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Gene therapy for BCR‐ABL+ human CML with dual phosphorylation resistant p27Kip1 and stable RNA interference using an EBV vector

BCR‐ABL‐mediated chronic myelogenous leukemia (CML) CD34+ cell proliferation mostly depends on the nucleo‐cytoplasmic ratio of the cyclin‐dependent kinase inhibitor p27. The ubiquitin‐ligase SCFSkp2 promotes degradation of phosphorylated p27 at T187 in the nucleus, resulting in G1/S progression of the cells. On the other hand, phosphatidylinositol‐3‐kinase (PI3K)‐directed T157 nuclear localization signal (NLS) phosphorylation results in cytoplasmic sequestration of p27, leading to abnormal integrin‐mediated proliferation of CD34+ CML cells.