BCR-ABL gene amplification in patients with chronic myeloid leukemia and imatinib resistance

Abstract

The treatment of Ph-positive chronic myeloid leukemia (CML) has achieved significant progress with the tyrosine kinase inhibitor (TKI) imatinib. Complete cytogenetic remission is a standard for patients treated in chronic phase. Nevertheless, primary and acquired resistance has been observed in few CML patients. Imatinib resistance in patients is related to heterogeneous mechanisms. The role of the BCR-ABL-related mechanism of imatinib resistance —BCR-ABL gene ampliphication in primary resistant cases was studied. The BCRABL gene ampliphication was established in 18% refractory to imatinib patients. Decreasing probability of complete cytogenetic response was revealed in these cases.

Keywords

• chronic myeloid leukemia
• imatinib resistance
• bcr-abl gene ampliphication