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. She is a Principal Research Fellow with SAHMRI and 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 the Australian and New Zealand Children’s Oncology Group (ANZCHOG) and the International Children’s Oncology Group (COG).

Professor White’s research focus is in Chronic Myeloid (CML) and Acute Lymphoblastic Leukaemia (ALL) and she holds/has held 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). She also plays an active role in Pharmaceutical Advisory Boards.

Professor White is an active member of the National Health & Medical Research Council (NHMRC) being a member of the NHMRC Academy, the Translational Research Program Advisory Committee, and the Women in Health Science Executive Committee. She is also the lead investigator of the ALL Stream of the Australian Genomics Healthcare Alliance (AGHA).  In addition, she is an active peer reviewer for the NHMRC, LFA and CCSA and for 16 Scientific Journals, and on the Editorial board of the Journal of Blood Research & Hematologic Diseases.  For the last 3 years Professor White has led an NHMRC Grant Review Panel as the Chair.  In 2014 she was recognised as the Australian Society for Medical Research (ASMR) Leading Light for her Medical Research, and in 2016 was awarded the University of Adelaide James McWha medal.

Over the last 5 years Professor White 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. Professor White is currently supervising four PhD students, one MPhil and one Honours student.

Prior to joining SAHMRI Professor White was employed as the Scientific Head of Haematology research at SA Pathology.

See my research publications

10 most significant papers over the last 5 years

  1. 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.
  2. Sieghart Sopper, Satu Mustjoki, Deborah White, Tim Hughes, Peter Valent, Andreas Burchert, Bjorn T. Gjertsen, Gunther Gastl, Matthias Baldauf, Zlatko Trajanoski, Frank Giles, Andreas Hochhaus, Thomas Ernst, Thomas Schenk, Jeroen JWM Janssen, Gert J Ossenkoppele, Kimmo Porkka, Dominik Wolf. Reduced CD62L expression on T cells and increased soluble CD62L levels predict molecular response to tyrosine kinase inhibitor (TKI) therapy in early Chronic Phase Chronic Myelogenous Leukemia (CML-CP). Journal of Clinical Oncology 2017 35 2 175-184 (I.F: 20.982)
  3. Laura N Eadie, Phuong Dang, David Yeung, Timothy P Hughes and Deborah L White. The clinical significance of ABCB1 overexpression in predicting outcome of CML patients undergoing first-line imatinib treatment. Leukemia. 2017 Jan;31(1):75-82. (I.F: 12.104)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.
  4. Eva Nievergall, John Reynolds, Chung H Kok, Dale B Watkins, Mark Biondo, Samantha J Busfield, Gino Vairo, David T Yeung, Angel F Lopez, Devendra K Hiwase, Timothy P Hughes and Deborah L White. TGF-α and IL-6 plasma levels selectively identify CML patients who fail to achieve an early molecular response or progress in the first year of therapy. Leukemia 2016 30 (6) 1263-1270. (I.F: 12.104)
  5. Watkins DB, Hughes TP, White DL. OCT1 and imatinib transport in CML: is it clinically relevant? Leukemia. 2015 29;10 1960-1969. (I.F: 12.104)
  6. Schafranek L, E Nievergall, JA Powell, DK Hiwase, T Leclercq, TP Hughes and DL White. Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia. Leukemia 2015 29(1): 76-85 (I.F: 12.104)
  7. D T Yeung, 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. Relapse of BCR-ABL1-like ALL mediated by the ABL1 kinase domain mutation T315I following initial response to dasatinib treatment. Leukemia 2015 29(1): 230-232. (I.F: 12.104)
  8. White DL, Eadie LN, Saunders VA, Hiwase DK, Hughes TP. Proton pump inhibitors significantly increase the intracellular concentration of nilotinib, but not imatinib in target CML cells. Leukemia. 2013;27(5):1201-1204. (I.F: 12.104)
  9. Kok CH, Watkins DB, Leclercq T, D'Andrea RJ, Hughes TP, White DL. 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. (I.F: 12.104)
  10. Richmond J, Robbins A, Evans K, Beck D, Raushan T. Kurmasheva RT, Billups CA, Carol H, Heatley S, Sutton R, Marshall GM, White DL, Pimanda J, Houghton PJ, Smith MA, Lock RB. Acute Sensitivity of Ph-like Acute Lymphoblastic Leukemia to the SMAC-Mimetic Birinapant. Cancer Res 2016 76 (15) 4579-1591. (I.F: 9.329)

10 most significant papers over career.

  1. 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 (I.F: 41.456)
  2. 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. (I.F:20.982)
  3. 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. (I.F: 12.104)
  4. DT Yeung, MP. Osborn, DL White, S Branford, J Braley, A Herschtal, M Kornhauser, S Issa, DK Hiwase, M Hertzberg, AP Schwarer, R Filshie, CK Arthur, YL Kwan, J Trotman, CJ Forsyth, J Taper, DM Ross, J Beresford, C Tam, AK Mills, AP Grigg, TP Hughes and Australasian Leukaemia and Lymphoma Group. TIDEL-II: first-line use of imatinib in CML with early switch to nilotinib for failure to achieve time-dependent molecular targets. Blood 2015 125(6): 915-923. (I.F: 11.841)
  5. 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 and Australasian Leukaemia and Lymphoma Group. 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. (I.F: 11.841)
  6. 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. (I.F: 11.841)
  7. 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. (I.F: 11.841)
  8. 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. (I.F: 11.841)
  9. 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. (I.F: 8.738)
  10. White DL, Hughes TP. Predicting the response of CML patients to tyrosine kinase inhibitor therapy. Curr Hematol Malig Rep. (2009);4(2):59-65. (I.F:2.53)
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