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Results 1-10 of 17 (Search time: 0.002 seconds).
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PreviewIssue DateTitleAuthor(s)
2017Reduced CD62L expression on T cells and increased soluble CD62L levels predict molecular response to tyrosine kinase inhibitor therapy in early chronic-phase chronic myelogenous leukemiaSopper, S.; Mustjoki, S.; White, D.; Hughes, T.; Valent, P.; Burchert, A.; Gjertsen, B.; Gastl, G.; Baldauf, M.; Trajanoski, Z.; Giles, F.; Hochhaus, A.; Ernst, T.; Schenk, T.; Janssen, J.; Ossenkoppele, G.; Porkka, K.; Wolf, D.
2013Safety and efficacy of imatinib cessation for CML patients with stable undetectable minimal residual disease: results from the TWISTER studyRoss, D.; Branford, S.; Seymour, J.; Schwarer, A.; Arthur, C.; Yeung, D.; Dang, P.; Goyne, J.; Slader, C.; Filshie, R.; Mills, A.; Vaz de Melo, J.; White, D.; Grigg, A.; Hughes, T.
2013Association between imatinib transporters and metabolizing enzymes genotype and response in newly diagnosed chronic myeloid leukemia patients receiving imatinib therapyAngelini, S.; Soverini, S.; Ravegnini, G.; Barnett, M.; Turrini, E.; Thornquist, M.; Pane, F.; Hughes, T.; White, D.; Radich, J.; Kim, D.; Saglio, G.; Cilloni, D.; Iacobucci, I.; Perini, G.; Woodman, R.; Cantelli-Forti, G.; Baccarani, M.; Hrelia, P.; Martinelli, G.
2011OCT-1 as a determinant of response to antileukemic treatmentEngler, J.; Hughes, T.; White, D.
2003Successful peripheral blood stem cell mobilisation with filgrastim in patients with chronic myeloid leukaemia achieving complete cytogenetic response with imatinib, without increasing disease burden as measured by quantitative real-time PCRHui, C.; Goh, K.; White, D.; Branford, S.; Grigg, A.; Seymour, J.; Kwan, Y.; Walsh, S.; Hoyt, R.; Trickett, A.; Rudzki, Z.; Ma, D.; To, L.; Hughes, T.
2010The poor response to imatinib observed in CML patients with low OCT-1 activity is not attributable to lower uptake of imatinib into their CD34⁺ cellsEngler, J.; Frede, A.; Saunders, V.; Zannettino, A.; White, D.; Hughes, T.
2005In vitro sensitivity to imatinib-induced inhibition of ABL kinase activity is predictive of molecular response in patients with de-novo CML.White, D.; Saunders, V.; Lyons, A.; Branford, S.; Grigg, A.; To, L.; Hughes, T.
2006OCT-1-mediated influx is a key determinant of the intraceflular uptake of imatinib but not nilotinib, (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinibWhite, D.; Saunders, V.; Dang, P.; Engler, J.; Zannettino, A.; Cambareri, A.; Quinn, S.; Manley, P.; Hughes, T.
2007Imatinib increases the intracellular concentration of nilotinib which may explain the observed synergy between these drugsWhite, D.; Saunders, V.; Quinn, S.; Manley, P.; Hughes, T.
2010Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with ImatinibWhite, D.; Dang, P.; Engler, J.; Frede, A.; Osborn, M.; Saunders, V.; Manley, P.; Zrim, S.; Hughes, T.

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