Prognostic implications of cumulative dosing in total therapy 3

摘要

Point mutations of the Bcr-Abl kinase domain (KD) are the most frequently identified mechanism of resistance in patients with chronic myeloid leukemia (CML) who fail tyrosine kinase inhibitor (TKI) therapy.1"4 The V299L mutation occurs rarely after imatinib therapy,3 but has been reported to confer resistance to dasatinib and bosutinib.5"6 The objective of this study was to assess the incidence, pattern of V299L development, and response to therapy in patients with TKI-resistant CML at our institution.