Clinically, CML progresses through three distinct phases of increasing refractoriness to therapy: chronic phase (median duration three to four years; median survival five to seven years with interferon), accelerated phase (median duration three to nine months; median survival eight to 18 months) and blast crisis (median survival three to six months). Blast crisis can be either of myeloid or, less commonly, lymphoid phenotype.2

The first-line treatment of patients with newly diagnosed CML has been extensively described in the consensus guidelines published by the American Society of Hematology.3 The standard therapeutic options that were available before the imatinib era were recombinant interferon-alpha (IFN-?), chemotherapy with hydroxyurea, low-dose cytarabine or busulfan and allogeneic bone-marrow transplantation (BMT). Allogeneic BMT has been recognised as the only potentially curative treatment of CML.4 It is, however, available to only 15% of newly diagnosed patients who are considered young enough (usually 50 years or younger) and have a suitable sibling marrow.5

The probability of long-term survival when BMT is performed in the first chronic phase is approximately 60%. However, the procedure is still associated with a high rate of transplant-related mortality of 20–30%.4 Introduced in the treatment of CML 20 years ago, IFN-?-based regimens were considered the standard therapy for newly diagnosed patients in the chronic phase. IFN-? was the only drug that had been consistently shown to prolong median survival by approximately two years compared with chemotherapy. The major goals of IFN-? therapy are to achieve control of the peripheral blood counts (haematological response) and, subsequently, a major decrease in the proportion of marrow cells harbouring the Ph chromosome to less than 35% (described as major cytogenetic response – MCyR). The achievement of both a haematological response and an MCyR has repeatedly been shown to be associated with prolonged survival.