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PreviewIssue DateTitleAuthor(s)
2002Juxtamembrane mutant V560GKit is more sensitive to Imatinib (STI571) compared with wild-type c-kit whereas the kinase domain mutant D816VKit is resistantFrost, M.; Ferrao, P.; Hughes, T.; Ashman, L.
2008Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemiale Coutre, P.; Ottmann, O.; Giles, F.; Kim, D.; Cortes, J.; Gattermann, N.; Apperley, J.; Larson, R.; Abruzzese, E.; O'Brien, S.; Kuliczkowski, K.; Hochhaus, A.; Mahon, F.; Saglio, G.; Gobbi, M.; Kwong, Y.; Baccarani, M.; Hughes, T.; Martinelli, G.; Radich, J.; et al.
2004Clinical resistance to imatinib: mechanisms and implicationsHochhaus, A.; Hughes, T.
2009Impact of baseline BCR-ABL mutations on response to Nilotinib in patients with chronic myeloid leukemia in chronic phaseHughes, T.; Saglio, G.; Branford, S.; Soverini, S.; Kim, J.; Muller, M.; Martinelli, G.; Cortes, J.; Beppu, L.; Gottardi, E.; Dongho, K.; Erben, P.; Shou, Y.; Haque, A.; Gallagher, N.; Radich, J.; Hochhaus, A.
2009Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter?Branford, S.; Vaz de Melo, J.; Hughes, T.
2009Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutationsMuller, M.; Cortes, J.; Kim, D.; Druker, B.; Erben, P.; Pasquini, R.; Branford, S.; Hughes, T.; Radich, J.; Ploughman, L.; Mukhopadhyay, J.; Hochhaus, A.
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.

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