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Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity

Background Targeted treatment of chronic myelogenous leukemia using imatinib has dramatically improved patient outcome. However, residual disease can be detected in the majority of patients treated with imatinib. Compensatory activation of MAP kinases (MAPK1/2) in response to BCR-ABL-inhibitors has...

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Bibliographic Details
Main Authors: Härtel, Nicolai (Author) , Hanfstein, Benjamin (Author) , Müller, Martin Christian (Author) , Erben, Philipp (Author)
Format: Article (Journal)
Language:English
Published: 2012
In: Journal of cancer research and clinical oncology
Year: 2011, Volume: 138, Issue: 2, Pages: 203-212
ISSN:1432-1335
DOI:10.1007/s00432-011-1086-x
Online Access:Verlag, Volltext: http://dx.doi.org/10.1007/s00432-011-1086-x
Verlag, Volltext: http://link.springer.com/10.1007/s00432-011-1086-x
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Author Notes:Nicolai Härtel, Thomas Klag, Benjamin Hanfstein, Martin C. Mueller, Thomas Schenk, Philipp Erben, Andreas Hochhaus, Paul La Rosée
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Summary:Background Targeted treatment of chronic myelogenous leukemia using imatinib has dramatically improved patient outcome. However, residual disease can be detected in the majority of patients treated with imatinib. Compensatory activation of MAP kinases (MAPK1/2) in response to BCR-ABL-inhibitors has been reported as a potential cytokine-dependent resistance mechanism leading to the rescue of leukemic progenitor cells.
Item Description:Published online: 17 November 2011
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Physical Description:Online Resource
ISSN:1432-1335
DOI:10.1007/s00432-011-1086-x

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