Chronic myeloid leukemia (CML) is a malignant hematopoietic stem cell proliferative disease driven by BCR-ABL tyrosine kinase, the product of the Philadelphia chromosome1. Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of CML. Such molecule directed against BCR-ABL firsrt introduced into clinical practice was imatinib mesylate (IM, Gleevec/Glivec, formerly STI571), which showed excellent efficacy in terms of prolonged major molecular response (MMR) and progression-free survival2. Replacing hematopoietic stem cell transplantation, IM is currently recommended as the first-line therapy for CML by the National Comprehensive Cancer Network (NCCN) and European Leukemia Net (ELN).

At the pre-TKI stage, IFN-α was the major choice for CML patients who were not candidates for allogeneic stem cell transplantation, and its observed complete cytogenetic response (CCyR) rates were approximately 20%. Moreover, IFN-α extends the leukemia-free survival (LFS) of patients3,4. In China, many patients begin with IFN-α treatment instead of IM at diagnosis for economic reasons. Previous studies have shown that the therapeutic efficacy of IM treatment is not affected by prior IFN-α treatment5,6. The results of our retrospective analysis of 137 CML cases suggest that IFN-α treatment before IM therapy is a risk factor associated with loss of MMR.

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