ABSTRACT

Chronic myeloid leukemia (CML) is a clonal stem cell disorder characterized by the formation of breakpoint cluster region–ABL1 fusion gene as a result of translocation leading to enhanced tyrosine kinase activity and proliferation of myeloid cells at all stages of differentiation. The main characteristics of CML include Philadelphia, leukocytosis with basophilia, hypercellular bone marrow (BM) with myeloid hyperplasia, and leftward shift, and hypolobated micromegakaryocytes. Histologic examination of the BM core biopsy reveals a hypercellular marrow with myeloid and often megakaryocytic hyperplasia, and myeloid leftward shift without an increased number of blasts. CML patients have reduced the Leukocyte alkaline phosphatase (LAP) index, which distinguishes them from leukemoid reaction in which the LAP score is usually high. Prominent neutrophilia is seen in infections and as a paraneoplastic syndrome in patients with malignant tumors, including plasma cell myeloma, carcinomas of the lung, stomach and kidney, and rarely sarcomas.