Abstract
Chronic myeloid leukemia is a hematopoietic malignancy resulting from the transformation of a primitive hematopoietic cell. It is a clonal myeloproliferative disease characterized by the presence of the Philadelphia chromosome, which results from a reciprocal translocation between chromosomes 9 and 22. CML is generally thought to develop from the transformation of primitive hematopoietic stem cells with the BCR-ABL fusion gene. The presence of a unique genetic abnormality with strong pathogenetic potential has enabled the development of specific pathological tyrosine kinase inhibitors. Their introduction into clinical practice, especially their effectiveness, have revolutionized the treatment management and prognosis of this disease, as evidenced by the median survival of patients diagnosed in the chronic phase.
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