Journal article
C. Hurtz, L. Chan, H. Geng, E. Ballabio, G. Xiao, Gauri Deb, H. Khoury, Chun-Wei Chen, S. Armstrong, Jianjun Chen, P. Ernst, A. Melnick, T. Milne, M. Müschen
Genes & Development, 2019
Genes & Development, 2019
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DOI
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APA
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Hurtz, C., Chan, L., Geng, H., Ballabio, E., Xiao, G., Deb, G., … Müschen, M. (2019). Rationale for targeting BCL6 in MLL-rearranged acute lymphoblastic leukemia. Genes &Amp; Development.
Chicago/Turabian
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Hurtz, C., L. Chan, H. Geng, E. Ballabio, G. Xiao, Gauri Deb, H. Khoury, et al. “Rationale for Targeting BCL6 in MLL-Rearranged Acute Lymphoblastic Leukemia.” Genes & Development (2019).
MLA
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Hurtz, C., et al. “Rationale for Targeting BCL6 in MLL-Rearranged Acute Lymphoblastic Leukemia.” Genes &Amp; Development, 2019.
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@article{c2019a,
title = {Rationale for targeting BCL6 in MLL-rearranged acute lymphoblastic leukemia},
year = {2019},
journal = {Genes & Development},
author = {Hurtz, C. and Chan, L. and Geng, H. and Ballabio, E. and Xiao, G. and Deb, Gauri and Khoury, H. and Chen, Chun-Wei and Armstrong, S. and Chen, Jianjun and Ernst, P. and Melnick, A. and Milne, T. and Müschen, M.}
}
Abstract
In this study, Hurtz et al. used genetic mouse models and patient-derived leukemia cells to show that the transcriptional repressor BCL6 functions as a central driver of drug resistance in MLL-rearranged B-cell leukemia. Their genetic and ChIP-seq analyses demonstrated that MLL-AF4 and MLL-ENL fusions directly bound to the BCL6 promoter and up-regulated BCL6 expression, thus providing new insights into a previously unrecognized requirement of malignant transformation by oncogenic MLL fusions.