Studies of Interferon as a Regulator on Hematopoietic Stem Cells in Chronic Myelogenous Leukemia

Chronic myelogenous leukemia (CML) is a myeloproliferative disorder in which the neoplastic transformation of a pluripotent stem cell results in the proliferation and accumulation of myeloid cells and their progenitors. Clinically, the disease is divided into three phases: a chronic phase of 3–4 years’ duration followed by an accelerated phase of 3–5 months, and then leading into an acute phase, i. e., blast crisis lasting 2–4 months [1]. During the chronic phase, the neoplastic clone represents the majority of the replicating myeloid cells. These cells and their progenitors normally respond to normal myelopoietic growth factors. In the acute phase, in contrast, the leukemic cells loose their ability to differentiate and mature normally. In CML a specific chromosome abnormality, the Philadelphia chromosome (Ph1) (22q-) is present in 90%–95% of patients [2]. The Ph1 chromosome results, in most instances, from a balanced reciprocal translocation between chromosome 9 and 22 [t(9;22)] [3].