Director of Cancer Research & Deputy Theme Leader
Professor Deborah White PhD FFSc(RCPA)
Professor White is the Director of Cancer Research and Deputy Cancer Theme Leader at SAHMRI. Deb is a Professor in both Medicine and Paediatrics at the University of Adelaide. In addition, she is a Fellow of the Faculty of Science (Royal College of Pathologists of Australia) a member of the American, European and Australian Societies of Haematology and the International Children’s Oncology Group (COG).
Deb holds Grants (peer reviewed) from The William Lawrence and Blanche Hughes Foundation and the Leukemia Lymphoma Society (USA), the NHMRC, the Leukaemia Foundation Australia (LFA), Channel 7 and the Cancer Council SA (CCSA) to continue her work on the underlying disease biology, drug transport and mechanisms of resistance in CML, Ph+ and Ph-like ALL. Over the last 5 years she has presented more than 130 papers at scientific meetings (both invited and peer reviewed). She has authored more than 60 scientific publications on CML and ALL, as well as being an inventor on several patents.
Deb is a member of the NHMRC Academy, the NHMRC Women in Health Science Executive Committee and was recently recognised as the 2014 Australian Society for Medical Research (ASMR) Leading Light for her Medical Research. Deb is currently supervising 4 PhD students, and welcomes Honours, Masters and PhD students to her group.
Prior to joining SAHMRI Deb was employed as the Scientific Head of Haematology research at SA Pathology.
10 most significant papers over the last 5 years
- Watkins, DB, Hughes, TP and White DL. (2015) "OCT1 and imatinib transport in CML: is it clinically relevant?" Accepted for Publication Leukemia May 1 2015.
- Schafranek, L., E. Nievergall, J. A. Powell, D. K. Hiwase, T. Leclercq, T. P. Hughes and D. L. White (2015). "Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia." Leukemia 29(1): 76-85.
- Yeung, D. T., D. J. Moulton, S. L. Heatley, E. Nievergall, P. Dang, J. Braley, S. Branford, S. Moore, C. G. Mullighan, T. P. Hughes and D. L. White (2015). "Relapse of BCR-ABL1-like ALL mediated by the ABL1 kinase domain mutation T315I following initial response to dasatinib treatment." Leukemia 29(1): 230-232
- Roberts, K. G., Y. Li, D. Payne-Turner, R. C. Harvey, Y. L…. D. L. White, T. P. Hughes… P. Hunger, C. L. Willman, J. Zhang and C. G. Mullighan (2014). "Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia." N Engl J Med 371(11): 1005-1015.
- Timothy P Hughes and Deborah L White. “Which TKI? An embarrassment of riches for CML patients…” ASH Education Book. American Society of Hematology. New Orleans (2013).1:168-175.
- White, D, Eadie, L., Saunders, V., Hiwase, D., and Hughes, T. 2013. Proton pump inhibitors significantly increase the intracellular concentration of nilotinib, but not imatinib in target CML cells. Leukemia (2013);27(5):1201-1204.
- Kok, C. H., D. B. Watkins, Leclercq, T. M. D'Andrea, R.J. Hughes, T.P. and White, D.L (2013). "Low GFI1 expression in white blood cells of CP-CML patients at diagnosis is strongly associated with subsequent blastic transformation." Leukemia. 2013;27(6):1427-1430.
- Engler, J.R., Zannettino, A.C.W., Bailey, C.G., Rasko, J.E.J., Hughes, T.P., and White, D.L. (2011). OCT-1 function varies with cell lineage but is not influenced by BCR-ABL. Haematologica 96:213-220.
- T.P. (2010). Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib. Journal of Clinical Oncology 28:2761-2767.
- Engler, J.R., Frede, A., Saunders, V.A., Zannettino, A.C., Hughes, T.P., and White, D.L. (2010). Chronic myeloid leukemia CD34+ cells have reduced uptake of imatinib due to low OCT-1 activity. Leukemia 24:765-770.
10 most significant papers over career.
- White D, Saunders V, Lyons AB, Branford S, Grigg A, To LB, Hughes T. In vitro sensitivity to imatinib-induced inhibition of ABL kinase activity is predictive of molecular response in patients with de novo CML. Blood. 2005;106(7):2520-2526
- White DL, Saunders VA, Dang P, Engler J, Zannettino AC, Cambareri AC, Quinn SR, Manley PW, Hughes TP. OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib. Blood. 2006;108(2):697-704.
- White D, Saunders V, Grigg A, Arthur C, Filshie R, Leahy MF, Lynch K, To LB, Hughes T. Measurement of in vivo BCR-ABL kinase inhibition to monitor imatinib-induced target blockade and predict response in chronic myeloid leukemia. J Clin Oncol. 2007;25(28):4445-4451.
- White DL, Saunders VA, Dang P, Engler J, Venables A, Zrim S, Zannettino A, Lynch K, Manley PW, Hughes T. Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity. Blood. 2007;110(12):4064-4072.
- White DL, Saunders VA, Quinn SR, Manley PW, Hughes TP. Imatinib increases the intracellular concentration of nilotinib, which may explain the observed synergy between these drugs. Blood. 2007;109(8):3609-3610.
- Hiwase DK, Saunders V, Hewett D, Frede A, Zrim S, Dang P, Eadie L, To LB, Melo J, Kumar S, Hughes TP, White DL. Dasatinib cellular uptake and efflux in chronic myeloid leukemia cells: therapeutic implications. Clin Cancer Res. 2008;14(12):3881-3888.
- Hughes TP, Branford S, White DL, Reynolds J, Koelmeyer R, Seymour JF, Taylor K, Arthur C, Schwarer A, Morton J, Cooney J, Leahy MF, Rowlings P, Catalano J, Hertzberg M, Filshie R, Mills AK, Fay K, Durrant S, Januszewicz H, Joske D, Underhill C, Dunkley S, Lynch K, Grigg A, Australasian L, Lymphoma G. Impact of early dose intensity on cytogenetic and molecular responses in chronic- phase CML patients receiving 600 mg/day of imatinib as initial therapy. Blood. 2008;112(10):3965-3973.
- Mullighan CG, Miller CB, Radtke I, Phillips LA, Dalton J, Ma J, White D, Hughes TP, Le Beau MM, Pui CH, Relling MV, Shurtleff SA, Downing JR. BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. Nature. 2008;453(7191):110-114.
- White DL, Hughes TP. Predicting the response of CML patients to tyrosine kinase inhibitor therapy. Curr Hematol Malig Rep. 2009;4(2):59-65.
- Eadie L, Hughes T, White DL. Nilotinib does not significantly reduce imatinib OCT-1 activity in either cell lines or primary CML cells. Leukemia. 2010;24(4):855-857.