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Results 1-10 of 26 (Search time: 0.002 seconds).
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PreviewIssue DateTitleAuthor(s)
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.)
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.)
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)
2010Limiting the variability within a BCR-ABL quantitative PCR (RQ-PCR) assay is essential for optimal concordance of results between laboratories generating BCR-ABL values on an international reporting scaleFletcher, L.; Prime, J.; Phillis, S.; Jamison, B.; Field, C.; Prime, H.; Sullivan, B.; Yeoman, A.; Georgievski, J.; Parker, W.; Slader, C.; Hughes, T.; Branford, S.; Haematology Association of Australasia Annual Meeting (2010 : Auckland, New Zealand)
2010Evidence that opioids may have toll-like receptor 4 and MD-2 effectsHutchinson, M.; Zhang, Y.; Shridhar, M.; Evans, J.; Buchanan, M.; Zhao, T.; Slivka, P.; Coats, B.; Rezvani, N.; Wieseler-Frank, J.; Hughes, T.; Landgraf, K.; Chan, S.; Fong, S.; Phipps, S.; Falke, J.; Maier, S.; Leinwand, L.; Yin, H.; Rice, K.; et al.
2010Nilotinib does not significantly reduce imatinib OCT-1 activity in either cell lines or primary CML cellsEadie, L.; Hughes, T.; White, D.
2010Nilotinib-mediated inhibition of ABCB1 increases intracellular concentration of dasatinib in CML cells: implications for combination TKI therapyHiwase, D.; White, D.; Zrim, S.; Saunders, V.; Vaz de Melo, J.; Hughes, T.