Abstract

Chronic myeloid leukemia (CML) is a clonal bone marrow (BM) disease characterized by neoplastic overproduction of, mainly, granulocytes. The treatment of CML has changed dramatically with the introduction of tyrosine kinase inhibitors (TKIs) targeting the product of the underlying cytogenetic and molecular lesion in CML. The Philadelphia chromosome was the first consistent neoplasia-associated chromosomal abnormality reported; its discovery was a milestone in cancer cytogenetics. Treatment of CML has changed dramatically over the last decades. The chfromosome t(9;22) (q34;q11) or its variant translocations (seen in 5-10%) are detected in the great majority of BM cells from patients with CML.The introduction of imatinib and other TKIs has dramatically improved the clinical outcome for CML patients, and today, the vast majority of patients receiving TKI treatment in chronic phase (CP) remain in complete hematologic and cytogenetic remission with low to undetectable BCR-ABL1 fusion transcripts. (Less)

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