This work, and that of colleagues Brian Druker and Novartis, led to the development of the kinase inhibitor imatinib (Gleevec) as primary therapy for chronic myelogenous leukemia (CML), and the discovery that
imatinib resistance is caused by BCR - ABL kinase domain mutations.
Not exact matches
In future, it may be possible to measure BCR - ABL levels in individual cells in the clinic — this will help us identify the resistant high BCR - ABL cells and better understand how patients develop
resistance to
imatinib treatment with the aim of combatting this
resistance to make response more durable and the treatment more effective.»
It has been shown in
imatinib - resistant CML that drug
resistance conferred by mutations does not necessarily correlate with proliferative advantage and increased kinase activity.34 Other, non-activating mutations or drug -
resistance mechanisms, might be acquired by tumor cells.