Abstract:Chronic myeloid leukemia (CML) is a clonal hematopoietic malignancy driven by the BCR::ABL1 fusion oncoprotein. The development of tyrosine kinase inhibitors (TKIs) has deeply increased long-term survival of CML patients. Nonetheless, one patient out of four will switch TKI off owing either to drug intolerance or resistance partly due to amplification or mutations of BCR::ABL1 oncogene and alteration of ATP-binding cassette (ABC) transporters. Increasing evidence suggests an involvement of the microRNA miR-495… Show more
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