Patients with splenomegaly and abnormally high leukocyte counts were first 
recognized in France, Germany, and Scotland in the 1840s. The only 
well-documented therapy in the 19th century was use of arsenic in one or other 
form, which did undoubtedly reduce the leukocyte count but probably did little 
or nothing to prolong life. These early cases were probably examples of chronic 
myeloid leukemia (CML) (then called chronic granulocytic leukemia). In the 20th 
century important steps in unraveling the pathogenesis of CML were the discovery 
of the Philadelphia chromosome in 1960, and of the (9;22) translocation in 1973. 
There followed definition of the breakpoint cluster region on chromosome 22 in 
1984 and the demonstration of the BCR-ABL transcript in CML in 1985. In the 
first half of the 20th century patients were treated predominantly with 
radiotherapy, and later on with busulfan, hydroxycarbamide, or interferon-alfa 
(IFN-α). From 1980 onwards allogeneic stem cell transplantation (SCT) became the 
treatment of choice for eligible patients. The era of tyrosine kinase inhibitors 
(TKI) began in 1998 and today the use of the original TKI, imatinib, has 
replaced SCT as initial therapy for patients who present with CML in chronic 
phase.