ABSTRACT
CHARACTERISTICS OF CML The advent of sophisticated molecular investigative techniques has allowed clinicians to understand the genetics and pathophysiology of CML in substantial detail [2]. As early as 1960, it was known that there was a shortening of chromosome 22, the so-called Philadelphia chromosome, associated with the disease. In 1973, this was further defined as a translocation of the long arms of chromosomes 9 and 22. As a result of this translocation, the fusion protein BCR-ABL, a tyrosine kinase that is constitutively active in the cytoplasm of hematopoietic progenitors, is produced; its unregulated activity leads to malignant transformation of the hematopoietic progenitor cells [1--4].
