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BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR–ABL1 kinase inhibition

Author

Listed:
  • Cihangir Duy

    (University of California San Francisco
    Children’s Hospital Los Angeles, University of Southern California)

  • Christian Hurtz

    (University of California San Francisco
    Faculty of Biology, BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-Universität Freiburg and Max-Planck-Institute for Immunobiology, Freiburg, Germany)

  • Seyedmehdi Shojaee

    (University of California San Francisco)

  • Leandro Cerchietti

    (Weill Cornell Medical College)

  • Huimin Geng

    (Weill Cornell Medical College)

  • Srividya Swaminathan

    (University of California San Francisco)

  • Lars Klemm

    (University of California San Francisco)

  • Soo-mi Kweon

    (Children’s Hospital Los Angeles, University of Southern California)

  • Rahul Nahar

    (University of California San Francisco
    Children’s Hospital Los Angeles, University of Southern California)

  • Melanie Braig

    (Universitätsklinikum Hamburg-Eppendorf)

  • Eugene Park

    (Children’s Hospital Los Angeles, University of Southern California)

  • Yong-mi Kim

    (Children’s Hospital Los Angeles, University of Southern California)

  • Wolf-Karsten Hofmann

    (Universität Heidelberg, Klinikum Mannheim, Mannheim, Germany)

  • Sebastian Herzog

    (Faculty of Biology, BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-Universität Freiburg and Max-Planck-Institute for Immunobiology, Freiburg, Germany)

  • Hassan Jumaa

    (Faculty of Biology, BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-Universität Freiburg and Max-Planck-Institute for Immunobiology, Freiburg, Germany)

  • H. Phillip Koeffler

    (Cedars Sinai Medical Center)

  • J. Jessica Yu

    (Albert Einstein College of Medicine)

  • Nora Heisterkamp

    (Children’s Hospital Los Angeles, University of Southern California)

  • Thomas G. Graeber

    (University of California Los Angeles)

  • Hong Wu

    (University of California Los Angeles)

  • B. Hilda Ye

    (Albert Einstein College of Medicine)

  • Ari Melnick

    (Weill Cornell Medical College)

  • Markus Müschen

    (University of California San Francisco
    Children’s Hospital Los Angeles, University of Southern California)

Abstract

Drug resistance in BCL6-dependent leukaemia Targeted cancer therapies are often associated with drug resistance, a phenomenon that has been observed with tyrosine kinase inhibitors (TKIs), widely used to treat leukaemia driven by BCR–ABL1 mutations. Markus Mueschen and colleagues describe a novel BCL6-dependent mechanism of drug resistance in leukaemia through which TKI-induced upregulation of BCL6 allows leukemia cells to cope with acute oncogene withdrawal. Targeted inhibition of BCL6 reduces the number of drug-resistant and self-renewing leukaemia-initiating cells. In xenograft models of acute lymphoblastic leukaemia cells carrying BCR–ABL1 mutations, dual inhibition of BCR–ABL1 and BCL6 prevents resistance and improves the anticancer response.

Suggested Citation

  • Cihangir Duy & Christian Hurtz & Seyedmehdi Shojaee & Leandro Cerchietti & Huimin Geng & Srividya Swaminathan & Lars Klemm & Soo-mi Kweon & Rahul Nahar & Melanie Braig & Eugene Park & Yong-mi Kim & Wo, 2011. "BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR–ABL1 kinase inhibition," Nature, Nature, vol. 473(7347), pages 384-388, May.
    • Handle: RePEc:nat:nature:v:473:y:2011:i:7347:d:10.1038_nature09883
    DOI: 10.1038/nature09883
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