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

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, Wolf-Karsten Hofmann, Sebastian Herzog, Hassan Jumaa, H. Phillip Koeffler, J. Jessica Yu, Nora Heisterkamp, Thomas G. Graeber, Hong Wu, B. Hilda Ye, Ari Melnick and Markus Müschen ()
Additional contact information
Cihangir Duy: University of California San Francisco
Christian Hurtz: University of California San Francisco
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
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

Nature, 2011, vol. 473, issue 7347, 384-388

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.

Date: 2011
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DOI: 10.1038/nature09883

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