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Background Chronic Myeloid Leukemia (CML) is a clonal myeloproliferative disorder characterized by formation of BCR-ABL fusion that encodes the p210 oncoprotein, which has a tyrosine kinase activity that confers an adaptive advantage to leukemic cells. Imatinib mesylate (IM) acts specifically on p210. Imatinib is able to reduce the differentiated cells (CD66b+) efficiently, but it has not the same effect on the stem cells (CD34+), which can be kept alive during treatment. Our aim was to identify expressed genes in CD34+ and CD66b+ cells as candidates for kinase inhibitors transport.

Differentially expressed genes responsible for insensitivity of CD34+ cells to kinase inhibitors in patients with chronic myeloid leukemia