Treatment Development of Chronic Myeloid Leukemia

Chronic Myeloid Leukemia (CML) is a hematologic stem cell disorder leading to myeloproliferation and its attendant consequences [1]. CML typically evolves in 3 distinct clinical phases; An indolent or chronic phase (CP) course easily controlled with therapy that can last for 3 to 5 years and accelerated phase (AP) that lasts for less than 12 months and blast phase (BP), characterized by rapid expansion of a population of myeloid or lymphoid blasts of at least 30% in the peripheral blood or bone marrow resulting in the patient’s death within 4 to 6 months [2]. Busulfan is the oral anti-CML alkylating agent in the 1950s and was convenient to administer and inexpensive but associated with severe and prolong myelosuppression. Busulfan was largely replaced by hydroxyurea in 1970s. Hydroxyurea was the available and effective anti-CML agents in the 1980s. These were able to control the clinical manifestations of the disease, but were rarely, if ever, capable of eliminating the malignant clone. In 1990s the interferon alpha has constituted first-line therapy for patients with CML resulted in major cytogenetic responses of 25% [3]. The combination of interferon alpha with hydroxyurea or with Ara-C was effective in clinical practice and induces cytogenetic remissions in some patients [4].