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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Foon, K.A. (1998). Interferon therapy of hematologic malignancies. In: Foon, K.A., Muss, H.B. (eds) Biological and Hormonal Therapies of Cancer. Cancer Treatment and Research, vol 94. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6189-7_1
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