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    Autophagy induction by Bcr-Abl-expressing cells facilitates their recovery from a targeted or nontargeted treatment.

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    Authors
    Crowley, Lisa C
    Elzinga, Baukje M
    O'Sullivan, Gerald C
    McKenna, Sharon L
    Affiliation
    Leslie C. Quick Laboratory, Cork Cancer Research Centre, BioSciences Institute,, University College Cork and Mercy University Hospital, Grenville Place, Cork,, Ireland.
    Issue Date
    2012-01-31T16:39:39Z
    MeSH
    Animals
    Autophagy/*drug effects/genetics
    Cell Line, Tumor
    DNA Damage
    Doxorubicin/*pharmacology
    Etoposide/*pharmacology
    Fusion Proteins, bcr-abl/*biosynthesis/genetics
    Gene Knockdown Techniques
    Humans
    K562 Cells
    Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug
    therapy/genetics/*metabolism
    Mice
    Molecular Targeted Therapy/methods
    Piperazines/*pharmacology
    Pyrimidines/*pharmacology
    RNA, Small Interfering/administration & dosage/genetics
    Transfection
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    Citation
    Am J Hematol. 2011 Jan;86(1):38-47.
    Journal
    American journal of hematology
    URI
    http://hdl.handle.net/10147/206351
    DOI
    10.1002/ajh.21914
    PubMed ID
    21132731
    Abstract
    Although Imatinib has transformed the treatment of chronic myeloid leukemia (CML), it is not curative due to the persistence of resistant cells that can regenerate the disease. We have examined how Bcr-Abl-expressing cells respond to two mechanistically different therapeutic agents, etoposide and Imatinib. We also examined Bcr-Abl expression at low and high levels as elevated expression has been associated with treatment failure. Cells expressing low levels of Bcr-Abl undergo apoptosis in response to the DNA-targeting agent (etoposide), whereas high-Bcr-Abl-expressing cells primarily induce autophagy. Autophagic populations engage a delayed nonapoptotic death; however, sufficient cells evade this and repopulate following the withdrawal of the drug. Non-Bcr-Abl-expressing 32D or Ba/F3 cells induce both apoptosis and autophagy in response to etoposide and can recover. Imatinib treatment induces both apoptosis and autophagy in all Bcr-Abl-expressing cells and populations rapidly recover. Inhibition of autophagy with ATG7 and Beclin1 siRNA significantly reduced the recovery of Imatinib-treated K562 cells, indicating the importance of autophagy for the recovery of treated cells. Combination regimes incorporating agents that disrupt Imatinib-induced autophagy would remain primarily targeted and may improve response to the treatment in CML.
    Language
    eng
    ISSN
    1096-8652 (Electronic)
    0361-8609 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1002/ajh.21914
    Scopus Count
    Collections
    Mercy University Hospital

    entitlement

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