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  • The regulation of bcr-abl in hypoxia is through the mTOR pathway

    Author(s)
    Clapper, Erin
    Di Trapani, Giovanna
    Tonissen, Kathryn F
    Griffith University Author(s)
    Di Trapani, Jenny
    Tonissen, Kathryn F.
    Year published
    2020
    Metadata
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    Abstract
    Chronic myeloid leukemia (CML) is usually characterized by the formation of the fusion onco-protein bcr-abl. Therefore, the majority of CML treatments are bcr-abl specific tyrosine kinase inhibitors (TKIs). TKI resistance in CML treatment is becoming a major obstacle in managing this disease. One well-studied form of drug resistance is hypoxia-induced drug resistance, a phenomenon observed in many other cancers. This study aimed to determine the efficacy of TKIs in CML cells cultured in hypoxia. It was observed that bcr-abl translation was severely halted in hypoxia, rendering TKIs ineffective. We found that the mechanism ...
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    Chronic myeloid leukemia (CML) is usually characterized by the formation of the fusion onco-protein bcr-abl. Therefore, the majority of CML treatments are bcr-abl specific tyrosine kinase inhibitors (TKIs). TKI resistance in CML treatment is becoming a major obstacle in managing this disease. One well-studied form of drug resistance is hypoxia-induced drug resistance, a phenomenon observed in many other cancers. This study aimed to determine the efficacy of TKIs in CML cells cultured in hypoxia. It was observed that bcr-abl translation was severely halted in hypoxia, rendering TKIs ineffective. We found that the mechanism by which bcr-abl protein levels were being suppressed in hypoxia was through the mTOR pathway, specifically via ribosomal protein S6 (RPS6). This information is vital to the improvement of CML treatments, as it can be used to determine how to best combat hypoxia-induced drug resistance in CML and subsequently to identify new targets for treatment.
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    Journal Title
    Leukemia & Lymphoma
    DOI
    https://doi.org/10.1080/10428194.2020.1849679
    Note
    This publication has been entered as an advanced online version in Griffith Research Online.
    Subject
    Clinical sciences
    Publication URI
    http://hdl.handle.net/10072/399938
    Collection
    • Journal articles

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