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

被引:0
|
作者
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
Markus Müschen
机构
[1] University of California San Francisco,Department of Laboratory Medicine
[2] Children’s Hospital Los Angeles,Department of Pediatrics
[3] University of Southern California,Departments of Medicine and Pharmacology
[4] Weill Cornell Medical College,Department of Hematology and Oncology
[5] Universitätsklinikum Hamburg-Eppendorf,Department of Hematology and Oncology
[6] Universität Heidelberg,Division of Hematology and Oncology
[7] Klinikum Mannheim,Department of Cell Biology
[8] Mannheim,Department of Molecular Pharmacology
[9] Germany,undefined
[10] Faculty of Biology,undefined
[11] BIOSS Centre for Biological Signalling Studies,undefined
[12] Albert-Ludwigs-Universität Freiburg and Max-Planck-Institute for Immunobiology,undefined
[13] Freiburg,undefined
[14] Germany ,undefined
[15] Cedars Sinai Medical Center,undefined
[16] Albert Einstein College of Medicine,undefined
[17] University of California Los Angeles,undefined
来源
Nature | 2011年 / 473卷
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摘要
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.
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页码:384 / 388
页数:4
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