Chronic granulocytic leukemia is a myeloproliferative tumor originating from multipotent stem cells. It is characterized by the translocation of chromosomes 9 and 22 forming the BCR/ABL fusion gene. The Philadelphia chromosome is a characteristic change in chronic granulocytic leukemia, first discovered and named in Philadelphia in 1960. Initially, it was observed as a deletion of the long arm of the primary chromosome in dividing blood cells of patients with this leukemia. Currently, studies have shown that abnormalities in the interaction between hematopoietic progenitor cells and the stroma might be central to treating the disease. Abnormal adhesion and anchoring characteristics of progenitor cells lead to disrupted cell maturation and proliferation. Chronic granulocytic cells do not adhere to stromal cells as normal cells do, particularly lacking integrin-mediated adhesion. Additionally, the expression of the adhesion molecule lymphocyte function-associated antigen 3 is also reduced in these cells. Therefore, the progression of the disease results from clonal changes. During the transformation of chronic granulocytic leukemia to acute myeloid leukemia, there is an increased rate of genetic mutations. Changes in gene expression during the progression involve various aspects, including nucleosome sugar metabolism, bone marrow myeloid differentiation, genomic instability of cell apoptosis genes, and processes related to DNA damage repair.