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Results 1-10 of 31 (Search time: 0.003 seconds).
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PreviewIssue DateTitleAuthor(s)
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.
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.
2002Dual transcription of b2a2 and b3a2 BCR-ABL transcripts in chronic myeloid leukaemia is confined to patients with a linked polymorphism within the BCR geneBranford, S.; Hughes, T.; Rudzki, Z.
2010Practical considerations for monitoring patients with chronic myeloid leukemiaBranford, S.; Hughes, T.
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.
2015A DNA real-time quantitative PCR method suitable for routine monitoring of low levels of minimal residual disease in chronic myeloid leukemiaBartley, P.; Latham, S.; Budgen, B.; Ross, D.; Hughes, E.; Branford, S.; White, D.; Hughes, T.; Morley, A.
2012BCR-ABL1 doubling times more reliably assess the dynamics of CML relapse compared with the BCR-ABL1 fold rise: implications for monitoring and managementBranford, S.; Yeung, D.; Prime, J.; Choi, S.; Bang, J.; Park, J.; Kim, D.; Ross, D.; 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.
2009Genomic translocation breakpoint sequences are conserved in BCR-ABL1 cell lines despite the presence of amplificationRoss, D.; Schafranek, L.; Hughes, T.; Nicola, M.; Branford, S.; Score, J.
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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