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

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BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition. / Duy, Cihangir; Hurtz, Christian; Shojaee, Seyedmehdi; Cerchietti, Leandro; Geng, Huimin; Swaminathan, Srividya; Klemm, Lars; Kweon, Soo-mi; Nahar, Rahul; Balabanov, Melanie; Park, Eugene; Kim, Yong-mi; Hofmann, Wolf-Karsten; Herzog, Sebastian; Jumaa, Hassan; Koeffler, H Phillip; Yu, J Jessica; Heisterkamp, Nora; Graeber, Thomas G; Wu, Hong; Ye, B Hilda; Melnick, Ari; Müschen, Markus.

in: NATURE, Jahrgang 473, Nr. 7347, 7347, 2011, S. 384-388.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Duy, C, Hurtz, C, Shojaee, S, Cerchietti, L, Geng, H, Swaminathan, S, Klemm, L, Kweon, S, Nahar, R, Balabanov, M, Park, E, Kim, Y, Hofmann, W-K, Herzog, S, Jumaa, H, Koeffler, HP, Yu, JJ, Heisterkamp, N, Graeber, TG, Wu, H, Ye, BH, Melnick, A & Müschen, M 2011, 'BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition.', NATURE, Jg. 473, Nr. 7347, 7347, S. 384-388. <http://www.ncbi.nlm.nih.gov/pubmed/21593872?dopt=Citation>

APA

Duy, C., Hurtz, C., Shojaee, S., Cerchietti, L., Geng, H., Swaminathan, S., Klemm, L., Kweon, S., Nahar, R., Balabanov, M., Park, E., Kim, Y., Hofmann, W-K., Herzog, S., Jumaa, H., Koeffler, H. P., Yu, J. J., Heisterkamp, N., Graeber, T. G., ... Müschen, M. (2011). BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition. NATURE, 473(7347), 384-388. [7347]. http://www.ncbi.nlm.nih.gov/pubmed/21593872?dopt=Citation

Vancouver

Duy C, Hurtz C, Shojaee S, Cerchietti L, Geng H, Swaminathan S et al. BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition. NATURE. 2011;473(7347):384-388. 7347.

Bibtex

@article{5964cab0250847d8a5f2eb8d996ec9ce,
title = "BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition.",
abstract = "Tyrosine kinase inhibitors (TKIs) are widely used to treat patients with leukaemia driven by BCR-ABL1 (ref. 1) and other oncogenic tyrosine kinases. Recent efforts have focused on developing more potent TKIs that also inhibit mutant tyrosine kinases. However, even effective TKIs typically fail to eradicate leukaemia-initiating cells (LICs), which often cause recurrence of leukaemia after initially successful treatment. Here we report the discovery of a novel mechanism of drug resistance, which is based on protective feedback signalling of leukaemia cells in response to treatment with TKI. We identify BCL6 as a central component of this drug-resistance pathway and demonstrate that targeted inhibition of BCL6 leads to eradication of drug-resistant and leukaemia-initiating subclones.",
keywords = "Animals, Humans, Mice, Transcription, Genetic, Tumor Suppressor Protein p53/metabolism, Mice, SCID, Cell Survival/drug effects, Mice, Inbred NOD, *Drug Resistance, Neoplasm, ADP-Ribosylation Factor 1/metabolism, DNA-Binding Proteins/biosynthesis/deficiency/genetics/*metabolism, Fusion Proteins, bcr-abl/*antagonists & inhibitors, Gene Expression Regulation, Neoplastic/drug effects, Precursor Cell Lymphoblastic Leukemia-Lymphoma/*drug therapy/genetics/metabolism/*pathology, Protein Kinase Inhibitors/*pharmacology/therapeutic use, Animals, Humans, Mice, Transcription, Genetic, Tumor Suppressor Protein p53/metabolism, Mice, SCID, Cell Survival/drug effects, Mice, Inbred NOD, *Drug Resistance, Neoplasm, ADP-Ribosylation Factor 1/metabolism, DNA-Binding Proteins/biosynthesis/deficiency/genetics/*metabolism, Fusion Proteins, bcr-abl/*antagonists & inhibitors, Gene Expression Regulation, Neoplastic/drug effects, Precursor Cell Lymphoblastic Leukemia-Lymphoma/*drug therapy/genetics/metabolism/*pathology, Protein Kinase Inhibitors/*pharmacology/therapeutic use",
author = "Cihangir Duy and Christian Hurtz and Seyedmehdi Shojaee and Leandro Cerchietti and Huimin Geng and Srividya Swaminathan and Lars Klemm and Soo-mi Kweon and Rahul Nahar and Melanie Balabanov and Eugene Park and Yong-mi Kim and Wolf-Karsten Hofmann and Sebastian Herzog and Hassan Jumaa and Koeffler, {H Phillip} and Yu, {J Jessica} and Nora Heisterkamp and Graeber, {Thomas G} and Hong Wu and Ye, {B Hilda} and Ari Melnick and Markus M{\"u}schen",
year = "2011",
language = "English",
volume = "473",
pages = "384--388",
journal = "NATURE",
issn = "0028-0836",
publisher = "NATURE PUBLISHING GROUP",
number = "7347",

}

RIS

TY - JOUR

T1 - BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition.

AU - Duy, Cihangir

AU - Hurtz, Christian

AU - Shojaee, Seyedmehdi

AU - Cerchietti, Leandro

AU - Geng, Huimin

AU - Swaminathan, Srividya

AU - Klemm, Lars

AU - Kweon, Soo-mi

AU - Nahar, Rahul

AU - Balabanov, Melanie

AU - Park, Eugene

AU - Kim, Yong-mi

AU - Hofmann, Wolf-Karsten

AU - Herzog, Sebastian

AU - Jumaa, Hassan

AU - Koeffler, H Phillip

AU - Yu, J Jessica

AU - Heisterkamp, Nora

AU - Graeber, Thomas G

AU - Wu, Hong

AU - Ye, B Hilda

AU - Melnick, Ari

AU - Müschen, Markus

PY - 2011

Y1 - 2011

N2 - Tyrosine kinase inhibitors (TKIs) are widely used to treat patients with leukaemia driven by BCR-ABL1 (ref. 1) and other oncogenic tyrosine kinases. Recent efforts have focused on developing more potent TKIs that also inhibit mutant tyrosine kinases. However, even effective TKIs typically fail to eradicate leukaemia-initiating cells (LICs), which often cause recurrence of leukaemia after initially successful treatment. Here we report the discovery of a novel mechanism of drug resistance, which is based on protective feedback signalling of leukaemia cells in response to treatment with TKI. We identify BCL6 as a central component of this drug-resistance pathway and demonstrate that targeted inhibition of BCL6 leads to eradication of drug-resistant and leukaemia-initiating subclones.

AB - Tyrosine kinase inhibitors (TKIs) are widely used to treat patients with leukaemia driven by BCR-ABL1 (ref. 1) and other oncogenic tyrosine kinases. Recent efforts have focused on developing more potent TKIs that also inhibit mutant tyrosine kinases. However, even effective TKIs typically fail to eradicate leukaemia-initiating cells (LICs), which often cause recurrence of leukaemia after initially successful treatment. Here we report the discovery of a novel mechanism of drug resistance, which is based on protective feedback signalling of leukaemia cells in response to treatment with TKI. We identify BCL6 as a central component of this drug-resistance pathway and demonstrate that targeted inhibition of BCL6 leads to eradication of drug-resistant and leukaemia-initiating subclones.

KW - Animals

KW - Humans

KW - Mice

KW - Transcription, Genetic

KW - Tumor Suppressor Protein p53/metabolism

KW - Mice, SCID

KW - Cell Survival/drug effects

KW - Mice, Inbred NOD

KW - Drug Resistance, Neoplasm

KW - ADP-Ribosylation Factor 1/metabolism

KW - DNA-Binding Proteins/biosynthesis/deficiency/genetics/metabolism

KW - Fusion Proteins, bcr-abl/antagonists & inhibitors

KW - Gene Expression Regulation, Neoplastic/drug effects

KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/genetics/metabolism/pathology

KW - Protein Kinase Inhibitors/pharmacology/therapeutic use

KW - Animals

KW - Humans

KW - Mice

KW - Transcription, Genetic

KW - Tumor Suppressor Protein p53/metabolism

KW - Mice, SCID

KW - Cell Survival/drug effects

KW - Mice, Inbred NOD

KW - Drug Resistance, Neoplasm

KW - ADP-Ribosylation Factor 1/metabolism

KW - DNA-Binding Proteins/biosynthesis/deficiency/genetics/metabolism

KW - Fusion Proteins, bcr-abl/antagonists & inhibitors

KW - Gene Expression Regulation, Neoplastic/drug effects

KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/genetics/metabolism/pathology

KW - Protein Kinase Inhibitors/pharmacology/therapeutic use

M3 - SCORING: Journal article

VL - 473

SP - 384

EP - 388

JO - NATURE

JF - NATURE

SN - 0028-0836

IS - 7347

M1 - 7347

ER -