Flis, K., Irvine, D., Copland, M. , Bhatia, R. and Skorski, T. (2012) Chronic myeloid leukemia stem cells display alterations in expression of genes involved in oxidative phosphorylation. Leukemia and Lymphoma, 53(12), pp. 2474-2478. (doi: 10.3109/10428194.2012.696313)

Faley, S., Copland, M. , Reboud, J. and Cooper, J. M. (2012) Intracellular protein trafficking kinetics in chronic myeloid leukemia stem cells using a microfluidic platform. Integrative Biology, 4(4), p. 368. (doi: 10.1039/c2ib00086e)

Pellicano, F., Simara, P., Sinclair, A., Helgason, G.V. , Copland, M. , Grant, S. and Holyoake, T.L. (2011) The MEK inhibitor PD184352 enhances BMS-214662-induced apoptosis in CD34+ CML stem/progenitor cells. Leukemia, 25(7), pp. 1159-67. (doi: 10.1038/leu.2011.67)

Lucas, C. M., Harris, R. J., Giannoudis, A., Copland, M. , Slupsky, J. R. and Clark, R. E. (2011) Cancerous inhibitor of PP2A (CIP2A) at diagnosis of chronic myeloid leukemia is a critical determinant of disease progression. Blood, 117(24), pp. 6660-6668. (doi: 10.1182/blood-2010-08-304477)

Pellicano, F., Copland, M. , Jorgensen, H. G. , Mountford, J., Leber, B. and Holyoake, T. L. (2009) BMS-214662 induces mitochondrial apoptosis in chronic myeloid leukemia (CML) stem/progenitor cells, including CD34⁺38^- cells, through activation of protein kinase Cβ. Blood, 114(19), pp. 4186-4196. (doi: 10.1182/blood-2009-05-219550)

Faley, S. L., Copland, M. , Wlodkowic, D., Kolch, W., Seale, K. T., Wikswo, J. P. and Cooper, J. M. (2009) Microfluidic single cell arrays to interrogate signalling dynamics of individual, patient-derived hematopoietic stem cells. Lab on a Chip, 9(18), pp. 2659-2664. (doi: 10.1039/b902083g)

Copland, M. (2009) Ikaros deletions are associated with poor prognosis in acute lymphoblastic leukemia. Future Oncology, 5(4), pp. 455-458. (doi: 10.2217/FON.09.16)

Copland, M. (2009) Chronic myelogenous leukemia stem cells: what's new? Current Hematologic Malignancy Reports, 4(2), pp. 66-73. (doi: 10.1007/s11899-009-0010-9)

Konig, H., Copland, M., Chu, S., Jove, R., Holyoake, T. L. and Bhatia, R. (2008) Effects of Dasatinib on Src Kinase Activity and Downstream Intracellular Signaling in Primitive Chronic Myelogenous Leukemia Hematopoietic Cells. Cancer Research, 68(23), pp. 9624-9633. (doi: 10.1158/0008-5472.CAN-08-1131)

Heaney, N. B., Copland, M., Stewart, K., Godden, J., Parker, A. N., McQuaker, I. G., Smith, G. M., Crawley, C., Shepherd, P. and Holyoake, T. L. (2008) Complete molecular responses are achieved after reduced intensity stem cell transplantation and donor lymphocyte infusion in chronic myeloid leukemia. Blood, 111(10), pp. 5252-5255. (doi: 10.1182/blood-2007-10-118141)

Copland, M., Pellicano, F., Richmond, L., Allan, E. K., Hamilton, A., Lee, F. Y., Weinmann, R. and Holyoake, T. L. (2008) BMS-214662 potently induces apoptosis of chronic myeloid leukemia stem and progenitor cells and synergizes with tyrosine kinase inhibitors. Blood, 111(5), pp. 2843-2853. (doi: 10.1182/blood-2007-09-112573)

Balabanov, S. et al. (2007) Hypusination of eukaryotic initiation factor 5A (eIF5A): a novel therapeutic target in BCR-ABL-positive leukemias identified by a proteomics approach. Blood, 109(4), pp. 1701-1711. (doi: 10.1182/blood-2005-03-037648)

Copland, M., Hamilton, A., Eirick, L., Baird, J., Allan, E., Jordanides, N., Barow, M., Mountford, J. and Holyoake, T. (2006) Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction. Blood, 107(11), pp. 4532-4539. (doi: 10.1182/blood-2005-07-2947)

Hamilton, A., Elrick, L., Myssina, S., Copland, M. , Jorgensen, H.G. , Melo, J.V. and Holyoake, T.L. (2006) BCR-ABL activity and its response to drugs can be determined in CD34⁺ CML stem cells by CrkL phosphorylation status using flow cytometry. Leukemia, 20(6), pp. 1035-1039. (doi: 10.1038/sj.leu.2404189)

Jorgensen, H.G. , Copland, M. , Allan, E.K., Jiang, X.Y., Eaves, A., Eaves, C. and Holyoake, T.L. (2006) Intermittent exposure of primitive quiescent chronic myeloid leukemia cells to granulocyte-colony stimulating factor in vitro promotes their elimination by imatinib mesylate. Clinical Cancer Research, 12(2), pp. 626-633. (doi: 10.1158/1078-0432.CCR-05-0429)