IMPORTANT PUBLICATIONS (pre-2009)

1. White D, Saunders V, Lyons A, Branford S, Grigg A, To L, Hughes T. In vitro sensitivity to imatinib-induced inhibition of ABL kinase activity is predictive of molecular response in patients with de novo CML. 2005. Blood 106:2520-2526 IF: 9.06
2. 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. 2006. Blood 108:697-704 IF: 9.06
3. 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. 2007. Journal of Clinical Oncology 25:4445-4451 IF: 18.04
4. 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. 2007. Blood 110:4064-4072 IF: 9.06
5. 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. 2008. Clinical Cancer Research 14:3881-3888 IF: 7.8
6. Mullighan CG, Miller CB, Radtke I, Phillips LA, Dalton J, Ma J,White D, Hughes TP, Le Beau MM, Pui CH, et al. BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. 2008. Nature 453:110-114 IF: 38.59