine kinase inhibitor, induces apoptosis in chronic myeloid leukemia cells. Resistance to imatinib is currently the most important concern of this treatment. One of the main mechanisms of this resistance is overexpression of BCR-ABL. METHODSIn the current study, the authors investigated the correlation between BCR-ABL overexpression and apoptosis in BaF/BCR-ABL and LAMA84 cell lines resistant to imatinib suddenly deprived of the inhibitor, and compared with their sensitive counterpart. RESULTSRemoval of imatinib from culture medium led to a decrease in Bcr-Abl protein expression by Day 5, which was sustained for > or = 3 weeks of imatinib deprivation. Apoptosis was observed after 3 days of imatinib deprivation in resistant lines accompanied by caspase activation, loss of membrane asymmetry (annexin V staining), and alteration of mitochondrial potential (dihexyloxacarbocyanine iodide [DiOC6]). Transient activation of the STAT5/Bcl-xL pathway and Akt kinase activity preceded these responses. CONCLUSIONSThus, imatinib removal led to apoptosis of BCR-ABL-overexpressing leukemic cells, a phenomenon that could be exploited to sensitize imatinib-resistant cells to the cytotoxic effect of other drugs.
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titleOverproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell lines.
descriptionBACKGROUNDImatinib mesylate, a BCR-ABL tyrosine kinase inhibitor, induces apoptosis in chronic myeloid leukemia cells. Resistance to imatinib is currently the most important concern of this treatment. One of the main mechanisms of this resistance is overexpression of BCR-ABL. METHODSIn the current study, the authors investigated the correlation between BCR-ABL overexpression and apoptosis in BaF/BCR-ABL and LAMA84 cell lines resistant to imatinib suddenly deprived of the inhibitor, and compared with their sensitive counterpart. RESULTSRemoval of imatinib from culture medium led to a decrease in Bcr-Abl protein expression by Day 5, which was sustained for > or = 3 weeks of imatinib deprivation. Apoptosis was observed after 3 days of imatinib deprivation in resistant lines accompanied by caspase activation, loss of membrane asymmetry (annexin V staining), and alteration of mitochondrial potential (dihexyloxacarbocyanine iodide [DiOC6]). Transient activation of the STAT5/Bcl-xL pathway and Akt kinase activity preceded these responses. CONCLUSIONSThus, imatinib removal led to apoptosis of BCR-ABL-overexpressing leukemic cells, a phenomenon that could be exploited to sensitize imatinib-resistant cells to the cytotoxic effect of other drugs.
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titleOverproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell lines.
authorDesplat, Vanessa ; Belloc, Francis ; Lagarde, Valérie ; Boyer, Catherine ; Melo, Junia V ; Reiffers, Josy ; Praloran, Vincent ; Mahon, François-Xavier
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abstractBACKGROUNDImatinib mesylate, a BCR-ABL tyrosine kinase inhibitor, induces apoptosis in chronic myeloid leukemia cells. Resistance to imatinib is currently the most important concern of this treatment. One of the main mechanisms of this resistance is overexpression of BCR-ABL. METHODSIn the current study, the authors investigated the correlation between BCR-ABL overexpression and apoptosis in BaF/BCR-ABL and LAMA84 cell lines resistant to imatinib suddenly deprived of the inhibitor, and compared with their sensitive counterpart. RESULTSRemoval of imatinib from culture medium led to a decrease in Bcr-Abl protein expression by Day 5, which was sustained for > or = 3 weeks of imatinib deprivation. Apoptosis was observed after 3 days of imatinib deprivation in resistant lines accompanied by caspase activation, loss of membrane asymmetry (annexin V staining), and alteration of mitochondrial potential (dihexyloxacarbocyanine iodide [DiOC6]). Transient activation of the STAT5/Bcl-xL pathway and Akt kinase activity preceded these responses. CONCLUSIONSThus, imatinib removal led to apoptosis of BCR-ABL-overexpressing leukemic cells, a phenomenon that could be exploited to sensitize imatinib-resistant cells to the cytotoxic effect of other drugs.
urlhttp://search.proquest.com/docview/67350458/
doi10.1002/cncr.20758
eissn10970142
date2005-01-01