BCR-ABL mutation analysis allows to provide "tailors therapy" for CML patients resistant to imatinib
Abstract
Chronic myeloid leukemia (CML) becomes a disease, treatment of which represents typical example of tailored therapy. The most frequent mechanism responsible for imatinib resistance is development of mutation in BCR-ABL kinase domain.
Mutation cause different level of imatinib resistance and while some of them can be overcome by increased dose of imatinib (M351T), others seem to be resistant to nilotinib. This review is focused only to clinically most important mutations occurring in 15 amino-acid substitutions, which account for more then 85% of all BCR-ABL mutations.
It has been shown recently that advances in molecular methods enable to better understand disease itself, weigh the benefit to risk ratio of the therapy, individualize therapeutic approach and eventually adjust CML therapy earlier in order to minimize the risk of CML, progression to advanced phases.