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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.
2008Long-term imatinib therapy promotes bone formation in CML patientsFitter, S.; Dewar, A.; Kostakis, P.; To, L.; Hughes, T.; Roberts, M.; Lynch, K.; Vernon-Roberts, B.; Zannettino, A.
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.
2007Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activityWhite, D.; Saunders, V.; Dang, P.; Engler, J.; Venables, A.; Zrim, S.; Zannettino, A.; Lynch, K.; Manley, P.; Hughes, T.
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.
2007Measurement of in vivo BCR-ABL kinase inhibition to monitor imatinib-induced target blockade and predict response in chronic myeloid leukemiaWhite, D.; Saunders, V.; Grigg, A.; Arthur, C.; Filshie, R.; Leahy, M.; Lynch, K.; To, L.; Hughes, T.

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