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PreviewIssue DateTitleAuthor(s)
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.
2013Early molecular response and female sex strongly predict stable undetectable BCR-ABL1, the criteria for imatinib discontinuation in patients with CMLBranford, S.; Yeung, D.; Ross, D.; Prime, J.; Field, C.; Altamura, H.; Yeoman, A.; Georgievski, J.; Jamison, B.; Phillis, S.; Sullivan, B.; Briggs, N.; Hertzberg, M.; Seymour, J.; Reynolds, J.; Hughes, T.
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.
2003Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemiaHughes, T.; Kaeda, J.; Branford, S.; Rudzki, Z.; Hochhaus, A.; Hensley, M.; Gathmann, I.; Bolton, A.; van Hoomissen, I.; Goldman, J.; Radich, J.
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.
2010Long-term prognostic significance of early molecular response to imatinib in newly diagnosed chronic myeloid leukemia: an analysis from the International Randomized Study of Interferon and STI571 (IRIS)Hughes, T.; Hochhaus, A.; Branford, S.; Muller, M.; Kaeda, J.; Foroni, L.; Druker, B.; Guilhot, F.; Larson, R.; O'Brien, S.; Rudoltz, M.; Mone, M.; Wehrle, E.; Modur, V.; Goldman, J.; Radich, J.
2003Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosisBranford, S.; Rudzki, Z.; Walsh, S.; Parkinson, I.; Grigg, A.; Szer, J.; Taylor, K.; Hermann, R.; Seymour, J.; Arthur, C.; Joske, D.; Lynch, K.; Hughes, T.
2010Phase III, randomized, open-label study of daily Imatinib Mesylate 400 mg versus 800 mg in patients with newly diagnosed, previously untreated chronic myeloid leukemia in chronic phase using molecular end points: Tyrosine Kinase Inhibitor Optimization and Selectivity StudyCortes, A.; Baccarani, M.; Guilhot, F.; Druker, B.; Branford, S.; Kim, D.; Pane, F.; Pasquini, R.; Goldberg, S.; Kalaycio, M.; Moiraghi, B.; Rowe, J.; Tothova, E.; de Souza, C.; Rudoltz, M.; Yu, R.; Krahnke, T.; Kantarjian, H.; Radich, J.; Hughes, T.
2011SHP-1 expression accounts for resistance to imatinib treatment in Philadelphia chromosome-positive cells derived from patients with chronic myeloid leukemiaEsposito, N.; Colavita, I.; Quintarelli, C.; Sica, A.; Peluso, A.; Luciano, L.; Picardi, M.; Vecchio, L.; Buonomo, T.; Hughes, T.; White, D.; Radich, J.; Russo, D.; Branford, S.; Saglio, G.; Vaz de Melo, J.; Martinelli, R.; Ruoppolo, M.; Kalebic, T.; Martinelli, G.; et al.

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