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Maintaining Low BCR-ABL Signaling Output to Restrict CML Progression and Enable Persistence
Current Hematologic Malignancy Reports Open Access 06 February 2014
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Acknowledgements
The authors thank members of the Leukemia/Bone Marrow Transplant Program of British Columbia for facilitating access to CML patients’ samples and clinical data; the Terry Fox Laboratory FACS Facility for assistance in cell sorting; the Stem Cell Assay Laboratory for cell processing and cryopreservation of CML samples; K Saw and K Lambie for excellent technical assistance; and Prof Richard I Christopherson (University of Sydney) and Prof Michael Neuberger (MRC Laboratory of Molecular Biology, Cambridge) for useful discussion. This work was supported in part by grants from the Canadian Cancer Society Research Institute (to XJ, AE and CE), the Cancer Research Society, the Leukemia & Lymphoma Society of Canada and the Canadian Cancer Society (to XJ) with core infrastructure support from the British Columbia Cancer Foundation. X Jiang is Michael Smith Foundation for Health Research Scholar.
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Grant, H., Jiang, X., Stebbing, J. et al. Analysis of BCR–ABL1 tyrosine kinase domain mutational spectra in primitive chronic myeloid leukemia cells suggests a unique mutator phenotype. Leukemia 24, 1817–1821 (2010). https://doi.org/10.1038/leu.2010.179
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DOI: https://doi.org/10.1038/leu.2010.179
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