Abstract
Chronic myelogenous leukemia (CML) is a hematologic neoplasm characterized by the proliferation and accumulation of mature myeloid cells and their progenitors. It is a clonal disorder caused by somatic mutation in a pluripotent hematopoietic stem cell; consequently, there is involvement of myeloid and erythroid cells, monocytes/macrophages, megakaryocytes, and lymphocytes. Clonality has been conclusively demonstrated by polymorphic genetic systems such as glucose 6-phosphate dehydrogenase (G6PD) in heterozygous individuals with CML, X-chromosome DNA restriction fragment-length polymorphism of hypoxanthine glucuronyl ribosyl phosphoryl transferase, and the presence of the Philadelphia (Ph’) chromosome and other clonal cytogenetic markers [1-5].
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