Imatinib mesylate provides good results in the treatment of CML in general. But what about the results of this treatment in CML associated with additional cytogenetic abnormalities at diagnosis among black Africans? For this, we retrospectively studied 27 cases of CML associated with additional cytogenetic abnormalities, diagnosed in the department of clinical hematology of the University Hospital of Yopougon in C？te d'Ivoire, from May 2005 to October 2011. The age of patients ranged from 13 to 68 years, with a mean age of 38 years and a sex ratio of 2. Patients were severely symptomatic with a high Sokal score of 67%. CML in chronic phase accounted for 67%. The prevalence of additional cytogenetic abnormalities was 29.7%. There were variants of the Philadelphia chromosome (18.5%), trisomy 8 (14.8%), complex cytogenetic abnormalities (18.5%), second Philadelphia chromosome (14.8%), and minor cytogenetic abnormalities (44.4%). Complete hematologic remission was achieved in 59%, with 52% of major cytogenetic remission. The outcome was fatal in 37% of patients. Death was related in 40% to hematologic toxicity and in 30% to acutisation. The median survival was 40 months. 1. Introduction Chronic myeloid leukemia (CML) is characterized by the predominant proliferation of cells of grainy line and by the existence of a cytogenetic abnormality that is the translocation t (9; 22) (q34; q11) with BCR/ABL rearrangement. If CML develops inexorably towards the acute transformation, the time necessary for this transformation is variable. Twenty five percent of patients will survive more than 5 years, 5% over 10 years. For others, the acute transformation occurs immediately or very soon after the diagnosis of the disease. This difference in overall survival may be partly explained by the Sokal score but also by the existence or not of additional cytogenetic abnormalities at diagnosis. Major additional cytogenetic abnormalities at diagnosis have a negative impact on survival and mean progression to the accelerated or blast phase [1–4]. Currently, the first-line treatment of this CML is based on imatinib mesylate. Imatinib mesylate or STI-571 or Glivec was discovered right in 1988 as a highly potent and selective inhibitor of ABL tyrosine kinases. This drug has become the first-line treatment of Ivorian patients with CML and with low income, since GIPAP (Glivec International Patient Assistance Program) kindly provides C？te d’Ivoire with it. Some resistance to this treatment may be associated with additional cytogenetic abnormalities [1, 5]. The aim of our study was to
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