Chronic myelogenous leukemia (CML) is a clonal disorder of a pluripotent stem cell and it usually evolves from a chronic, relatively indolent disease to a more aggressive leukemia whose progressive stages characterized by increased cellular proliferation, maturation arrest, and karyotypic evolution ( Anastasi and Roulston, 2001). To elucidate the genetic events that perturbing important roles in the progression of CML to blastic crisis, we performed FISH on a series of 25 Philadelphia positive cases of CML in different stages of disease using D20S108 probe for 20q12 locus flanking the tumour suppressor genes regulating these genetic events. D20S108 deletion was found in 1/16(6.25%) of cases in the chronic phase, and in 7/14 (50%) of cases in the evolution phases.The higher incidence of D20S108 deletion as additional cytogenetic abnormalities to Philadelphia chromosome in the acceleration and blastic crises speculates that 20q12 deletion marks the site of tumour suppressor genes that perturb the regulation of multipotent haemopoietic progenitors. Also, being more common in myeloid than the lymphoid phenotype of the acute phase, suggests that D20S108 can be considered as a poor prognostic value in the progression of CML. This study clarifies the value of additional chromosomal aberrations in the progression of CML, and provides guidance for future molecular approaches to isolate tumour suppressor genes that are probably associated with the transformation to lethal crisis.