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PreviewIssue DateTitleAuthor(s)
2014Achieving the deep molecular response levels required for an imatinib discontinuation trial is strongly associated with the BCR-ABL level at the first qualifying timepointBranford, S.; Ross, D.; Yeung, D.; Braley, J.; Hughes, T.; 56th ASH Annual Meeting (6 Dec 2014 - 9 Dec 2014 : San Francisco, California)
2010Selective escalation of imatinib therapy and early switching to nilotinib in de novo chronic phase CML patients: interim results from the TIDELL-II trialYeung, D.; Osborn, M.; White, D.; Branford, S.; Haswell, L.; Slader, C.; Issa, S.; Hiwase, D.; Hertzberg, M.; Schwarer, A.; Filshie, R.; Arthur, C.; Kwan, Y.; Forsyth, C.; Ross, D.; Mills, A.; Grigg, A.; Hughes, T.; Annual Meeting of the American Society of Hematology (52nd : 2010 : Orlando, Fl.)
2010Mutation analysis of BCR-ABL tyrosine kinase domain in new chronic phase-chronic myeloid leukemia patients with suboptimal response or treatment failure from imatinib treatmentKim, D.; Kim, D.; Kim, S.; Goh, H.; Pane, F.; Hughes, T.; Radich, J.; Lin, P.; Saglio, G.; Branford, S.; Martinelli, G.; Soverini, S.; Hochhaus, A.; American Society of Hematology Meeting (52nd : 2010 : Florida, CA.)
2003Imatinib produces significantly superior molecular responses compared to interferon alfa plus cytarabine in patients with newly diagnosed chronic myeloid leukemia in chronic phaseBranford, S.; Rudzki, Z.; Harper, A.; Grigg, A.; Taylor, K.; Durrant, S.; Arthur, C.; Browett, P.; Schwarer, A.; Ma, D.; Seymour, J.; Bradstock, K.; Joske, D.; Lynch, K.; Gathmann, I.; Hughes, T.
2010A Review of Mutation Analysis In the TOPS Trial of Standard Dose Versus High Dose IM In CML Suggests That Refinements to the ELN Recommendations for Mutation Screening May Be AppropriateBranford, S.; Goh, H.; Izzo, B.; Beppu, L.; Ortmann, C.; Duniec, K.; Jin, Y.; Woodman, R.; Pane, F.; Kim, D.; Radich, J.; Hughes, T.; American Society of Hematology Meeting (52nd : 2010 : Florida, CA.)
2010Detection of low level nilotinib or dasatinib resistant BCR-ABL mutations by mass spectrometry in CML patients who fail Imatinib is highly predivtive of their subsequent clonal expansion when treated with the drug for which their mutation confers resistanceParker, W.; Ho, M.; Lawrence, R.; Irwin, D.; Scott, H.; Hughes, T.; Branford, S.; American Society of Hematology Meeting (52nd : 2010 : Florida, CA.)
2002High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistanceBranford, S.; Rudzki, Z.; Walsh, S.; Grigg, A.; Arthur, C.; Taylor, K.; Herrmann, R.; Lynch, K.; Hughes, T.
2010Towards DNA-based monitoring of therapy in chronic myeloid leukemiaMorley, A.; Bartley, P.; Ross, D.; Latham, S.; Budgen, B.; Branford, S.; Hughes, T.; American Society of Hematology Meeting (52nd : 2010 : Florida, CA.)
2010Contrasting response of patients with chronic myeloid leukaemia (CML) and the highly imatinib resistant L248V mutation that may be related to an increased propensity of some patients to form an associated deletion mutant with increased imatinib sensitivityPrime, H.; Romeo, G.; Phillis, S.; Field, C.; Jamison, B.; Prime, J.; Parker, W.; Joske, D.; Hughes, T.; Branford, S.; Haematology Association of Australasia Annual Meeting (2010 : Auckland, New Zealand)
2007Monitoring disease responseHughes, T.; Branford, S.; Melo, J.; Goldman, J.

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