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Access through your institution Buy or subscribe Acute myeloid leukemia (AML) is a heterogeneous hematologic disease characterized by the accumulation of immature myeloid cells. Despite the
recent advances in the treatment of AML, drug resistance and disease relapse remain a substantial clinical problem. AML cells are characterized by their recurrent contact with the stromal
microenvironment in the bone marrow (BM).1 This interplay between the BM stroma and AML cells protects malignant cells from spontaneous apoptosis, promotes proliferation and drug resistance.
Increasing evidence suggests that this stromal refuge has a pivotal role in paving the way for disease relapse. This is a preview of subscription content, access via your institution ACCESS
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institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * Ayala F, Dewar R, Kieran M, Kalluri R . Contribution of bone microenvironment to leukemogenesis and
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Google Scholar Download references ACKNOWLEDGEMENTS MQ was supported by the IZKF Erlangen. RJ was supported by the ELAN program of the University of Erlangen. FAK was supported by the EC
FP7-funded project RADIANT. DM was supported by the IZKF Erlangen and the Max-Eder program of the Deutsche Krebshilfe. We acknowledge the assistance of the Core Unit Cell Sorting and
Immunomonitoring Erlangen. AUTHOR CONTRIBUTIONS MB performed research, analyzed data and helped writing the manuscript. MQ, MB, FK, DS and WH performed research and analyzed data. MA
collected patient material and provided patient data. AM provided patient material and helped writing the manuscript. RJ performed research, helped designing the study and writing the
manuscript. DM designed the study, analyzed data and wrote the manuscript. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Internal Medicine 5, Hematology and Oncology,
University of Erlangen-Nuremberg, Erlangen, Germany M Braun, M Qorraj, D Saul, M Aigner, A Mackensen, R Jitschin & D Mougiakakos * Department of Nephropathology, Institute of Pathology,
University of Erlangen-Nuremberg, Erlangen, Germany M Büttner * European Molecular Biology Laboratory (EMBL), Heidelberg, Germany F A Klein & W Huber Authors * M Braun View author
publications You can also search for this author inPubMed Google Scholar * M Qorraj View author publications You can also search for this author inPubMed Google Scholar * M Büttner View
author publications You can also search for this author inPubMed Google Scholar * F A Klein View author publications You can also search for this author inPubMed Google Scholar * D Saul View
author publications You can also search for this author inPubMed Google Scholar * M Aigner View author publications You can also search for this author inPubMed Google Scholar * W Huber
View author publications You can also search for this author inPubMed Google Scholar * A Mackensen View author publications You can also search for this author inPubMed Google Scholar * R
Jitschin View author publications You can also search for this author inPubMed Google Scholar * D Mougiakakos View author publications You can also search for this author inPubMed Google
Scholar CORRESPONDING AUTHOR Correspondence to D Mougiakakos. ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no conflict of interest. ADDITIONAL INFORMATION Supplementary
Information accompanies this paper on the Leukemia website SUPPLEMENTARY INFORMATION SUPPLEMENTARY INFORMATION (DOCX 795 KB) RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS
ARTICLE CITE THIS ARTICLE Braun, M., Qorraj, M., Büttner, M. _et al._ CXCL12 promotes glycolytic reprogramming in acute myeloid leukemia cells via the CXCR4/mTOR axis. _Leukemia_ 30,
1788–1792 (2016). https://doi.org/10.1038/leu.2016.58 Download citation * Published: 08 March 2016 * Issue Date: August 2016 * DOI: https://doi.org/10.1038/leu.2016.58 SHARE THIS ARTICLE
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