Clinical implications of clonal chromosomal abnormalities in Philadelphia negative cells in CML patients after treated with tyrosine kinase inhibitors

Chronic myelogenous leukemia (CML) is a clonal hematologic disorder characterized by the presence of a fusion oncogene, BCR-ABL, which leads to uncontrolled proliferation of myeloid cells. The fusion gene is the results of reciprocal translocation (9;22) (q34; q11) known as Philadelphia (Ph) chromosome[1]. The successful use of tyrosine kinase inhibitors (TKIs) targeting the BCR-ABL oncoprotein has significantly improved the prognosis of this disease, so that the survival of CML patients is nearly identical to that of the general population[2,3].
Source: Cancer Genetics and Cytogenetics - Category: Genetics & Stem Cells Authors: Source Type: research