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: Hongyu Ni, Xinlai Sun, Yin Xu, Derek Lyle, Paris Petersen, Xianfeng Zhao, Hong Drum, Bei You, Dongfang Liu, Chen Liu, Jie-Gen Jiang Source Type: research
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