This disease occurs more commonly in young adults. It is rare in children and is seen especially in older children and adolescents. It is a myeloproliferative disorder characterized by the presence of translocation t (9;22) commonly referred to as the Philadelphia (Ph1) chromosome.

The disease has three phases: the chronic, accelerated, and acute. The If CML is not adequately treated, the transition from chronic to acute phases can occur with disastrous consequences between forms if not treated adequately can occur rapidly with disastrous consequences.

Philadelphia (Ph1) chromosome is the result of a translocation between 2 chromosomes: 9 and 22 (q34q11). This translocation leads to the juxtaposition of proto-oncogene c-ABL (chromosome 9) and BCL gene (chromosome 22). The chimeric gene produces a tyrosine kinase protein which has an anti-apoptotic effect with loss of adhesion to the stromal matrix molecules.

Few symptoms are noticed during the chronic phase. Some CML may be asymptomatic. Nonspecific signs such as fever, night sweats, or a vague pain of the left hypochondria are the most commonly reported symptoms. Clinical examination is in most cases dominated by a grossly enlarged spleen and sometimes moderate anemia. Complete blood count shows a leukocytosis often exceeding 100,000/mm³ with a left shift extending to blast cells, basophilia, thrombocytosis, and a moderate normochromic anemia. The bone marrow aspirate adds valuable information and is characterized by a hyperplasia of the granulocytic lineage with normal maturation. During accelerated phase, an increased rate of immature blasts is found in bone marrow. Acute transformation can give rise to myeloid or lymphoid leukemia. The disease may rarely lead to thrombotic events and in particular to priapism. The thrombosis is related to the blood hyperviscosity caused by leukocytosis, lower deformability of the blasts, and thrombocytosis.

A complete diagnosis of the disease requires the karyotype or molecular analysis. However, in African setting these analyses may not be available.

A high degree of suspicion is present in an older child or young adult with a chronic anemia , tiredness , and splenomegaly . The suspicion is in most cases confirmed by a high leucocyte count with a left shift.

The initial treatment may be started with Hydroxyurea (10–20 mg/kg/day) and will provide hematologic response but without eradication of the malignant clone.

The drug of choice remains a tyrosine kinase inhibitor and hematopoietic stem cell transplantation for patients who fail to respond to TKI. or allogeneic bone marrow transplantation . In the absence of the ideal therapy, the inevitably progressing to the refractory acute form. Interferon therapy allows in less than 20 % of the cases an eradication of the malignant clone proved by the negativity of the BCR-ABL chimeric protein. The allogeneic hematopoietic stem cells transplant from HLA compatible donor and particularly in the siblings is a treatment that allows the eradication of malignant clone. This approach however has a significant morbidity and mortality.