Molecular analysis as an aid to identify imatinib resistance unrelated to BCR-ABL mutations. Rising BCR-ABL levels of two patients (Ai and Bi) indicated potential imatinib resistance. No BCR-ABL mutations were detected.

Cytogenetic analysis indicated duplication of the Ph chromosome and the presence of additional cytogenetic abnormalities at loss of CCR for both patients (Aii and Bii). (A) The 57-year-old female was diagnosed in accelerated phase CML and commenced imatinib at 600 mg. An increased imatinib dose of 800 mg upon the rise in BCR-ABL failed to prevent progression to myeloid blast crisis (MBC). Dasatinib therapy reestablished CCR, but the patient relapsed. (B) The 42-year-old male commenced 600 mg imatinib upon diagnosis of chronic-phase CML. CCR was maintained after commencing nilotinib therapy.