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Results 1-10 of 17 (Search time: 0.003 seconds).
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PreviewIssue DateTitleAuthor(s)
2014Interaction of the efflux transporters ABCB1 and ABCG2 with imatinib, nilotinib, and dasatinibEadie, L.; Hughes, T.; White, 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.
2010Nilotinib does not significantly reduce imatinib OCT-1 activity in either cell lines or primary CML cellsEadie, L.; Hughes, T.; White, D.
2013Proton pump inhibitors significantly increase the intracellular concentration of nilotinib, but not imatinib in target CML cellsWhite, D.; Eadie, L.; Saunders, V.; Hiwase, D.; Hughes, T.
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.

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