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Results 21-30 of 30 (Search time: 0.003 seconds).
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PreviewIssue DateTitleAuthor(s)
2011Sensitive detection of BCR-ABL1 mutations in patients with chronic myeloid leukemia after Imatinib resistance is predictive of outcome during subsequent therapyParker, W.; Lawrence, R.; Ho, M.; Irwin, D.; Scott, H.; Hughes, T.; Branford, S.
2004Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutationsBranford, S.; Rudzki, Z.; Parkinson, I.; Grigg, A.; Taylor, K.; Seymour, J.; Durrant, S.; Browett, P.; Schwarer, A.; Arthur, C.; Catalano, J.; Leahy, M.; Filshie, R.; Bradstock, K.; Herrmann, R.; Joske, D.; Lynch, K.; Hughes, T.
2011Dynamics of chronic myeloid leukemia response to long-term targeted therapy reveal treatment effects on leukemic stem cellsTang, M.; Gonen, M.; Quintas-Cardama, A.; Cortes, J.; Kantarjian, H.; Field, C.; Hughes, T.; Branford, S.; Michor, F.
2012Poor response to second-line kinase inhibitors in chronic myeloid leukemia patients with multiple low-level mutations, irrespective of their resistance profileParker, W.; Ho, M.; Scott, H.; Hughes, T.; Branford, S.
2012Initial molecular response at 3 months may predict both response and event-free survival at 24 months in Imatinib-resistant or -intolerant patients with Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase treated with NilotinibBranford, S.; Kim, D.; Soverini, S.; Haque, A.; Shou, Y.; Woodman, R.; Kantarjian, H.; Martinelli, G.; Radich, J.; Saglio, G.; Hochhaus, A.; Hughes, T.; Muller, M.
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.
2011BCR-ABL transcript dynamics support the hypothesis that leukemic stem cells are reduced during imatinib teatmentStein, A.; Bottino, D.; Modur, V.; Branford, S.; Kaeda, J.; Goldman, J.; Hughes, T.; Radich, J.; Hochhaus, A.
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.
2008Reverse transcription with random pentadecamer primers improves the detection limit of a quantitative PCR assay for BCR-ABL transcripts in chronic myeloid leukemia: Implications for defining sensitivity in minimal residual diseaseRoss, D.; Watkins, D.; Hughes, T.; Branford, S.

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